\n \n\n \n \n \n \n \n \n Tuberculosis treatment-shortening.\n \n \n \n \n\n\n \n Singh, V.\n\n\n \n\n\n\n Drug Discovery Today, 29(5): 103955. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Tuberculosis$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{singh_tuberculosis_2024,\n\ttitle = {Tuberculosis treatment-shortening},\n\tvolume = {29},\n\tissn = {13596446},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1359644624000801},\n\tdoi = {10.1016/j.drudis.2024.103955},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-25},\n\tjournal = {Drug Discovery Today},\n\tauthor = {Singh, Vinayak},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {103955},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Influence of individuals’ determinants including vaccine type on cellular and humoral responses to SARS-CoV-2 vaccination.\n \n \n \n \n\n\n \n Chambers, E. S.; Cai, W.; Vivaldi, G.; Jolliffe, D. A.; Perdek, N.; Li, W.; Faustini, S. E.; Gibbons, J. M.; Pade, C.; Richter, A. G.; Coussens, A. K.; and Martineau, A. R.\n\n\n \n\n\n\n npj Vaccines, 9(1): 87. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Influence$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{chambers_influence_2024,\n\ttitle = {Influence of individuals’ determinants including vaccine type on cellular and humoral responses to {SARS}-{CoV}-2 vaccination},\n\tvolume = {9},\n\tissn = {2059-0105},\n\turl = {https://www.nature.com/articles/s41541-024-00878-0},\n\tdoi = {10.1038/s41541-024-00878-0},\n\tabstract = {Abstract \n            Vaccine development targeting SARS-CoV-2 in 2020 was of critical importance in reducing COVID-19 severity and mortality. In the U.K. during the initial roll-out most individuals either received two doses of Pfizer COVID-19 vaccine (BNT162b2) or the adenovirus-based vaccine from Oxford/AstraZeneca (ChAdOx1-nCoV-19). There are conflicting data as to the impact of age, sex and body habitus on cellular and humoral responses to vaccination, and most studies in this area have focused on determinants of mRNA vaccine immunogenicity. Here, we studied a cohort of participants in a population-based longitudinal study (COVIDENCE UK) to determine the influence of age, sex, body mass index (BMI) and pre-vaccination anti-Spike (anti-S) antibody status on vaccine-induced humoral and cellular immune responses to two doses of BNT162b2 or ChAdOx-n-CoV-19 vaccination. Younger age and pre-vaccination anti-S seropositivity were both associated with stronger antibody responses to vaccination. BNT162b2 generated higher neutralising and anti-S antibody titres to vaccination than ChAdOx1-nCoV-19, but cellular responses to the two vaccines were no different. Irrespective of vaccine type, increasing age was also associated with decreased frequency of cytokine double-positive CD4+T cells. Increasing BMI was associated with reduced frequency of SARS-CoV-2-specific TNF+CD8\\% T cells for both vaccines. Together, our findings demonstrate that increasing age and BMI are associated with attenuated cellular and humoral responses to SARS-CoV-2 vaccination. Whilst both vaccines induced T cell responses, BNT162b2 induced significantly elevated humoral immune response as compared to ChAdOx-n-CoV-19.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-25},\n\tjournal = {npj Vaccines},\n\tauthor = {Chambers, Emma S. and Cai, Weigang and Vivaldi, Giulia and Jolliffe, David A. and Perdek, Natalia and Li, Wenhao and Faustini, Sian E. and Gibbons, Joseph M. and Pade, Corinna and Richter, Alex G. and Coussens, Anna K. and Martineau, Adrian R.},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {87},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A first-in-class leucyl-tRNA synthetase inhibitor, ganfeborole, for rifampicin-susceptible tuberculosis: a phase 2a open-label, randomized trial.\n \n \n \n \n\n\n \n Diacon, A. H.; Barry, C. E.; Carlton, A.; Chen, R. Y.; Davies, M.; De Jager, V.; Fletcher, K.; Koh, G. C. K. W.; Kontsevaya, I.; Heyckendorf, J.; Lange, C.; Reimann, M.; Penman, S. L.; Scott, R.; Maher-Edwards, G.; Tiberi, S.; Vlasakakis, G.; Upton, C. M.; and Aguirre, D. B.\n\n\n \n\n\n\n Nature Medicine, 30(3): 896–904. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{diacon_first--class_2024,\n\ttitle = {A first-in-class leucyl-{tRNA} synthetase inhibitor, ganfeborole, for rifampicin-susceptible tuberculosis: a phase 2a open-label, randomized trial},\n\tvolume = {30},\n\tissn = {1078-8956, 1546-170X},\n\tshorttitle = {A first-in-class leucyl-{tRNA} synthetase inhibitor, ganfeborole, for rifampicin-susceptible tuberculosis},\n\turl = {https://www.nature.com/articles/s41591-024-02829-7},\n\tdoi = {10.1038/s41591-024-02829-7},\n\tabstract = {Abstract \n             \n              New tuberculosis treatments are needed to address drug resistance, lengthy treatment duration and adverse reactions of available agents. GSK3036656 (ganfeborole) is a first-in-class benzoxaborole inhibiting the \n              Mycobacterium tuberculosis \n              leucyl-tRNA synthetase. Here, in this phase 2a, single-center, open-label, randomized trial, we assessed early bactericidal activity (primary objective) and safety and pharmacokinetics (secondary objectives) of ganfeborole in participants with untreated, rifampicin-susceptible pulmonary tuberculosis. Overall, 75 males were treated with ganfeborole (1/5/15/30 mg) or standard of care (Rifafour e-275 or generic alternative) once daily for 14 days. We observed numerical reductions in daily sputum-derived colony-forming units from baseline in participants receiving 5, 15 and 30 mg once daily but not those receiving 1 mg ganfeborole. Adverse event rates were comparable across groups; all events were grade 1 or 2. In a participant subset, post hoc exploratory computational analysis of \n              18 \n              F-fluorodeoxyglucose positron emission tomography/computed tomography findings showed measurable treatment responses across several lesion types in those receiving ganfeborole 30 mg at day 14. Analysis of whole-blood transcriptional treatment response to ganfeborole 30 mg at day 14 revealed a strong association with neutrophil-dominated transcriptional modules. The demonstrated bactericidal activity and acceptable safety profile suggest that ganfeborole is a potential candidate for combination treatment of pulmonary tuberculosis. \n             \n             \n              ClinicalTrials.gov identifier: \n              NCT03557281 \n              .},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Nature Medicine},\n\tauthor = {Diacon, Andreas H. and Barry, Clifton E. and Carlton, Alex and Chen, Ray Y. and Davies, Matt and De Jager, Veronique and Fletcher, Kim and Koh, Gavin C. K. W. and Kontsevaya, Irina and Heyckendorf, Jan and Lange, Christoph and Reimann, Maja and Penman, Sophie L. and Scott, Rhona and Maher-Edwards, Gareth and Tiberi, Simon and Vlasakakis, Georgios and Upton, Caryn M. and Aguirre, David Barros},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {896--904},\n}\n\n\n\n

\n

\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Mycobacterial FtsEX-RipC interaction is required for normal growth and cell morphology in rifampicin and low ionic strength conditions.\n \n \n \n \n\n\n \n Samuels, V.; Mulelu, A. E.; Ndlovu, H.; and Marakalala, M. J.\n\n\n \n\n\n\n Microbiology Spectrum, 12(3): e02515–23. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Mycobacterial$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{samuels_mycobacterial_2024,\n\ttitle = {Mycobacterial {FtsEX}-{RipC} interaction is required for normal growth and cell morphology in rifampicin and low ionic strength conditions},\n\tvolume = {12},\n\tissn = {2165-0497},\n\turl = {https://journals.asm.org/doi/10.1128/spectrum.02515-23},\n\tdoi = {10.1128/spectrum.02515-23},\n\tabstract = {ABSTRACT \n \n \n \n Tuberculosis, a lung disease caused by \n Mycobacterium tuberculosis \n ( \n Mtb \n ), remains a major global health problem ranking as the second leading cause of death from a single infectious agent. One of the major factors contributing toward \n Mtb’s \n success as a pathogen is its unique cell wall and its ability to counteract various arms of the host’s immune response. A recent genome-scale study profiled a list of candidate genes that are predicted to be essential for \n Mtb \n survival of host-mediated responses. One candidate was FtsEX, a protein complex composed of an ATP-binding domain, FtsE, and a transmembrane domain, FtsX. FtsEX functions through interaction with a periplasmic hydrolase, RipC. Homologs of FtsEX exist in other bacteria and have been linked with playing a key role in regulating peptidoglycan hydrolysis during cell elongation and division. Here, we report on \n Mycobacterium smegmatis, \n FtsE, FtsX, and RipC and their protective roles in stressful conditions. We demonstrate that the individual genes of FtsEX complex and RipC are not essential for survival in normal growth conditions but conditionally essential in low-salt media and antibiotic-treated media. Growth defects in these conditions were characterized by short and bulgy cells as well as elongated filamentous cells. Our results suggest that FtsE, FtsX, and RipC are required for both normal cell elongation and division and ultimately for survival in stressful conditions. \n \n \n \n IMPORTANCE \n \n Mycobacterial cell growth and division are coordinated with regulated peptidoglycan hydrolysis. Understanding cell wall gene complexes that govern normal cell division and elongation will aid in the development of tools to disarm the ability of mycobacteria to survive immune-like and antibiotic stresses. We combined genetic analyses and scanning electron microscopy to analyze morphological changes of mycobacterial FtsEX and RipC mutants in stressful conditions. We demonstrate that FtsE, FtsX, FtsEX, and RipC are conditionally required for the survival of \n Mycobacterium smegmatis \n during rifampicin treatment and in low-salt conditions. Growth defects in these conditions were characterized by short and bulgy cells as well as elongated filamentous cells. We also show that the FtsEX-RipC interaction is essential for the survival of \n M. smegmatis \n in rifampicin. Our results suggest that FtsE, FtsX, and RipC are required for normal cell wall regulation and ultimately for survival in stressful conditions. \n \n \n , \n \n Mycobacterial cell growth and division are coordinated with regulated peptidoglycan hydrolysis. Understanding cell wall gene complexes that govern normal cell division and elongation will aid in the development of tools to disarm the ability of mycobacteria to survive immune-like and antibiotic stresses. We combined genetic analyses and scanning electron microscopy to analyze morphological changes of mycobacterial FtsEX and RipC mutants in stressful conditions. We demonstrate that FtsE, FtsX, FtsEX, and RipC are conditionally required for the survival of \n Mycobacterium smegmatis \n during rifampicin treatment and in low-salt conditions. Growth defects in these conditions were characterized by short and bulgy cells as well as elongated filamentous cells. We also show that the FtsEX-RipC interaction is essential for the survival of \n M. smegmatis \n in rifampicin. Our results suggest that FtsE, FtsX, and RipC are required for normal cell wall regulation and ultimately for survival in stressful conditions.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Microbiology Spectrum},\n\tauthor = {Samuels, Veneshley and Mulelu, Andani E. and Ndlovu, Hlumani and Marakalala, Mohlopheni J.},\n\teditor = {Unnikrishnan, Meera},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {e02515--23},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Tuberculosis, a lung disease caused by Mycobacterium tuberculosis ( Mtb ), remains a major global health problem ranking as the second leading cause of death from a single infectious agent. One of the major factors contributing toward Mtb’s success as a pathogen is its unique cell wall and its ability to counteract various arms of the host’s immune response. A recent genome-scale study profiled a list of candidate genes that are predicted to be essential for Mtb survival of host-mediated responses. One candidate was FtsEX, a protein complex composed of an ATP-binding domain, FtsE, and a transmembrane domain, FtsX. FtsEX functions through interaction with a periplasmic hydrolase, RipC. Homologs of FtsEX exist in other bacteria and have been linked with playing a key role in regulating peptidoglycan hydrolysis during cell elongation and division. Here, we report on Mycobacterium smegmatis, FtsE, FtsX, and RipC and their protective roles in stressful conditions. We demonstrate that the individual genes of FtsEX complex and RipC are not essential for survival in normal growth conditions but conditionally essential in low-salt media and antibiotic-treated media. Growth defects in these conditions were characterized by short and bulgy cells as well as elongated filamentous cells. Our results suggest that FtsE, FtsX, and RipC are required for both normal cell elongation and division and ultimately for survival in stressful conditions. IMPORTANCE Mycobacterial cell growth and division are coordinated with regulated peptidoglycan hydrolysis. Understanding cell wall gene complexes that govern normal cell division and elongation will aid in the development of tools to disarm the ability of mycobacteria to survive immune-like and antibiotic stresses. We combined genetic analyses and scanning electron microscopy to analyze morphological changes of mycobacterial FtsEX and RipC mutants in stressful conditions. We demonstrate that FtsE, FtsX, FtsEX, and RipC are conditionally required for the survival of Mycobacterium smegmatis during rifampicin treatment and in low-salt conditions. Growth defects in these conditions were characterized by short and bulgy cells as well as elongated filamentous cells. We also show that the FtsEX-RipC interaction is essential for the survival of M. smegmatis in rifampicin. Our results suggest that FtsE, FtsX, and RipC are required for normal cell wall regulation and ultimately for survival in stressful conditions. , Mycobacterial cell growth and division are coordinated with regulated peptidoglycan hydrolysis. Understanding cell wall gene complexes that govern normal cell division and elongation will aid in the development of tools to disarm the ability of mycobacteria to survive immune-like and antibiotic stresses. We combined genetic analyses and scanning electron microscopy to analyze morphological changes of mycobacterial FtsEX and RipC mutants in stressful conditions. We demonstrate that FtsE, FtsX, FtsEX, and RipC are conditionally required for the survival of Mycobacterium smegmatis during rifampicin treatment and in low-salt conditions. Growth defects in these conditions were characterized by short and bulgy cells as well as elongated filamentous cells. We also show that the FtsEX-RipC interaction is essential for the survival of M. smegmatis in rifampicin. Our results suggest that FtsE, FtsX, and RipC are required for normal cell wall regulation and ultimately for survival in stressful conditions.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Rapid dynamic changes of FL.2 variant: A case report of COVID-19 breakthrough infection.\n \n \n \n \n\n\n \n Choga, W. T.; Kurusa (Gasenna), G. K.; San, J. E.; Ookame, T.; Gobe, I.; Chand, M.; Phafane, B.; Seru, K.; Matshosi, P.; Zuze, B.; Ndlovu, N.; Matsuru, T.; Maruapula, D.; Bareng, O. T.; Macheke, K.; Kuate-Lere, L.; Tlale, L.; Lesetedi, O.; Tau, M.; Mbulawa, M. B.; Smith-Lawrence, P.; Matshaba, M.; Shapiro, R.; Makhema, J.; Martin, D. P.; De Oliveira, T.; Lessells, R. J.; Lockman, S.; Gaseitsiwe, S.; and Moyo, S.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 138: 91–96. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Rapid$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{choga_rapid_2024,\n\ttitle = {Rapid dynamic changes of {FL}.2 variant: {A} case report of {COVID}-19 breakthrough infection},\n\tvolume = {138},\n\tissn = {12019712},\n\tshorttitle = {Rapid dynamic changes of {FL}.2 variant},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971223007725},\n\tdoi = {10.1016/j.ijid.2023.11.011},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Choga, Wonderful T. and Kurusa (Gasenna), Gobuiwang Khilly and San, James Emmanuel and Ookame, Tidimalo and Gobe, Irene and Chand, Mohammed and Phafane, Badisa and Seru, Kedumetse and Matshosi, Patience and Zuze, Boitumelo and Ndlovu, Nokuthula and Matsuru, Teko and Maruapula, Dorcas and Bareng, Ontlametse T. and Macheke, Kutlo and Kuate-Lere, Lesego and Tlale, Labapotswe and Lesetedi, Onalethata and Tau, Modiri and Mbulawa, Mpaphi B. and Smith-Lawrence, Pamela and Matshaba, Mogomotsi and Shapiro, Roger and Makhema, Joseph and Martin, Darren P. and De Oliveira, Tulio and Lessells, Richard J. and Lockman, Shahin and Gaseitsiwe, Simani and Moyo, Sikhulile},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {91--96},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n The Genetic Architecture of Amygdala Nuclei.\n \n \n \n \n\n\n \n Mufford, M. S.; Van Der Meer, D.; Kaufmann, T.; Frei, O.; Ramesar, R.; Thompson, P. M.; Jahanshad, N.; Morey, R. A.; Andreassen, O. A.; Stein, D. J.; and Dalvie, S.\n\n\n \n\n\n\n Biological Psychiatry, 95(1): 72–84. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{mufford_genetic_2024,\n\ttitle = {The {Genetic} {Architecture} of {Amygdala} {Nuclei}},\n\tvolume = {95},\n\tissn = {00063223},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0006322323013951},\n\tdoi = {10.1016/j.biopsych.2023.06.022},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Biological Psychiatry},\n\tauthor = {Mufford, Mary S. and Van Der Meer, Dennis and Kaufmann, Tobias and Frei, Oleksandr and Ramesar, Raj and Thompson, Paul M. and Jahanshad, Neda and Morey, Rajendra A. and Andreassen, Ole A. and Stein, Dan J. and Dalvie, Shareefa},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {72--84},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Editorial: An outlook on urobiome: advances in understanding the role of urobiome in urological health and disease and its potential in biotherapeutics.\n \n \n \n \n\n\n \n Onywera, H.; Chambuso, R.; Benjamin, D. J.; Hilt, E. E.; and Thomas-White, K.\n\n\n \n\n\n\n Frontiers in Urology, 4: 1380340. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Editorial:$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{onywera_editorial_2024,\n\ttitle = {Editorial: {An} outlook on urobiome: advances in understanding the role of urobiome in urological health and disease and its potential in biotherapeutics},\n\tvolume = {4},\n\tissn = {2673-9828},\n\tshorttitle = {Editorial},\n\turl = {https://www.frontiersin.org/articles/10.3389/fruro.2024.1380340/full},\n\tdoi = {10.3389/fruro.2024.1380340},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Urology},\n\tauthor = {Onywera, Harris and Chambuso, Ramadhani and Benjamin, David J. and Hilt, Evann E. and Thomas-White, Krystal},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {1380340},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Development and validation of quantitative PCR assays for HIV-associated cryptococcal meningitis in sub-Saharan Africa: a diagnostic accuracy study.\n \n \n \n \n\n\n \n Mbangiwa, T.; Sturny-Leclère, A.; Lechiile, K.; Kajanga, C.; Boyer-Chammard, T.; Hoving, J. C; Leeme, T.; Moyo, M.; Youssouf, N.; Lawrence, D. S; Mwandumba, H.; Mosepele, M.; Harrison, T. S; Jarvis, J. N; Lortholary, O.; Alanio, A.; Goodall, J; Mawoko, N; Milburn, J; Mmipi, R; Muthoga, C; Ponatshego, P; Rulaganyang, I; Seatla, K; Tlhako, N; Tsholo, K; April, S; Bekiswa, A; Boloko, L; Bookholane, H; Crede, T; Davids, L; Goliath, R; Hlungulu, S; Hoffman, R; Kyepa, H; Masina, N; Maughan, D; Mnguni, T; Moosa, S; Morar, T; Mpalali, M; Naude, J; Oliphant, I; Sayed, S; Sebesho, L; Shey, M; Swanepoel, L; Chasweka, M; Chimang’anga, W; Chimphambano, T; Dziwani, E; Gondwe, E; Kadzilimbile, A; Kateta, S; Kossam, E; Kukacha, C; Lipenga, B; Ndaferankhande, J; Ndalama, M; Shah, R; Singini, A; Stott, K; Zambasa, A; Banda, T; Chikaonda, T; Chitulo, G; Chiwoko, L; Chome, N; Gwin, M; Kachitosi, T; Kamanga, B; Kazembe, M; Kumwenda, E; Kumwenda, M; Maya, C; Mhango, W; Mphande, C; Msumba, L; Munthali, T; Ngoma, D; Nicholas, S; Simwinga, L; Stambuli, A; Tegha, G; Zambezi, J; Ahimbisibwe, C; Akampurira, A; Alice, A; Cresswell, F; Gakuru, J; Kiiza, D; Kisembo, J; Kwizera, R; Kugonza, F; Laker, E; Luggya, T; Lule, A; Musubire, A; Muyise, R; Namujju, O; Ndyetukira, J; Nsangi, L; Okirwoth, M; Sadiq, A; Tadeo, K; Tukundane, A; Williams, D; Atwine, L; Buzaare, P; Collins, M; Emily, N; Inyakuwa, C; Kariisa, S; Mwesigye, J; Niwamanya, S; Rodgers, A; Rukundo, J; Rwomushana, I; Ssemusu, M; Stead, G; Boyd, K; Gondo, S; Kufa, P; Makaha, E; Moyo, C; Mtisi, T; Mudzingwa, S; Mwarumba, T; Zinyandu, T; Dromer, F; Johnstone, P; and Hafeez, S\n\n\n \n\n\n\n The Lancet Microbe, 5(3): e261–e271. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Development$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{mbangiwa_development_2024,\n\ttitle = {Development and validation of quantitative {PCR} assays for {HIV}-associated cryptococcal meningitis in sub-{Saharan} {Africa}: a diagnostic accuracy study},\n\tvolume = {5},\n\tissn = {26665247},\n\tshorttitle = {Development and validation of quantitative {PCR} assays for {HIV}-associated cryptococcal meningitis in sub-{Saharan} {Africa}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524723003622},\n\tdoi = {10.1016/S2666-5247(23)00362-2},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Mbangiwa, Tshepiso and Sturny-Leclère, Aude and Lechiile, Kwana and Kajanga, Cheusisime and Boyer-Chammard, Timothée and Hoving, Jennifer C and Leeme, Tshepo and Moyo, Melanie and Youssouf, Nabila and Lawrence, David S and Mwandumba, Henry and Mosepele, Mosepele and Harrison, Thomas S and Jarvis, Joseph N and Lortholary, Olivier and Alanio, Alexandre and Goodall, J and Mawoko, N and Milburn, J and Mmipi, R and Muthoga, C and Ponatshego, P and Rulaganyang, I and Seatla, K and Tlhako, N and Tsholo, K and April, S and Bekiswa, A and Boloko, L and Bookholane, H and Crede, T and Davids, L and Goliath, R and Hlungulu, S and Hoffman, R and Kyepa, H and Masina, N and Maughan, D and Mnguni, T and Moosa, S and Morar, T and Mpalali, M and Naude, J and Oliphant, I and Sayed, S and Sebesho, L and Shey, M and Swanepoel, L and Chasweka, M and Chimang’anga, W and Chimphambano, T and Dziwani, E and Gondwe, E and Kadzilimbile, A and Kateta, S and Kossam, E and Kukacha, C and Lipenga, B and Ndaferankhande, J and Ndalama, M and Shah, R and Singini, A and Stott, K and Zambasa, A and Banda, T and Chikaonda, T and Chitulo, G and Chiwoko, L and Chome, N and Gwin, M and Kachitosi, T and Kamanga, B and Kazembe, M and Kumwenda, E and Kumwenda, M and Maya, C and Mhango, W and Mphande, C and Msumba, L and Munthali, T and Ngoma, D and Nicholas, S and Simwinga, L and Stambuli, A and Tegha, G and Zambezi, J and Ahimbisibwe, C and Akampurira, A and Alice, A and Cresswell, F and Gakuru, J and Kiiza, D and Kisembo, J and Kwizera, R and Kugonza, F and Laker, E and Luggya, T and Lule, A and Musubire, A and Muyise, R and Namujju, O and Ndyetukira, J and Nsangi, L and Okirwoth, M and Sadiq, A and Tadeo, K and Tukundane, A and Williams, D and Atwine, L and Buzaare, P and Collins, M and Emily, N and Inyakuwa, C and Kariisa, S and Mwesigye, J and Niwamanya, S and Rodgers, A and Rukundo, J and Rwomushana, I and Ssemusu, M and Stead, G and Boyd, K and Gondo, S and Kufa, P and Makaha, E and Moyo, C and Mtisi, T and Mudzingwa, S and Mwarumba, T and Zinyandu, T and Dromer, F and Johnstone, P and Hafeez, S},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {e261--e271},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n HIV latency potential may be influenced by intra-subtype genetic differences in the viral long-terminal repeat.\n \n \n \n \n\n\n \n Doolabh, D. S.; Selhorst, P.; Williamson, C.; Chopera, D.; and Abrahams, M.\n\n\n \n\n\n\n Frontiers in Virology, 4: 1393475. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"HIV$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{doolabh_hiv_2024,\n\ttitle = {{HIV} latency potential may be influenced by intra-subtype genetic differences in the viral long-terminal repeat},\n\tvolume = {4},\n\tissn = {2673-818X},\n\turl = {https://www.frontiersin.org/articles/10.3389/fviro.2024.1393475/full},\n\tdoi = {10.3389/fviro.2024.1393475},\n\tabstract = {Introduction \n              Elucidation of mechanisms that drive HIV latency is essential to identifying cure strategies. While host mechanisms associated with viral persistence on antiretroviral therapy (ART) have been well studied, less is known about the viral properties that influence latency. The viral promoter element, the 5’ long terminal repeat (LTR), has been shown to affect the number of latently infected cells shortly after infection. Here we investigated the role of subtype C LTR genotypic variation on the establishment of latency in a dual reporter HIV-1 infection model. \n             \n             \n              Methods \n               \n                The LTR U3 and R regions from 11 women with acute/early subtype C HIV infection were cloned into the dual reporter pRGH plasmid. Latency potential was calculated based on the expression of fluorescent reporter genes in Jurkat E6–1 cells measured by flow cytometry as the proportion of latent (mCherry \n                +ve \n                cells)/proportion of active (eGFP \n                +ve \n                mCherry \n                +ve \n                cells) infection. Reversal of latency was performed using PMA/Ionomycin stimulation 24 hours before fixing of cells. LTR transcriptional capacity, in the presence and absence of a heterologous subtype C Tat, was measured for the same LTRs cloned into a pGL4.10 luciferase expression vector following transfection of HEK293T cells. \n               \n             \n             \n              Results \n              The majority of proviruses were latent at day 8 post-infection, yet the proportion of latently infected cells varied significantly across participants. We observed a median latent:active infection ratio of 1.79 (range 0.86–2.83) across LTRs with the hierarchy of latency potential remaining consistent across repeat experiments. The median latent:active infection ratio decreased by a median of 3-fold following PMA/Ionomycin stimulation to 0.55 (range 0.46–0.78) indicating that a proportion of latently infected cells could produce viral proteins upon activation. Latency potential did not correlate with LTR transcriptional capacity. \n             \n             \n              Conclusions \n              We found intra-subtype level differences in the latency potential of LTRs from South African women independent of their transcriptional capacity, suggesting that HIV-1 LTRs have intrinsic properties that influence the proportion of latently infected cells shortly after infection. The inability to reactivate viral expression in all latently infected cells supports the complex nature of mechanisms driving latency and the need for continued advancements in methods used to study these mechanisms.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Virology},\n\tauthor = {Doolabh, Deelan Sudhir and Selhorst, Philippe and Williamson, Carolyn and Chopera, Denis and Abrahams, Melissa-Rose},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {1393475},\n}\n\n\n\n

\n

\n\n\n

\n Introduction Elucidation of mechanisms that drive HIV latency is essential to identifying cure strategies. While host mechanisms associated with viral persistence on antiretroviral therapy (ART) have been well studied, less is known about the viral properties that influence latency. The viral promoter element, the 5’ long terminal repeat (LTR), has been shown to affect the number of latently infected cells shortly after infection. Here we investigated the role of subtype C LTR genotypic variation on the establishment of latency in a dual reporter HIV-1 infection model. Methods The LTR U3 and R regions from 11 women with acute/early subtype C HIV infection were cloned into the dual reporter pRGH plasmid. Latency potential was calculated based on the expression of fluorescent reporter genes in Jurkat E6–1 cells measured by flow cytometry as the proportion of latent (mCherry +ve cells)/proportion of active (eGFP +ve mCherry +ve cells) infection. Reversal of latency was performed using PMA/Ionomycin stimulation 24 hours before fixing of cells. LTR transcriptional capacity, in the presence and absence of a heterologous subtype C Tat, was measured for the same LTRs cloned into a pGL4.10 luciferase expression vector following transfection of HEK293T cells. Results The majority of proviruses were latent at day 8 post-infection, yet the proportion of latently infected cells varied significantly across participants. We observed a median latent:active infection ratio of 1.79 (range 0.86–2.83) across LTRs with the hierarchy of latency potential remaining consistent across repeat experiments. The median latent:active infection ratio decreased by a median of 3-fold following PMA/Ionomycin stimulation to 0.55 (range 0.46–0.78) indicating that a proportion of latently infected cells could produce viral proteins upon activation. Latency potential did not correlate with LTR transcriptional capacity. Conclusions We found intra-subtype level differences in the latency potential of LTRs from South African women independent of their transcriptional capacity, suggesting that HIV-1 LTRs have intrinsic properties that influence the proportion of latently infected cells shortly after infection. The inability to reactivate viral expression in all latently infected cells supports the complex nature of mechanisms driving latency and the need for continued advancements in methods used to study these mechanisms.\n

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\n \n\n \n \n \n \n \n \n Exploring perceptions of gender roles amongst sexually active adolescents in rural KwaZulu-Natal, South Africa.\n \n \n \n \n\n\n \n Marshall, B.; Mehou-Loko, C.; Mazibuko, S.; Madladla, M.; Knight, L.; and Humphries, H.\n\n\n \n\n\n\n PLOS ONE, 19(1): e0296806. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Exploring$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{marshall_exploring_2024,\n\ttitle = {Exploring perceptions of gender roles amongst sexually active adolescents in rural {KwaZulu}-{Natal}, {South} {Africa}},\n\tvolume = {19},\n\tissn = {1932-6203},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0296806},\n\tdoi = {10.1371/journal.pone.0296806},\n\tabstract = {Traditional gender and social norms reinforce asymmetrical power relations, increase the risk of experiencing gender-based violence and mediate poor engagement with sexual and reproductive health services. This study explored gender norms and expectations amongst cisgender adolescents in rural KwaZulu-Natal, South Africa. A purposive sample of 29 adolescents aged 16–19 years old were enrolled as part of a longitudinal qualitative study. The current analysis reports on the first round of in-depth interviews, which focused on the role of men and women in their community. A theoretically informed thematic analysis identified three broad themes: 1) \n              Adolescent interpretation and understanding of gender identity \n              , 2) \n              Gendered essentialism and Gender roles \n              (two sub-themes: Young men: Power through providing, and Young women: The domestication process which highlighted that gender roles were defined by being the provider for men, and the successful fulfilment of traditional domestic behaviours amongst women), 3) \n              Gender and fertility \n              highlighted how participants highly valued fertility as affirming of manhood/womanhood. These norms reinforce gender roles that maintain asymmetrical power relations, carrying them over into adulthood. The subtle social pressure to prove fertility could have unintended consequences for driving teenage pregnancy. Structural, gender-based interventions emphasising positive gender-role development in early childhood are needed.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Marshall, Brett and Mehou-Loko, Celia and Mazibuko, Sindisiwe and Madladla, Makhosazana and Knight, Lucia and Humphries, Hilton},\n\teditor = {Bolarinwa, Obasanjo Afolabi},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {e0296806},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Women in STEM becoming independent: The journey to independence is an immensely gratifying odyssey.\n \n \n \n \n\n\n \n Campbell, C.; Funk, M. C.; Hattori, Y.; Hu, W.; Jeschke, J.; Lau, C. M.; Ling, G. S.; Liu, S.; Lloréns-Rico, V.; and Nemes, E.\n\n\n \n\n\n\n Journal of Experimental Medicine, 221(7): e20240842. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Women$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{campbell_women_2024,\n\ttitle = {Women in {STEM} becoming independent: {The} journey to independence is an immensely gratifying odyssey},\n\tvolume = {221},\n\tissn = {0022-1007, 1540-9538},\n\tshorttitle = {Women in {STEM} becoming independent},\n\turl = {https://rupress.org/jem/article/221/7/e20240842/276795/Women-in-STEM-becoming-independent-The-journey-to},\n\tdoi = {10.1084/jem.20240842},\n\tabstract = {This year at JEM, we are highlighting women in science by sharing their stories and amplifying their voices. In this Viewpoint, we hear from a cross section of women, across multiple research fields, discussing their science and the process of setting up a lab as an independent researcher.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Experimental Medicine},\n\tauthor = {Campbell, Clarissa and Funk, Maja C. and Hattori, Yuki and Hu, Wei and Jeschke, Jana and Lau, Colleen M. and Ling, Guang Sheng and Liu, Siqi and Lloréns-Rico, Verónica and Nemes, Elisa},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {e20240842},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Negative clinic experiences as a barrier to care for people with HIV and their impact on patient preferences for intervention support: a qualitative study in Cape Town, South Africa.\n \n \n \n \n\n\n \n Killian, C.; West, R. L.; Orrell, C.; Gifford, A.; Haberer, J. E.; Halim, N.; Jennings, L.; Berkowitz, N.; Fourie, S.; and Sabin, L.\n\n\n \n\n\n\n AIDS Care, 36(9): 1222–1231. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Negative$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{killian_negative_2024,\n\ttitle = {Negative clinic experiences as a barrier to care for people with {HIV} and their impact on patient preferences for intervention support: a qualitative study in {Cape} {Town}, {South} {Africa}},\n\tvolume = {36},\n\tissn = {0954-0121, 1360-0451},\n\tshorttitle = {Negative clinic experiences as a barrier to care for people with {HIV} and their impact on patient preferences for intervention support},\n\turl = {https://www.tandfonline.com/doi/full/10.1080/09540121.2024.2346255},\n\tdoi = {10.1080/09540121.2024.2346255},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {AIDS Care},\n\tauthor = {Killian, Clare and West, Rebecca L. and Orrell, Catherine and Gifford, Allen and Haberer, Jessica E. and Halim, Nafisa and Jennings, Lauren and Berkowitz, Natacha and Fourie, Stephanie and Sabin, Lora},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {1222--1231},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The prevalence of pulmonary hypertension in post-tuberculosis and active tuberculosis populations: a systematic review and meta-analysis.\n \n \n \n \n\n\n \n Van Heerden, J. K.; Louw, E. H.; Thienemann, F.; Engel, M. E.; and Allwood, B. W.\n\n\n \n\n\n\n European Respiratory Review, 33(171): 230154. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{van_heerden_prevalence_2024,\n\ttitle = {The prevalence of pulmonary hypertension in post-tuberculosis and active tuberculosis populations: a systematic review and meta-analysis},\n\tvolume = {33},\n\tissn = {0905-9180, 1600-0617},\n\tshorttitle = {The prevalence of pulmonary hypertension in post-tuberculosis and active tuberculosis populations},\n\turl = {https://publications.ersnet.org/lookup/doi/10.1183/16000617.0154-2023},\n\tdoi = {10.1183/16000617.0154-2023},\n\tabstract = {Background: \n              The prevalence of tuberculosis (TB)-associated pulmonary hypertension (PH) has not previously been quantified, resulting in an underappreciated burden of disease. We aimed to estimate the prevalence of PH in post-TB and active TB populations. \n             \n             \n              Methods: \n              In this systematic review and meta-analysis, we searched PubMed/Medline, Cochrane Library, EBSCOhost, Scopus, African Journals Online and Google Scholar, with no language restriction, for available literature published after 1950. Eligible studies described adult participants (≥16 years), with documented evidence of active or prior TB, diagnosed with PH. Study quality was assessed using a risk of bias tool specifically developed for prevalence studies. Aggregate prevalence estimates with 95\\% confidence intervals were synthesised using a random-effects meta-analysis model, incorporating the Freeman–Tukey transformation. Subgroup analysis was conducted to ascertain prevalence estimates in specific patient populations. \n             \n             \n              Results: \n               \n                We identified 1452 unique records, of which 34 met our inclusion criteria. 23 studies, with an acceptable risk of bias and where PH was diagnosed at right heart catheterisation or echocardiography, were included in the meta-analysis. In post-TB studies (14/23), the prevalence of PH was 67.0\\% (95\\% CI 50.8–81.4) in patients with chronic respiratory failure, 42.4\\% (95\\% CI 31.3–54.0) in hospitalised or symptomatic patients and 6.3\\% (95\\% CI 2.3–11.8) in nonhealthcare-seeking outpatients (I \n                2 \n                =96\\%). There was a lower estimated prevalence of PH in studies of populations with active TB (9.4\\%, 95\\% CI 6.3–13.0), I \n                2 \n                =84\\%). \n               \n             \n             \n              Conclusion: \n              Our results highlight the significant burden of PH in post-TB and active TB populations. We emphasise the need for increased recognition of TB-associated PH and additional high-quality prevalence data.},\n\tlanguage = {en},\n\tnumber = {171},\n\turldate = {2025-06-24},\n\tjournal = {European Respiratory Review},\n\tauthor = {Van Heerden, Jennifer K. and Louw, Elizabeth H. and Thienemann, Friedrich and Engel, Mark E. and Allwood, Brian W.},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {230154},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Slicing through the challenge of maintaining Pneumocystis in the laboratory.\n \n \n \n \n\n\n \n Nev, O. A.; Duvenage, L.; Brown, A. J. P.; Dangarembizi, R.; and Hoving, J. C.\n\n\n \n\n\n\n mBio, 15(3): e03277–23. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Slicing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{nev_slicing_2024,\n\ttitle = {Slicing through the challenge of maintaining \\textit{{Pneumocystis}} in the laboratory},\n\tvolume = {15},\n\tissn = {2150-7511},\n\turl = {https://journals.asm.org/doi/10.1128/mbio.03277-23},\n\tdoi = {10.1128/mbio.03277-23},\n\tabstract = {ABSTRACT \n             \n               \n               \n                Pneumocystis jirovecii \n                is a major fungal pathogen of humans that causes life-threatening lung infections in immunocompromised individuals. Despite its huge global impact upon human health, our understanding of the pathobiology of this deadly fungus remains extremely limited, largely because it is not yet possible to cultivate \n                Pneumocystis in vitro, \n                independently of the host. However, a recent paper by Munyonho et al. offers a major step forward (F. T. Munyonho, R. D. Clark, D. Lin, M. S. Khatun, et al., 2023, mBio 15:e01464-23, \n                https://doi.org/10.1128/mbio.01464-23 \n                ). They show that it is possible to maintain both the trophozoite and cyst forms of the mouse pathogen, \n                Pneumocystis murina, \n                in precision-cut lung slices for several weeks. Furthermore, they demonstrate that this offers the exciting opportunity to examine potential virulence factors such as possible biofilm formation as well as antifungal drug responses in the lung.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {mBio},\n\tauthor = {Nev, Olga A. and Duvenage, Lucian and Brown, Alistair J. P. and Dangarembizi, Rachael and Hoving, Jennifer Claire},\n\teditor = {Heitman, Joseph},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {e03277--23},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n HLA-E/Mtb specific CD4+ and CD8+ T cells have a memory phenotype in individuals with TB infection.\n \n \n \n \n\n\n \n Voogd, L.; Riou, C.; Scriba, T. J.; Van Wolfswinkel, M.; Van Meijgaarden, K. E.; Franken, K. L. M. C.; Wilkinson, R. J.; Ottenhoff, T. H. M.; and Joosten, S. A.\n\n\n \n\n\n\n Frontiers in Immunology, 15: 1505329. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"HLA-E/Mtb$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{voogd_hla-emtb_2024,\n\ttitle = {{HLA}-{E}/{Mtb} specific {CD4}+ and {CD8}+ {T} cells have a memory phenotype in individuals with {TB} infection},\n\tvolume = {15},\n\tissn = {1664-3224},\n\turl = {https://www.frontiersin.org/articles/10.3389/fimmu.2024.1505329/full},\n\tdoi = {10.3389/fimmu.2024.1505329},\n\tabstract = {Introduction \n               \n                Tuberculosis (TB) is the deadliest infectious disease worldwide and novel vaccines are urgently needed. HLA-E is a virtually monomorphic antigen presentation molecule and is not downregulated upon HIV co-infection. HLA-E restricted \n                Mtb \n                specific CD8 \n                + \n                T cells are present in the circulation of individuals with active TB (aTB) and \n                Mtb \n                infection (TBI) with or without HIV co-infection, making HLA-E restricted T cells interesting vaccination targets for TB. \n               \n             \n             \n              Methods \n               \n                Here, we performed in-depth phenotyping of HLA-E/ \n                Mtb \n                specific and total T cell populations in individuals with TBI and in individuals with aTB or TBI and HIV using HLA-E/ \n                Mtb \n                tetramers. \n               \n             \n             \n              Results and Discussion \n               \n                We show that HIV co-infection is the main driver in changing the memory distribution of HLA-E/ \n                Mtb \n                specific CD4 \n                + \n                and CD8 \n                + \n                T cell subsets. HLA-E/ \n                Mtb \n                specific CD4 \n                + \n                and CD8 \n                + \n                T cells were found to circulate with comparable frequencies in all individuals and displayed expression of KLRG1, PD-1 and 2B4 similar to that of total T cells. The presence of HLA-E/ \n                Mtb \n                specific T cells in individuals with aTB and TBI highlights the potential of HLA-E as a vaccine target for TB.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Immunology},\n\tauthor = {Voogd, Linda and Riou, Catherine and Scriba, Thomas J. and Van Wolfswinkel, Marjolein and Van Meijgaarden, Krista E. and Franken, Kees L. M. C. and Wilkinson, Robert J. and Ottenhoff, Tom H. M. and Joosten, Simone A.},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {1505329},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Protective efficacy of a plant-produced beta variant rSARS-CoV-2 VLP vaccine in golden Syrian hamsters.\n \n \n \n \n\n\n \n Lemmer, Y.; Chapman, R.; Abolnik, C.; Smith, T.; Schäfer, G.; Hermanus, T.; Du Preez, I.; Goosen, K.; Sepotokele, K. M.; Gers, S.; Suliman, T.; Preiser, W.; Shaw, M. L.; Roth, R.; Truyts, A.; Chipangura, J.; Magwaza, M.; Mahanjana, O.; Moore, P. L.; and O'Kennedy, M. M.\n\n\n \n\n\n\n Vaccine, 42(4): 738–744. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Protective$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{lemmer_protective_2024,\n\ttitle = {Protective efficacy of a plant-produced beta variant {rSARS}-{CoV}-2 {VLP} vaccine in golden {Syrian} hamsters},\n\tvolume = {42},\n\tissn = {0264410X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0264410X24000367},\n\tdoi = {10.1016/j.vaccine.2024.01.036},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {Vaccine},\n\tauthor = {Lemmer, Yolandy and Chapman, Ros and Abolnik, Celia and Smith, Tanja and Schäfer, Georgia and Hermanus, Tandile and Du Preez, Ilse and Goosen, Kruger and Sepotokele, Kamogelo M. and Gers, Sophette and Suliman, Tasnim and Preiser, Wolfgang and Shaw, Megan L. and Roth, Robyn and Truyts, Alma and Chipangura, John and Magwaza, Martin and Mahanjana, Osborn and Moore, Penny L. and O'Kennedy, Martha M.},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {738--744},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Webinar report: stakeholder perspectives on informed consent for the use of genomic data by commercial entities.\n \n \n \n \n\n\n \n Schultz, B.; Agamah, F. E; Ewuoso, C.; Madden, E. B; Troyer, J.; Skelton, M.; and Mwaka, E.\n\n\n \n\n\n\n Journal of Medical Ethics, 50(1): 57–61. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Webinar$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{schultz_webinar_2024,\n\ttitle = {Webinar report: stakeholder perspectives on informed consent for the use of genomic data by commercial entities},\n\tvolume = {50},\n\tissn = {0306-6800, 1473-4257},\n\tshorttitle = {Webinar report},\n\turl = {https://jme.bmj.com/lookup/doi/10.1136/jme-2022-108650},\n\tdoi = {10.1136/jme-2022-108650},\n\tabstract = {In July 2020, the H3Africa Ethics and Community Engagement (E\\&CE) Working Group organised a webinar with ethics committee members and biomedical researchers from various African institutions throughout the Continent to discuss the issue of whether and how biological samples for scientific research may be accessed by commercial entities when broad consents obtained for the samples are silent. 128 people including Research Ethics Committee members (10), H3Africa researchers (46) including members of the E\\&CE working group, biomedical researchers not associated with H3Africa (27), representatives from the National Institutes of Health (16) and 10 other participants attended the webinar and shared their views. Several major themes emerged during the webinar, with the topics of broad versus explicit informed consent, defining commercial use, legacy samples and benefit sharing prevailing in the discussion. This report describes the consensus concerns and recommendations raised during the meeting and will be informative for future research on ethical considerations for genomic research in the African research context.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Medical Ethics},\n\tauthor = {Schultz, Baergen and Agamah, Francis E and Ewuoso, Cornelius and Madden, Ebony B and Troyer, Jennifer and Skelton, Michelle and Mwaka, Erisa},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {57--61},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Minimising the threat of bedaquiline-resistant tuberculosis: better diagnosis as prevention.\n \n \n \n \n\n\n \n Zemanay, W.; and Cox, H.\n\n\n \n\n\n\n The Lancet Infectious Diseases, 24(3): 226–228. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Minimising$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{zemanay_minimising_2024,\n\ttitle = {Minimising the threat of bedaquiline-resistant tuberculosis: better diagnosis as prevention},\n\tvolume = {24},\n\tissn = {14733099},\n\tshorttitle = {Minimising the threat of bedaquiline-resistant tuberculosis},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1473309923005509},\n\tdoi = {10.1016/S1473-3099(23)00550-9},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Infectious Diseases},\n\tauthor = {Zemanay, Widaad and Cox, Helen},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {226--228},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Triglyceride-glucose index, low-density lipoprotein levels, and cardiovascular outcomes in chronic stable cardiovascular disease: results from the ONTARGET and TRANSCEND trials.\n \n \n \n \n\n\n \n Haring, B.; Schumacher, H.; Mancia, G.; Teo, K. K; Lonn, E. M; Mahfoud, F.; Schmieder, R.; Mann, J. F E; Sliwa, K.; Yusuf, S.; and Böhm, M.\n\n\n \n\n\n\n European Journal of Preventive Cardiology, 31(3): 311–319. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Triglyceride-glucose$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{haring_triglyceride-glucose_2024,\n\ttitle = {Triglyceride-glucose index, low-density lipoprotein levels, and cardiovascular outcomes in chronic stable cardiovascular disease: results from the {ONTARGET} and {TRANSCEND} trials},\n\tvolume = {31},\n\tcopyright = {https://academic.oup.com/pages/standard-publication-reuse-rights},\n\tissn = {2047-4873, 2047-4881},\n\tshorttitle = {Triglyceride-glucose index, low-density lipoprotein levels, and cardiovascular outcomes in chronic stable cardiovascular disease},\n\turl = {https://academic.oup.com/eurjpc/article/31/3/311/7331252},\n\tdoi = {10.1093/eurjpc/zwad340},\n\tabstract = {Abstract \n             \n              Aims \n              The triglyceride-glucose index (TyG) has been proposed as an alternative to insulin resistance and as a predictor of cardiovascular outcomes. Little is known on its role in chronic stable cardiovascular disease and its predictive power at controlled low density lipoprotein (LDL) levels. \n             \n             \n              Methods and results \n              Our study population consisted of 29 960 participants in the ONTARGET and TRANSCEND trials that enrolled patients with known atherosclerotic disease. Triglycerides and glucose were measured at baseline. TyG was calculated as the logarithmized product of fasting triglycerides and glucose divided by 2. The primary endpoint of both trials was a composite of cardiovascular death, myocardial infarction, stroke, or hospitalization for heart failure. The secondary endpoint was all-cause death and the components of the primary endpoint. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95\\% confidence intervals (CI) with extensive covariate adjustment for demographic, medical history, and lifestyle factors. During a mean follow-up of 4.3 years, 4895 primary endpoints and 3571 all-cause deaths occurred. In fully adjusted models, individuals in the highest compared to the lowest quartile of the TyG index were at higher risk for the primary endpoint (HR 1.14; 95\\% CI 1.05–1.25) and for myocardial infarction (HR 1.30; 95\\% CI 1.11–1.53). A higher TyG index did not associate with the primary endpoint in individuals with LDL levels \\&lt; 100 mg/dL. \n             \n             \n              Conclusion \n              A higher TyG index is associated with a modestly increased cardiovascular risk in chronic stable cardiovascular disease. This association is largely attenuated when LDL levels are controlled. \n             \n             \n              Registration \n              www.clinicaltrials.gov: NCT00153101},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {European Journal of Preventive Cardiology},\n\tauthor = {Haring, Bernhard and Schumacher, Helmut and Mancia, Giuseppe and Teo, Koon K and Lonn, Eva M and Mahfoud, Felix and Schmieder, Roland and Mann, Johannes F E and Sliwa, Karen and Yusuf, Salim and Böhm, Michael},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {311--319},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Relationship Between Tenofovir Diphosphate Concentrations in Dried Blood Spots and Virological Outcomes After Initiating Tenofovir–Lamivudine–Dolutegravir as First-Line or Second-Line Antiretroviral Therapy.\n \n \n \n \n\n\n \n Van Heerden, J. K.; Meintjes, G.; Barr, D.; Zhao, Y.; Griesel, R.; Keene, C. M.; Wiesner, L.; Galileya, L. T.; Denti, P.; and Maartens, G.\n\n\n \n\n\n\n JAIDS Journal of Acquired Immune Deficiency Syndromes, 95(3): 260–267. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Relationship$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{van_heerden_relationship_2024,\n\ttitle = {Relationship {Between} {Tenofovir} {Diphosphate} {Concentrations} in {Dried} {Blood} {Spots} and {Virological} {Outcomes} {After} {Initiating} {Tenofovir}–{Lamivudine}–{Dolutegravir} as {First}-{Line} or {Second}-{Line} {Antiretroviral} {Therapy}},\n\tvolume = {95},\n\tissn = {1525-4135},\n\turl = {https://journals.lww.com/10.1097/QAI.0000000000003341},\n\tdoi = {10.1097/QAI.0000000000003341},\n\tabstract = {Background: \n              Tenofovir diphosphate (TFV-DP) concentration in dried blood spots is a marker of long-term adherence. We investigated the relationship between TFV-DP concentrations and virological outcomes in participants initiating tenofovir–lamivudine–dolutegravir (TLD) as first-line or second-line antiretroviral therapy. \n             \n             \n              Setting: \n              Three primary care clinics in Khayelitsha, Cape Town, South Africa. \n             \n             \n              Methods: \n              We conducted a post hoc analysis of 2 randomized controlled trials of participants initiating TLD. TFV-DP concentrations and viral loads were measured at 12, 24, and 48 weeks. Multivariable logistic regression was performed to assess the association with virological suppression ({\\textless}50 copies/mL) per natural logarithm increase in TFV-DP concentration. Generalized estimating equations with logit link were used to assess associations with virological rebound. The Akaike Information Criterion and Quasi-likelihood Information Criteria were used to compare models built on continuous TFV-DP data to 4 previously defined concentration categories. \n             \n             \n              Results: \n              We included 294 participants in the analysis, 188 (64\\%) of whom initiated TLD as second-line therapy. Adjusted odds ratios (95\\% CIs) of virological suppression were 2.12 (1.23, 3.75), 3.11 (1.84, 5.65), and 4.69 (2.81, 8.68) per natural logarithm increase in TFV-DP concentration at weeks 12, 24, and 48, respectively. In participants with virological suppression at week 12, the adjusted odds ratio for remaining virologically suppressed was 3.63 (95\\% CI: 2.21 to 5.69) per natural logarithm increase in TFV-DP concentration. Models using continuous TFV-DP data had lower Akaike Information Criterion and Quasi-likelihood Information Criteria values than those using categorical data for predicting virological outcomes. \n             \n             \n              Conclusion: \n              TFV-DP concentrations in dried blood spots exhibit a dose–response relationship with viral load. Analyzing TFV-DP concentrations as continuous variables rather than conventional categorization may be appropriate.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},\n\tauthor = {Van Heerden, Jennifer Kate and Meintjes, Graeme and Barr, David and Zhao, Ying and Griesel, Rulan and Keene, Claire Marriott and Wiesner, Lubbe and Galileya, Lufina Tsirizani and Denti, Paolo and Maartens, Gary},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {260--267},\n}\n\n\n\n

\n

\n\n\n

\n Background: Tenofovir diphosphate (TFV-DP) concentration in dried blood spots is a marker of long-term adherence. We investigated the relationship between TFV-DP concentrations and virological outcomes in participants initiating tenofovir–lamivudine–dolutegravir (TLD) as first-line or second-line antiretroviral therapy. Setting: Three primary care clinics in Khayelitsha, Cape Town, South Africa. Methods: We conducted a post hoc analysis of 2 randomized controlled trials of participants initiating TLD. TFV-DP concentrations and viral loads were measured at 12, 24, and 48 weeks. Multivariable logistic regression was performed to assess the association with virological suppression (\\textless50 copies/mL) per natural logarithm increase in TFV-DP concentration. Generalized estimating equations with logit link were used to assess associations with virological rebound. The Akaike Information Criterion and Quasi-likelihood Information Criteria were used to compare models built on continuous TFV-DP data to 4 previously defined concentration categories. Results: We included 294 participants in the analysis, 188 (64%) of whom initiated TLD as second-line therapy. Adjusted odds ratios (95% CIs) of virological suppression were 2.12 (1.23, 3.75), 3.11 (1.84, 5.65), and 4.69 (2.81, 8.68) per natural logarithm increase in TFV-DP concentration at weeks 12, 24, and 48, respectively. In participants with virological suppression at week 12, the adjusted odds ratio for remaining virologically suppressed was 3.63 (95% CI: 2.21 to 5.69) per natural logarithm increase in TFV-DP concentration. Models using continuous TFV-DP data had lower Akaike Information Criterion and Quasi-likelihood Information Criteria values than those using categorical data for predicting virological outcomes. Conclusion: TFV-DP concentrations in dried blood spots exhibit a dose–response relationship with viral load. Analyzing TFV-DP concentrations as continuous variables rather than conventional categorization may be appropriate.\n

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\n \n\n \n \n \n \n \n \n OMIP‐101: 27‐color flow cytometry panel for immunophenotyping of major leukocyte populations in fixed whole blood.\n \n \n \n \n\n\n \n Imbratta, C.; Reid, T. D.; Toefy, A.; Scriba, T. J.; and Nemes, E.\n\n\n \n\n\n\n Cytometry Part A, 105(3): 165–170. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"OMIP‐101:$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{imbratta_omip101_2024,\n\ttitle = {{OMIP}‐101: 27‐color flow cytometry panel for immunophenotyping of major leukocyte populations in fixed whole blood},\n\tvolume = {105},\n\tissn = {1552-4922, 1552-4930},\n\tshorttitle = {{OMIP}‐101},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/cyto.a.24827},\n\tdoi = {10.1002/cyto.a.24827},\n\tabstract = {Abstract \n            This 27‐color flow cytometry antibody panel allows broad immune‐profiling of major leukocyte subsets in human whole blood (WB). It includes lineage markers to identify myeloid and lymphoid cell populations including granulocytes, monocytes, myeloid dendritic cells (mDCs), natural killer (NK) cells, NKT‐like cells, B cells, conventional CD4 and CD8 T cells, γδ T cells, mucosa‐associated invariant T (MAIT) cells and innate lymphoid cells (ILC). To further characterize each of these populations, markers defining stages of cell differentiation (CCR7, CD27, CD45RA, CD127, CD57), cytotoxic potential (perforin, granzyme B) and cell activation/proliferation (HLA‐DR, CD38, Ki‐67) were included. This panel was developed for quantifying absolute counts and phenotyping major leukocyte populations in cryopreserved, fixed WB collected from participants enrolled in large multi‐site tuberculosis (TB) vaccine clinical trials. This antibody panel can be applied to profile major leukocyte subsets in other sample types such as fresh WB or peripheral blood mononuclear cells (PBMCs) with only minor additional optimization.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Cytometry Part A},\n\tauthor = {Imbratta, Claire and Reid, Timothy D. and Toefy, Asma and Scriba, Thomas J. and Nemes, Elisa},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {165--170},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Towards Uncovering the Role of Incomplete Penetrance in Maculopathies through Sequencing of 105 Disease-Associated Genes.\n \n \n \n \n\n\n \n Hitti-Malin, R. J.; Panneman, D. M.; Corradi, Z.; Boonen, E. G. M.; Astuti, G.; Dhaenens, C.; Stöhr, H.; Weber, B. H. F.; Sharon, D.; Banin, E.; Karali, M.; Banfi, S.; Ben-Yosef, T.; Glavač, D.; Farrar, G. J.; Ayuso, C.; Liskova, P.; Dudakova, L.; Vajter, M.; Ołdak, M.; Szaflik, J. P.; Matynia, A.; Gorin, M. B.; Kämpjärvi, K.; Bauwens, M.; De Baere, E.; Hoyng, C. B.; Li, C. H. Z.; Klaver, C. C. W.; Inglehearn, C. F.; Fujinami, K.; Rivolta, C.; Allikmets, R.; Zernant, J.; Lee, W.; Podhajcer, O. L.; Fakin, A.; Sajovic, J.; AlTalbishi, A.; Valeina, S.; Taurina, G.; Vincent, A. L.; Roberts, L.; Ramesar, R.; Sartor, G.; Luppi, E.; Downes, S. M.; Van Den Born, L. I.; McLaren, T. L.; De Roach, J. N.; Lamey, T. M.; Thompson, J. A.; Chen, F. K.; Tracewska, A. M.; Kamakari, S.; Sallum, J. M. F.; Bolz, H. J.; Kayserili, H.; Roosing, S.; and Cremers, F. P. M.\n\n\n \n\n\n\n Biomolecules, 14(3): 367. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Towards$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{hitti-malin_towards_2024,\n\ttitle = {Towards {Uncovering} the {Role} of {Incomplete} {Penetrance} in {Maculopathies} through {Sequencing} of 105 {Disease}-{Associated} {Genes}},\n\tvolume = {14},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2218-273X},\n\turl = {https://www.mdpi.com/2218-273X/14/3/367},\n\tdoi = {10.3390/biom14030367},\n\tabstract = {Inherited macular dystrophies (iMDs) are a group of genetic disorders, which affect the central region of the retina. To investigate the genetic basis of iMDs, we used single-molecule Molecular Inversion Probes to sequence 105 maculopathy-associated genes in 1352 patients diagnosed with iMDs. Within this cohort, 39.8\\% of patients were considered genetically explained by 460 different variants in 49 distinct genes of which 73 were novel variants, with some affecting splicing. The top five most frequent causative genes were ABCA4 (37.2\\%), PRPH2 (6.7\\%), CDHR1 (6.1\\%), PROM1 (4.3\\%) and RP1L1 (3.1\\%). Interestingly, variants with incomplete penetrance were revealed in almost one-third of patients considered solved (28.1\\%), and therefore, a proportion of patients may not be explained solely by the variants reported. This includes eight previously reported variants with incomplete penetrance in addition to CDHR1:c.783G{\\textgreater}A and CNGB3:c.1208G{\\textgreater}A. Notably, segregation analysis was not routinely performed for variant phasing—a limitation, which may also impact the overall diagnostic yield. The relatively high proportion of probands without any putative causal variant (60.2\\%) highlights the need to explore variants with incomplete penetrance, the potential modifiers of disease and the genetic overlap between iMDs and age-related macular degeneration. Our results provide valuable insights into the genetic landscape of iMDs and warrant future exploration to determine the involvement of other maculopathy genes.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Biomolecules},\n\tauthor = {Hitti-Malin, Rebekkah J. and Panneman, Daan M. and Corradi, Zelia and Boonen, Erica G. M. and Astuti, Galuh and Dhaenens, Claire-Marie and Stöhr, Heidi and Weber, Bernhard H. F. and Sharon, Dror and Banin, Eyal and Karali, Marianthi and Banfi, Sandro and Ben-Yosef, Tamar and Glavač, Damjan and Farrar, G. Jane and Ayuso, Carmen and Liskova, Petra and Dudakova, Lubica and Vajter, Marie and Ołdak, Monika and Szaflik, Jacek P. and Matynia, Anna and Gorin, Michael B. and Kämpjärvi, Kati and Bauwens, Miriam and De Baere, Elfride and Hoyng, Carel B. and Li, Catherina H. Z. and Klaver, Caroline C. W. and Inglehearn, Chris F. and Fujinami, Kaoru and Rivolta, Carlo and Allikmets, Rando and Zernant, Jana and Lee, Winston and Podhajcer, Osvaldo L. and Fakin, Ana and Sajovic, Jana and AlTalbishi, Alaa and Valeina, Sandra and Taurina, Gita and Vincent, Andrea L. and Roberts, Lisa and Ramesar, Raj and Sartor, Giovanna and Luppi, Elena and Downes, Susan M. and Van Den Born, L. Ingeborgh and McLaren, Terri L. and De Roach, John N. and Lamey, Tina M. and Thompson, Jennifer A. and Chen, Fred K. and Tracewska, Anna M. and Kamakari, Smaragda and Sallum, Juliana Maria Ferraz and Bolz, Hanno J. and Kayserili, Hülya and Roosing, Susanne and Cremers, Frans P. M.},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {367},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The African Human Microbiome Portal: a public web portal of curated metagenomic metadata.\n \n \n \n \n\n\n \n Kiran, A.; Hanachi, M.; Alsayed, N.; Fassatoui, M.; Oduaran, O. H; Allali, I.; Maslamoney, S.; Meintjes, A.; Zass, L.; Rocha, J. D.; Kefi, R.; Benkahla, A.; Ghedira, K.; Panji, S.; Mulder, N.; Fadlelmola, F. M; and Souiai, O.\n\n\n \n\n\n\n Database, 2024: baad092. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kiran_african_2024,\n\ttitle = {The {African} {Human} {Microbiome} {Portal}: a public web portal of curated metagenomic metadata},\n\tvolume = {2024},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1758-0463},\n\tshorttitle = {The {African} {Human} {Microbiome} {Portal}},\n\turl = {https://academic.oup.com/database/article/doi/10.1093/database/baad092/7514669},\n\tdoi = {10.1093/database/baad092},\n\tabstract = {Abstract \n            There is growing evidence that comprehensive and harmonized metadata are fundamental for effective public data reusability. However, it is often challenging to extract accurate metadata from public repositories. Of particular concern is the metagenomic data related to African individuals, which often omit important information about the particular features of these populations. As part of a collaborative consortium, H3ABioNet, we created a web portal, namely the African Human Microbiome Portal (AHMP), exclusively dedicated to metadata related to African human microbiome samples. Metadata were collected from various public repositories prior to cleaning, curation and harmonization according to a pre-established guideline and using ontology terms. These metadata sets can be accessed at https://microbiome.h3abionet.org/. This web portal is open access and offers an interactive visualization of 14 889 records from 70 bioprojects associated with 72 peer reviewed research articles. It also offers the ability to download harmonized metadata according to the user’s applied filters. The AHMP thereby supports metadata search and retrieve operations, facilitating, thus, access to relevant studies linked to the African Human microbiome. \n            Database URL:  https://microbiome.h3abionet.org/.},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Database},\n\tauthor = {Kiran, Anmol and Hanachi, Mariem and Alsayed, Nihad and Fassatoui, Meriem and Oduaran, Ovokeraye H and Allali, Imane and Maslamoney, Suresh and Meintjes, Ayton and Zass, Lyndon and Rocha, Jorge Da and Kefi, Rym and Benkahla, Alia and Ghedira, Kais and Panji, Sumir and Mulder, Nicola and Fadlelmola, Faisal M and Souiai, Oussema},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {baad092},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Multi-omics analysis of overexpressed tumor-associated proteins: gene expression, immunopeptide presentation, and antibody response in oropharyngeal squamous cell carcinoma, with a focus on cancer-testis antigens.\n \n \n \n \n\n\n \n Abou Kors, T.; Meier, M.; Mühlenbruch, L.; Betzler, A. C.; Oliveri, F.; Bens, M.; Thomas, J.; Kraus, J. M.; Doescher, J.; Von Witzleben, A.; Hofmann, L.; Ezic, J.; Huber, D.; Benckendorff, J.; Barth, T. F. E.; Greve, J.; Schuler, P. J.; Brunner, C.; Blackburn, J. M.; Hoffmann, T. K.; Ottensmeier, C.; Kestler, H. A.; Rammensee, H.; Walz, J. S.; and Laban, S.\n\n\n \n\n\n\n Frontiers in Immunology, 15: 1408173. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Multi-omics$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{abou_kors_multi-omics_2024,\n\ttitle = {Multi-omics analysis of overexpressed tumor-associated proteins: gene expression, immunopeptide presentation, and antibody response in oropharyngeal squamous cell carcinoma, with a focus on cancer-testis antigens},\n\tvolume = {15},\n\tissn = {1664-3224},\n\tshorttitle = {Multi-omics analysis of overexpressed tumor-associated proteins},\n\turl = {https://www.frontiersin.org/articles/10.3389/fimmu.2024.1408173/full},\n\tdoi = {10.3389/fimmu.2024.1408173},\n\tabstract = {Introduction \n              The human leukocyte antigen complex (HLA) is essential for inducing specific immune responses to cancer by presenting tumor-associated peptides (TAP) to T cells. Overexpressed tumor associated antigens, mainly cancer-testis antigens (CTA), are outlined as essential targets for immunotherapy in oropharyngeal squamous cell carcinoma (OPSCC). This study assessed the degree to which presentation, gene expression, and antibody response (AR) of TAP, mainly CTA, are correlated in OPSCC patients to evaluate their potential as immunotherapy targets. \n             \n             \n              Materials and methods \n               \n                Snap-frozen tumor (N \n                Ligand/RNA \n                =40), healthy mucosa (N \n                RNA \n                =6), and healthy tonsils (N \n                Ligand \n                =5) samples were obtained. RNA-Seq was performed using Illumina HiSeq 2500/NovaSeq 6000 and whole exome sequencing (WES) utilizing NextSeq500. HLA ligands were isolated from tumor tissue using immunoaffinity purification, UHPLC, and analyzed by tandem MS. Antibodies were measured in serum (N \n                Ab \n                =27) utilizing the KREX™ CT262 protein array. Data analysis focused on 312 proteins (KREX™ CT262 panel + overexpressed self-proteins). \n               \n             \n             \n              Results \n              183 and 94 of HLA class I and II TAP were identified by comparative profiling with healthy tonsils. Genes from 26 TAP were overexpressed in tumors compared to healthy mucosa (LFC\\&gt;1; FDR\\&lt;0.05). Low concordance (r=0.25; p\\&lt;0.0001) was found between upregulated mRNA and class I TAP. The specific mode of correlation of TAP was found to be dependent on clinical parameters. A lack of correlation was observed both between mRNA and class II TAP, as well as between class II tumor-unique TAP (TAP-U) presentation and antibody response (AR) levels. \n             \n             \n              Discussion \n              This study demonstrates that focusing exclusively on gene transcript levels fails to capture the full extent of TAP presentation in OPSCC. Furthermore, our findings reveal that although CTA are presented at relatively low levels, a few CTA TAP-U show potential as targets for immunotherapy.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Immunology},\n\tauthor = {Abou Kors, Tsima and Meier, Matthias and Mühlenbruch, Lena and Betzler, Annika C. and Oliveri, Franziska and Bens, Martin and Thomas, Jaya and Kraus, Johann M. and Doescher, Johannes and Von Witzleben, Adrian and Hofmann, Linda and Ezic, Jasmin and Huber, Diana and Benckendorff, Julian and Barth, Thomas F. E. and Greve, Jens and Schuler, Patrick J. and Brunner, Cornelia and Blackburn, Jonathan M. and Hoffmann, Thomas K. and Ottensmeier, Christian and Kestler, Hans A. and Rammensee, Hans-Georg and Walz, Juliane S. and Laban, Simon},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {1408173},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Investigating antimicrobial resistance genes in Kenya, Uganda and Tanzania cattle using metagenomics.\n \n \n \n \n\n\n \n Omar, K. M.; Kitundu, G. L.; Jimoh, A. O.; Namikelwa, D. N.; Lisso, F. M.; Babajide, A. A.; Olufemi, S. E.; and Awe, O. I.\n\n\n \n\n\n\n PeerJ, 12: e17181. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Investigating$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{omar_investigating_2024,\n\ttitle = {Investigating antimicrobial resistance genes in {Kenya}, {Uganda} and {Tanzania} cattle using metagenomics},\n\tvolume = {12},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2167-8359},\n\turl = {https://peerj.com/articles/17181},\n\tdoi = {10.7717/peerj.17181},\n\tabstract = {Antimicrobial resistance (AMR) is a growing problem in African cattle production systems, posing a threat to human and animal health and the associated economic value chain. However, there is a poor understanding of the resistomes in small-holder cattle breeds in East African countries. This study aims to examine the distribution of antimicrobial resistance genes (ARGs) in Kenya, Tanzania, and Uganda cattle using a metagenomics approach. We used the SqueezeMeta-Abricate (assembly-based) pipeline to detect ARGs and benchmarked this approach using the Centifuge-AMRplusplus (read-based) pipeline to evaluate its efficiency. Our findings reveal a significant number of ARGs of critical medical and economic importance in all three countries, including resistance to drugs of last resort such as carbapenems, suggesting the presence of highly virulent and antibiotic-resistant bacterial pathogens (ESKAPE) circulating in East Africa. Shared ARGs such as aph(6)-id (aminoglycoside phosphotransferase), tet (tetracycline resistance gene), sul2 (sulfonamide resistance gene) and cfxA\\_gen (betalactamase gene) were detected. Assembly-based methods revealed fewer ARGs compared to read-based methods, indicating the sensitivity and specificity of read-based methods in resistome characterization. Our findings call for further surveillance to estimate the intensity of the antibiotic resistance problem and wider resistome classification. Effective management of livestock and antibiotic consumption is crucial in minimizing antimicrobial resistance and maximizing productivity, making these findings relevant to stakeholders, agriculturists, and veterinarians in East Africa and Africa at large.},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {PeerJ},\n\tauthor = {Omar, Kauthar M. and Kitundu, George L. and Jimoh, Adijat O. and Namikelwa, Dorcus N. and Lisso, Felix M. and Babajide, Abiola A. and Olufemi, Seun E. and Awe, Olaitan I.},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {e17181},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Navigating US participant data sharing requirements: implications for international clinical trials.\n \n \n \n \n\n\n \n Dal-Ré, R.; Bekker, L.; Jha, V.; Le Louarn, A.; and Naudet, F.\n\n\n \n\n\n\n BMJ,e079701. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Navigating$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{dal-re_navigating_2024,\n\ttitle = {Navigating {US} participant data sharing requirements: implications for international clinical trials},\n\tissn = {1756-1833},\n\tshorttitle = {Navigating {US} participant data sharing requirements},\n\turl = {https://www.bmj.com/lookup/doi/10.1136/bmj-2024-079701},\n\tdoi = {10.1136/bmj-2024-079701},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {BMJ},\n\tauthor = {Dal-Ré, Rafael and Bekker, Linda-Gail and Jha, Vivekanand and Le Louarn, Anne and Naudet, Florian},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {e079701},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Blood transcriptomic signatures for symptomatic tuberculosis in an African multicohort study.\n \n \n \n \n\n\n \n Muwanga, V. M.; Mendelsohn, S. C.; Leukes, V.; Stanley, K.; Mbandi, S. K.; Erasmus, M.; Flinn, M.; Fisher, T.; Raphela, R.; Bilek, N.; Malherbe, S. T.; Tromp, G.; Van Der Spuy, G.; Walzl, G.; Chegou, N. N.; and Scriba, T. J.\n\n\n \n\n\n\n European Respiratory Journal, 64(2): 2400153. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Blood$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{muwanga_blood_2024,\n\ttitle = {Blood transcriptomic signatures for symptomatic tuberculosis in an {African} multicohort study},\n\tvolume = {64},\n\tissn = {0903-1936, 1399-3003},\n\turl = {https://publications.ersnet.org/lookup/doi/10.1183/13993003.00153-2024},\n\tdoi = {10.1183/13993003.00153-2024},\n\tabstract = {Background \n               \n                Multiple host blood transcriptional signatures have been developed as non-sputum triage tests for tuberculosis (TB). We aimed to compare the diagnostic performance of 20 blood transcriptomic TB signatures for differentiating between symptomatic patients who have TB \n                versus \n                other respiratory diseases (ORD). \n               \n             \n             \n              Methods \n              As part of a nested case–control study, individuals presenting with respiratory symptoms at primary healthcare clinics in Ethiopia, Malawi, Namibia, Uganda, South Africa and The Gambia were enrolled. TB was diagnosed based on clinical, microbiological and radiological findings. Transcriptomic signatures were measured in whole blood using microfluidic real-time quantitative PCR. Diagnostic performance was benchmarked against the World Health Organization Target Product Profile (TPP) for a non-sputum TB triage test. \n             \n             \n              Results \n              Among 579 participants, 158 had definite, microbiologically confirmed TB, 32 had probable TB, while 389 participants had ORD. Nine signatures differentiated between ORD and TB with equivalent performance (Satproedprai7: area under the curve 0.83 (95\\% CI 0.79–0.87); Jacobsen3: 0.83 (95\\% CI 0.79–0.86); Suliman2: 0.82 (95\\% CI 0.78–0.86); Roe1: 0.82 (95\\% CI 0.78–0.86); Kaforou22: 0.82 (95\\% CI 0.78–0.86); Sambarey10: 0.81 (95\\% CI 0.77–0.85); Duffy9: 0.81 (95\\% CI 0.76–0.86); Gliddon3: 0.8 (95\\% CI 0.75–0.85); Suliman4 0.79 (95\\% CI 0.75–0.84)). Benchmarked against a 90\\% sensitivity, these signatures achieved specificities between 44\\% (95\\% CI 38–49\\%) and 54\\% (95\\% CI 49–59\\%), not meeting the TPP criteria. Signature scores significantly varied by HIV status and country. In country-specific analyses, several signatures, such as Satproedprai7 and Penn-Nicholson6, met the minimal TPP criteria for a triage test in Ethiopia, Malawi and South Africa. \n             \n             \n              Conclusion \n              No signatures met the TPP criteria in a pooled analysis of all countries, but several signatures met the minimum criteria for a non-sputum TB triage test in some countries.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {European Respiratory Journal},\n\tauthor = {Muwanga, Vanessa Mwebaza and Mendelsohn, Simon C. and Leukes, Vinzeigh and Stanley, Kim and Mbandi, Stanley Kimbung and Erasmus, Mzwandile and Flinn, Marika and Fisher, Tarryn-Lee and Raphela, Rodney and Bilek, Nicole and Malherbe, Stephanus T. and Tromp, Gerard and Van Der Spuy, Gian and Walzl, Gerhard and Chegou, Novel N. and Scriba, Thomas J.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {2400153},\n}\n\n\n\n

\n

\n\n\n

\n Background Multiple host blood transcriptional signatures have been developed as non-sputum triage tests for tuberculosis (TB). We aimed to compare the diagnostic performance of 20 blood transcriptomic TB signatures for differentiating between symptomatic patients who have TB versus other respiratory diseases (ORD). Methods As part of a nested case–control study, individuals presenting with respiratory symptoms at primary healthcare clinics in Ethiopia, Malawi, Namibia, Uganda, South Africa and The Gambia were enrolled. TB was diagnosed based on clinical, microbiological and radiological findings. Transcriptomic signatures were measured in whole blood using microfluidic real-time quantitative PCR. Diagnostic performance was benchmarked against the World Health Organization Target Product Profile (TPP) for a non-sputum TB triage test. Results Among 579 participants, 158 had definite, microbiologically confirmed TB, 32 had probable TB, while 389 participants had ORD. Nine signatures differentiated between ORD and TB with equivalent performance (Satproedprai7: area under the curve 0.83 (95% CI 0.79–0.87); Jacobsen3: 0.83 (95% CI 0.79–0.86); Suliman2: 0.82 (95% CI 0.78–0.86); Roe1: 0.82 (95% CI 0.78–0.86); Kaforou22: 0.82 (95% CI 0.78–0.86); Sambarey10: 0.81 (95% CI 0.77–0.85); Duffy9: 0.81 (95% CI 0.76–0.86); Gliddon3: 0.8 (95% CI 0.75–0.85); Suliman4 0.79 (95% CI 0.75–0.84)). Benchmarked against a 90% sensitivity, these signatures achieved specificities between 44% (95% CI 38–49%) and 54% (95% CI 49–59%), not meeting the TPP criteria. Signature scores significantly varied by HIV status and country. In country-specific analyses, several signatures, such as Satproedprai7 and Penn-Nicholson6, met the minimal TPP criteria for a triage test in Ethiopia, Malawi and South Africa. Conclusion No signatures met the TPP criteria in a pooled analysis of all countries, but several signatures met the minimum criteria for a non-sputum TB triage test in some countries.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Higher Sensitivity of Xpert MTB/RIF Ultra Over Tuberculosis Culture for the Diagnosis of Spinal Tuberculosis With Open or Computed Tomography–Guided Biopsies.\n \n \n \n \n\n\n \n Waters, R.; Laubscher, M.; Dunn, R. N; Adikary, N.; Coussens, A. K; and Held, M.\n\n\n \n\n\n\n Open Forum Infectious Diseases, 11(1): ofad621. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Higher$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{waters_higher_2024,\n\ttitle = {Higher {Sensitivity} of {Xpert} {MTB}/{RIF} {Ultra} {Over} {Tuberculosis} {Culture} for the {Diagnosis} of {Spinal} {Tuberculosis} {With} {Open} or {Computed} {Tomography}–{Guided} {Biopsies}},\n\tvolume = {11},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2328-8957},\n\turl = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofad621/7462171},\n\tdoi = {10.1093/ofid/ofad621},\n\tabstract = {Abstract \n             \n              Background \n              Diagnostic specimens for spinal tuberculosis (STB) are mostly collected via open surgery. Percutaneous computed tomography (CT)–guided biopsies are used in times of limited surgical availability. However, poor diagnostic accuracy of Mycobacterium tuberculosis (Mtb) culture has been reported with this method, due to limited sample volume and the paucibacillary nature of STB. We evaluated Xpert MTB/RIF Ultra on open and CT-guided biopsies as compared with the gold standard Mtb culture and histopathology. \n             \n             \n              Methods \n              We conducted a prospective diagnostic accuracy study of Xpert Ultra, as compared with tuberculosis culture and histopathology, in adults with signs and symptoms of STB at a tertiary academic hospital in South Africa from November 2020 to December 2021. Diagnostic testing was performed on 31 patients with available samples. \n             \n             \n              Results \n              Xpert Ultra had a sensitivity of 94.7\\% (95\\% CI, 75.3\\%–99.7\\%) and specificity of 100\\% (95\\% CI, 75.7\\%–100.0\\%) against a reference standard of Mtb culture and histopathology. Xpert Ultra had high diagnostic accuracy in open and CT-guided biopsy samples with sensitivity and specificity of 100\\% and 100\\% (open) and 89\\% and 100\\% (CT), respectively. Mtb culture had limited specificity for CT-guided biopsies (43\\%; 95\\% CI, 15.8\\%–74.9\\%). HIV-1 coinfection did not affect Mtb abundance measures by Xpert Ultra or culture. Xpert Ultra was also superior to culture for STB diagnosis in patients concurrently treated for pulmonary tuberculosis. \n             \n             \n              Conclusions \n              Xpert Ultra detected more STB cases than culture for CT-guided biopsy samples. There was also no difference in sensitivity for open biopsies, irrespective of HIV-1 status, making it an important tool for rapid diagnosis, especially during times or in locations where open surgery is not possible or concurrent pulmonary tuberculosis treatment is initiated.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Open Forum Infectious Diseases},\n\tauthor = {Waters, Robyn and Laubscher, Maritz and Dunn, Robert N and Adikary, Nawaal and Coussens, Anna K and Held, Michael},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {ofad621},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Power Relations in Optimisation of Therapies and Equity in Access to Antibiotics (PROTEA) Study: investigating the intersection of socio-economic and cultural drivers on antimicrobial resistance (AMR) and its influence on healthcare access and health-providing behaviours in India and South Africa.\n \n \n \n \n\n\n \n Charani, E.; Dlamini, S.; Koch, A.; Singh, S.; Hodes, R.; Laxminarayan, R.; Batheja, D.; Ramugondo, E.; Mukherjee, A. S.; and Mendelson, M.\n\n\n \n\n\n\n Wellcome Open Research, 9: 400. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Power$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{charani_power_2024,\n\ttitle = {Power {Relations} in {Optimisation} of {Therapies} and {Equity} in {Access} to {Antibiotics} ({PROTEA}) {Study}: investigating the intersection of socio-economic and cultural drivers on antimicrobial resistance ({AMR}) and its influence on healthcare access and health-providing behaviours in {India} and {South} {Africa}},\n\tvolume = {9},\n\tissn = {2398-502X},\n\tshorttitle = {Power {Relations} in {Optimisation} of {Therapies} and {Equity} in {Access} to {Antibiotics} ({PROTEA}) {Study}},\n\turl = {https://wellcomeopenresearch.org/articles/9-400/v1},\n\tdoi = {10.12688/wellcomeopenres.20193.1},\n\tabstract = {Across social structures within society, including healthcare, power relations manifest according to gender, socioeconomic status, race, ethnicity, and class influencing infection related healthcare access and health providing-behaviours. Therefore, accounting for sociocultural drivers, including gender, race, and class, and their influence on economic status can improve healthcare access and health-providing behaviours in infection prevention and control (IPC) as well as antibiotic use, which in turn helps mitigate the spread of antimicrobial resistance (AMR). This Wellcome funded research will investigate how and why the social determinants of health and economic status influence how people seek, experience, and provide healthcare for suspected or proven (bacterial) infections and how these factors influence antibiotic prescribing and use in South Africa (upper middle-income country) and India (lower middle-income country). The aim of this body of work is to, (1) define and estimate the sociocultural and economic drivers for AMR in different resource settings, (2) design, implement and evaluate context-sensitive IPC and antimicrobial stewardship (AMS) interventions, and (3) inform policy and strategy for AMR mitigation. The population will be healthcare workers (HCWs), patients, and their carers across acute medical and surgical pathways where IPC and antibiotic-related healthcare access and health-providing behaviours will be studied. Qualitative methods will include ethnographic research, semi-structured in-depth interviews, and focus groups with healthcare providers, patients and carers. Quantitative analysis of bedside observational data from hospitals and population level data on antibiotic use will study the various predictors of AMR using bivariable and multivariable regression analyses. The research will provide high-quality evidence on how social determinants intersect with health, social well-being, and vulnerability in IPC practices and antibiotic use. Using this knowledge we will: 1) design, implement, and measure effects of interventions accounting for these factors; 2) provide a toolkit for advocacy for actors in AMR, and healthcare to assist them to promote dialogue, including policy dialogue on this issue. This work directly benefits the target population and informs healthcare services and practice across the participating countries with potential for wider translation. The setting will be hospitals in South Africa (middle-income country) and India (lower middle-income country). The population will be healthcare workers (HCWs), patients, and their carers across acute medical and surgical pathways where IPC and antibiotic-related health-seeking and health-providing behaviours will be studied. These populations represent communities most affected by infections and AMR because existing interventions do not address a) differences in how surgical versus medical teams manage infections; b) the role of the wider social network of individuals on their decision-making, c) intersection of the social determinants of health including race, gender, socioeconomic deprivation with AMR.},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Wellcome Open Research},\n\tauthor = {Charani, Esmita and Dlamini, Sipho and Koch, Anastasia and Singh, Sanjeev and Hodes, Rebecca and Laxminarayan, Ramanan and Batheja, Deepshikha and Ramugondo, Elelwani and Mukherjee, Arunima Sehgal and Mendelson, Marc},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {400},\n}\n\n\n\n

\n

\n\n\n

\n Across social structures within society, including healthcare, power relations manifest according to gender, socioeconomic status, race, ethnicity, and class influencing infection related healthcare access and health providing-behaviours. Therefore, accounting for sociocultural drivers, including gender, race, and class, and their influence on economic status can improve healthcare access and health-providing behaviours in infection prevention and control (IPC) as well as antibiotic use, which in turn helps mitigate the spread of antimicrobial resistance (AMR). This Wellcome funded research will investigate how and why the social determinants of health and economic status influence how people seek, experience, and provide healthcare for suspected or proven (bacterial) infections and how these factors influence antibiotic prescribing and use in South Africa (upper middle-income country) and India (lower middle-income country). The aim of this body of work is to, (1) define and estimate the sociocultural and economic drivers for AMR in different resource settings, (2) design, implement and evaluate context-sensitive IPC and antimicrobial stewardship (AMS) interventions, and (3) inform policy and strategy for AMR mitigation. The population will be healthcare workers (HCWs), patients, and their carers across acute medical and surgical pathways where IPC and antibiotic-related healthcare access and health-providing behaviours will be studied. Qualitative methods will include ethnographic research, semi-structured in-depth interviews, and focus groups with healthcare providers, patients and carers. Quantitative analysis of bedside observational data from hospitals and population level data on antibiotic use will study the various predictors of AMR using bivariable and multivariable regression analyses. The research will provide high-quality evidence on how social determinants intersect with health, social well-being, and vulnerability in IPC practices and antibiotic use. Using this knowledge we will: 1) design, implement, and measure effects of interventions accounting for these factors; 2) provide a toolkit for advocacy for actors in AMR, and healthcare to assist them to promote dialogue, including policy dialogue on this issue. This work directly benefits the target population and informs healthcare services and practice across the participating countries with potential for wider translation. The setting will be hospitals in South Africa (middle-income country) and India (lower middle-income country). The population will be healthcare workers (HCWs), patients, and their carers across acute medical and surgical pathways where IPC and antibiotic-related health-seeking and health-providing behaviours will be studied. These populations represent communities most affected by infections and AMR because existing interventions do not address a) differences in how surgical versus medical teams manage infections; b) the role of the wider social network of individuals on their decision-making, c) intersection of the social determinants of health including race, gender, socioeconomic deprivation with AMR.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Modelling the health and economic impacts of M72/AS01E vaccination and BCG-revaccination: Estimates for South Africa.\n \n \n \n \n\n\n \n Sumner, T.; Clark, R. A.; Mukandavire, C.; Portnoy, A.; Weerasuriya, C. K.; Bakker, R.; Scarponi, D.; Hatherill, M.; Menzies, N. A.; and White, R. G.\n\n\n \n\n\n\n Vaccine, 42(6): 1311–1318. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Modelling$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{sumner_modelling_2024,\n\ttitle = {Modelling the health and economic impacts of {M72}/{AS01E} vaccination and {BCG}-revaccination: {Estimates} for {South} {Africa}},\n\tvolume = {42},\n\tissn = {0264410X},\n\tshorttitle = {Modelling the health and economic impacts of {M72}/{AS01E} vaccination and {BCG}-revaccination},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0264410X24000963},\n\tdoi = {10.1016/j.vaccine.2024.01.072},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {Vaccine},\n\tauthor = {Sumner, Tom and Clark, Rebecca A. and Mukandavire, Christinah and Portnoy, Allison and Weerasuriya, Chathika K. and Bakker, Roel and Scarponi, Danny and Hatherill, Mark and Menzies, Nicolas A. and White, Richard G.},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {1311--1318},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Investigating somatic variants and pathways in mismatch repair-deficient (dMMR) colorectal carcinoma in South Africa.\n \n \n \n \n\n\n \n Aldera, A. P.; Van Der Westhuizen, J.; Tsai, W.; Krause, M. J; Yildiz, S.; Pillay, K.; Boutall, A.; and Ramesar, R.\n\n\n \n\n\n\n Journal of Clinical Pathology,jcp–2024–209526. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Investigating$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{aldera_investigating_2024,\n\ttitle = {Investigating somatic variants and pathways in mismatch repair-deficient ({dMMR}) colorectal carcinoma in {South} {Africa}},\n\tissn = {0021-9746, 1472-4146},\n\turl = {https://jcp.bmj.com/lookup/doi/10.1136/jcp-2024-209526},\n\tdoi = {10.1136/jcp-2024-209526},\n\tabstract = {Aims \n              Colorectal carcinoma (CRC) is a common cause of morbidity and mortality worldwide, and an emerging public health problem in sub-Saharan Africa. Several authors have described an increased frequency of mismatch repair-deficient (dMMR) CRC in sub-Saharan Africa, but these tumours remain poorly characterised molecularly. We sought to interrogate the somatic molecular genetic landscape of dMMR CRC in a cohort of young patients to better inform Lynch syndrome (LS) screening strategies and personalised medicine approaches in our setting. \n             \n             \n              Methods \n              32 patients (aged {\\textless}60 years) were identified with dMMR CRC. DNA was extracted from selected formalin-fixed paraffin-embedded (FFPE) tissue resection samples and subjected to amplicon-based next-generation sequencing (NGS). \n             \n             \n              Results \n               \n                Pathogenic or likely pathogenic variants were detected in the corresponding MMR gene in 14 of 18 (78\\%) MLH1/PMS2-deficient tumours, 5 of 8 (63\\%) MSH2/MSH6-deficient tumours, 1 of 4 (25\\%) tumours with isolated MSH6 loss and 0 of 2 tumours with isolated PMS2 loss. Previously unreported variants were identified in \n                MLH1 \n                (three) and \n                MSH2 \n                (one). Cases with a variant allele frequency suggesting a germline mutation were identified in \n                MLH1 \n                (eight), \n                MSH2 \n                (two) and \n                MSH6 \n                (one). Only one MMR gene variant was detected in more than one patient ( \n                MLH1 \n                p.Q510*). Four \n                POLE/POLD1 \n                exonuclease domain variants were identified, one of which was previously unreported. \n               \n             \n             \n              Conclusion \n              The spectrum of disease-causing MMR gene variants in our population necessitates NGS testing for LS screening. This study also highlights the role of somatic testing on readily available FFPE samples to generate data on the epidemiology of CRC in different settings.},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Clinical Pathology},\n\tauthor = {Aldera, Alessandro Pietro and Van Der Westhuizen, Jana and Tsai, Wan-Jung and Krause, May J and Yildiz, Safiye and Pillay, Komala and Boutall, Adam and Ramesar, Raj},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {jcp--2024--209526},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n SARS-CoV-2 Infections in a Triad of Primary School Learners (Grades 1-7), Their Parents, and Teachers in KwaZulu-Natal, South Africa: Protocol for a Cross-Sectional and Nested Case-Cohort Study.\n \n \n \n \n\n\n \n Dassaye, R.; Chetty, T.; Daniels, B.; Gaffoor, Z.; Spooner, E.; Ramraj, T.; Mthethwa, N.; Nsibande, D. F.; Pillay, S.; Bhana, A.; Magasana, V.; Reddy, T.; Mohlabi, K.; Moore, P. L.; Burgers, W. A; De Oliveira, T.; Msomi, N.; and Goga, A.\n\n\n \n\n\n\n JMIR Research Protocols, 13: e52713. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"SARS-CoV-2$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{dassaye_sars-cov-2_2024,\n\ttitle = {{SARS}-{CoV}-2 {Infections} in a {Triad} of {Primary} {School} {Learners} ({Grades} 1-7), {Their} {Parents}, and {Teachers} in {KwaZulu}-{Natal}, {South} {Africa}: {Protocol} for a {Cross}-{Sectional} and {Nested} {Case}-{Cohort} {Study}},\n\tvolume = {13},\n\tissn = {1929-0748},\n\tshorttitle = {{SARS}-{CoV}-2 {Infections} in a {Triad} of {Primary} {School} {Learners} ({Grades} 1-7), {Their} {Parents}, and {Teachers} in {KwaZulu}-{Natal}, {South} {Africa}},\n\turl = {https://www.researchprotocols.org/2024/1/e52713},\n\tdoi = {10.2196/52713},\n\tabstract = {Background \n              In low- and middle-income countries (LMICs) such as South Africa, there is paucity of data on SARS-CoV-2 infections among children attending school, including seroprevalence and transmission dynamics. \n             \n             \n              Objective \n              This pilot study aims to assess (1) the prevalence of self-reported or confirmed SARS-CoV-2 prior infections, COVID-19 symptoms (including long COVID), seroprevalence of SARS-CoV-2 antibodies, and general/mental health, (2) longitudinal changes in SARS-CoV-2 seroprevalence, and (3) SARS-CoV-2 acute infections, immune responses, transmission dynamics, and symptomatic versus asymptomatic contacts in a unique cohort of unvaccinated primary school learners, their parents, teachers, and close contacts in semirural primary school settings. \n             \n             \n              Methods \n              Learners (grades 1-7) from primary schools in KwaZulu-Natal, South Africa, their parents, and teachers will be invited to enroll into the COVID kids school study (CoKiDSS). CoKiDSS comprises 3 parts: a cross-sectional survey (N=640), a follow-up survey (n=300), and a nested case-cohort substudy. Finger-prick blood and saliva samples will be collected for serological and future testing, respectively, in the cross-sectional (451 learners:147 parents:42 teachers) and follow-up (210 learners:70 parents:20 teachers) surveys. The nested case-cohort substudy will include cases from the cross-sectional survey with confirmed current SARS-CoV-2 infection (n=30) and their close contacts (n=up to 10 per infected participant). Finger-prick blood (from all substudy participants), venous blood (from cases), and nasal swabs (from cases and contacts) will be collected for serological testing, immunological testing, and viral genome sequencing, respectively. Questionnaires covering sociodemographic and general and mental health information, prior and current SARS-CoV-2 symptoms and testing information, vaccination status, preventative behavior, and lifestyle will be administered. Statistical methods will include generalized linear mixed models, intracluster correlation, descriptive analysis, and graphical techniques. \n             \n             \n              Results \n              A total of 645 participants were enrolled into the cross-sectional survey between May and August 2023. A subset of 300 participants were followed up in the follow-up survey in October 2023. Screening of the participants into the nested case-cohort substudy is planned between November 2023 and September 2024. Data cleanup and analysis for the cross-sectional survey is complete, while those for the follow-up survey and nested case substudy will be completed by the third quarter of 2024. The dissemination and publication of results is anticipated for the fourth quarter of 2024. \n             \n             \n              Conclusions \n              This study provides data from an LMIC setting on the impact of SARS-CoV-2 on school-attending learners, their parents, and teachers 3 years after the SARS-CoV-2 pandemic was declared and 21-24 months after resumption of normal school attendance. In particular, this study will provide data on the prevalence of self-reported or confirmed SARS-CoV-2 prior infection, prior and current symptoms, seroprevalence, changes in seroprevalence, SARS-CoV-2 transmission, SARS-CoV-2 adaptive immune responses, and symptoms of long COVID and mental health among a triad of learners, their parents, and teachers. \n             \n             \n              International Registered Report Identifier (IRRID) \n              DERR1-10.2196/52713},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {JMIR Research Protocols},\n\tauthor = {Dassaye, Reshmi and Chetty, Terusha and Daniels, Brodie and Gaffoor, Zakir and Spooner, Elizabeth and Ramraj, Trisha and Mthethwa, Ncengani and Nsibande, Duduzile Faith and Pillay, Saresha and Bhana, Arvin and Magasana, Vuyolwethu and Reddy, Tarylee and Mohlabi, Khanya and Moore, Penelope Linda and Burgers, Wendy A and De Oliveira, Tulio and Msomi, Nokukhanya and Goga, Ameena},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {e52713},\n}\n\n\n\n

\n

\n\n\n

\n Background In low- and middle-income countries (LMICs) such as South Africa, there is paucity of data on SARS-CoV-2 infections among children attending school, including seroprevalence and transmission dynamics. Objective This pilot study aims to assess (1) the prevalence of self-reported or confirmed SARS-CoV-2 prior infections, COVID-19 symptoms (including long COVID), seroprevalence of SARS-CoV-2 antibodies, and general/mental health, (2) longitudinal changes in SARS-CoV-2 seroprevalence, and (3) SARS-CoV-2 acute infections, immune responses, transmission dynamics, and symptomatic versus asymptomatic contacts in a unique cohort of unvaccinated primary school learners, their parents, teachers, and close contacts in semirural primary school settings. Methods Learners (grades 1-7) from primary schools in KwaZulu-Natal, South Africa, their parents, and teachers will be invited to enroll into the COVID kids school study (CoKiDSS). CoKiDSS comprises 3 parts: a cross-sectional survey (N=640), a follow-up survey (n=300), and a nested case-cohort substudy. Finger-prick blood and saliva samples will be collected for serological and future testing, respectively, in the cross-sectional (451 learners:147 parents:42 teachers) and follow-up (210 learners:70 parents:20 teachers) surveys. The nested case-cohort substudy will include cases from the cross-sectional survey with confirmed current SARS-CoV-2 infection (n=30) and their close contacts (n=up to 10 per infected participant). Finger-prick blood (from all substudy participants), venous blood (from cases), and nasal swabs (from cases and contacts) will be collected for serological testing, immunological testing, and viral genome sequencing, respectively. Questionnaires covering sociodemographic and general and mental health information, prior and current SARS-CoV-2 symptoms and testing information, vaccination status, preventative behavior, and lifestyle will be administered. Statistical methods will include generalized linear mixed models, intracluster correlation, descriptive analysis, and graphical techniques. Results A total of 645 participants were enrolled into the cross-sectional survey between May and August 2023. A subset of 300 participants were followed up in the follow-up survey in October 2023. Screening of the participants into the nested case-cohort substudy is planned between November 2023 and September 2024. Data cleanup and analysis for the cross-sectional survey is complete, while those for the follow-up survey and nested case substudy will be completed by the third quarter of 2024. The dissemination and publication of results is anticipated for the fourth quarter of 2024. Conclusions This study provides data from an LMIC setting on the impact of SARS-CoV-2 on school-attending learners, their parents, and teachers 3 years after the SARS-CoV-2 pandemic was declared and 21-24 months after resumption of normal school attendance. In particular, this study will provide data on the prevalence of self-reported or confirmed SARS-CoV-2 prior infection, prior and current symptoms, seroprevalence, changes in seroprevalence, SARS-CoV-2 transmission, SARS-CoV-2 adaptive immune responses, and symptoms of long COVID and mental health among a triad of learners, their parents, and teachers. International Registered Report Identifier (IRRID) DERR1-10.2196/52713\n

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\n \n\n \n \n \n \n \n \n Prevention efficacy of the broadly neutralizing antibody VRC01 depends on HIV-1 envelope sequence features.\n \n \n \n \n\n\n \n Juraska, M.; Bai, H.; deCamp , A. C.; Magaret, C. A.; Li, L.; Gillespie, K.; Carpp, L. N.; Giorgi, E. E.; Ludwig, J.; Molitor, C.; Hudson, A.; Williamson, B. D.; Espy, N.; Simpkins, B.; Rudnicki, E.; Shao, D.; Rossenkhan, R.; Edlefsen, P. T.; Westfall, D. H.; Deng, W.; Chen, L.; Zhao, H.; Bhattacharya, T.; Pankow, A.; Murrell, B.; Yssel, A.; Matten, D.; York, T.; Beaume, N.; Gwashu-Nyangiwe, A.; Ndabambi, N.; Thebus, R.; Karuna, S. T.; Morris, L.; Montefiori, D. C.; Hural, J. A.; Cohen, M. S.; Corey, L.; Rolland, M.; Gilbert, P. B.; Williamson, C.; and Mullins, J. I.\n\n\n \n\n\n\n Proceedings of the National Academy of Sciences, 121(4): e2308942121. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Prevention$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{juraska_prevention_2024,\n\ttitle = {Prevention efficacy of the broadly neutralizing antibody {VRC01} depends on {HIV}-1 envelope sequence features},\n\tvolume = {121},\n\tissn = {0027-8424, 1091-6490},\n\turl = {https://pnas.org/doi/10.1073/pnas.2308942121},\n\tdoi = {10.1073/pnas.2308942121},\n\tabstract = {In the Antibody Mediated Prevention (AMP) trials (HVTN 704/HPTN 085 and HVTN 703/HPTN 081), prevention efficacy (PE) of the monoclonal broadly neutralizing antibody (bnAb) VRC01 (vs. placebo) against HIV-1 acquisition diagnosis varied according to the HIV-1 Envelope (Env) neutralization sensitivity to VRC01, as measured by 80\\% inhibitory concentration (IC80). Here, we performed a genotypic sieve analysis, a complementary approach to gaining insight into correlates of protection that assesses how PE varies with HIV-1 sequence features. We analyzed HIV-1 Env amino acid (AA) sequences from the earliest available HIV-1 RNA-positive plasma samples from AMP participants diagnosed with HIV-1 and identified Env sequence features that associated with PE. The strongest Env AA sequence correlate in both trials was VRC01 epitope distance that quantifies the divergence of the VRC01 epitope in an acquired HIV-1 isolate from the VRC01 epitope of reference HIV-1 strains that were most sensitive to VRC01-mediated neutralization. In HVTN 704/HPTN 085, the Env sequence-based predicted probability that VRC01 IC80 against the acquired isolate exceeded 1 µg/mL also significantly associated with PE. In HVTN 703/HPTN 081, a physicochemical-weighted Hamming distance across 50 VRC01 binding-associated Env AA positions of the acquired isolate from the most VRC01-sensitive HIV-1 strain significantly associated with PE. These results suggest that incorporating mutation scoring by BLOSUM62 and weighting by the strength of interactions at AA positions in the epitope:VRC01 interface can optimize performance of an Env sequence-based biomarker of VRC01 prevention efficacy. Future work could determine whether these results extend to other bnAbs and bnAb combinations.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {Proceedings of the National Academy of Sciences},\n\tauthor = {Juraska, Michal and Bai, Hongjun and deCamp, Allan C. and Magaret, Craig A. and Li, Li and Gillespie, Kevin and Carpp, Lindsay N. and Giorgi, Elena E. and Ludwig, James and Molitor, Cindy and Hudson, Aaron and Williamson, Brian D. and Espy, Nicole and Simpkins, Brian and Rudnicki, Erika and Shao, Danica and Rossenkhan, Raabya and Edlefsen, Paul T. and Westfall, Dylan H. and Deng, Wenjie and Chen, Lennie and Zhao, Hong and Bhattacharya, Tanmoy and Pankow, Alec and Murrell, Ben and Yssel, Anna and Matten, David and York, Talita and Beaume, Nicolas and Gwashu-Nyangiwe, Asanda and Ndabambi, Nonkululeko and Thebus, Ruwayhida and Karuna, Shelly T. and Morris, Lynn and Montefiori, David C. and Hural, John A. and Cohen, Myron S. and Corey, Lawrence and Rolland, Morgane and Gilbert, Peter B. and Williamson, Carolyn and Mullins, James I.},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {e2308942121},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Important Guide for Natural Compounds Inclusion in Precision Medicine.\n \n \n \n \n\n\n \n Oluwole, O. G.\n\n\n \n\n\n\n OBM Genetics, 08(04): 1–8. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Important$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{oluwole_important_2024,\n\ttitle = {Important {Guide} for {Natural} {Compounds} {Inclusion} in {Precision} {Medicine}},\n\tvolume = {08},\n\tissn = {25775790},\n\turl = {https://www.lidsen.com/journals/genetics/genetics-08-04-273},\n\tdoi = {10.21926/obm.genet.2404273},\n\tabstract = {Precision medicine describes the definition of disease at a higher resolution by genomic and other technologies to enable more precise targeting of disease subgroups with new therapies. Preventative or therapeutic interventions can be developed with the knowledge of how a compound acts safely in the body to target receptors and produce the desirable effect. With the completion of the Human Genome Project in 2003 and the rapid increase in sequencing and bioinformatics tools, obtaining information about a person's genome is becoming more accessible. To make use of genetic information in precision or personalised medicine, it is important to examine the roles of natural remedies in the individualization of treatment - to use as the right drug, at the correct dose, for the right person, at the right time. Integrating biomarkers, especially within clinical workflows, plays a crucial role in implementing precision medicine. Though the horizon in precision medicine looks promising, one major issue resides in the precise mapping into clearly defined medical conditions associated with biomarker identification and precedence ranking. This communication is met to provide guidelines that could improve biomarker discovery and enhance the participation and integration of novel natural compounds in the processes of implementing precision or personalized medicine.},\n\tnumber = {04},\n\turldate = {2025-06-24},\n\tjournal = {OBM Genetics},\n\tauthor = {Oluwole, Oluwafemi G.},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {1--8},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A call to intensify prostate cancer education and screening in Africa: a case study of Ghana.\n \n \n \n \n\n\n \n Osei Agyemang, R.; Bannor, R.; Osei-Yeboah, R.; and Okyere, P.\n\n\n \n\n\n\n International Journal of Health Promotion and Education, 62(5): 367–380. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{osei_agyemang_call_2024,\n\ttitle = {A call to intensify prostate cancer education and screening in {Africa}: a case study of {Ghana}},\n\tvolume = {62},\n\tissn = {1463-5240, 2164-9545},\n\tshorttitle = {A call to intensify prostate cancer education and screening in {Africa}},\n\turl = {https://www.tandfonline.com/doi/full/10.1080/14635240.2021.2014344},\n\tdoi = {10.1080/14635240.2021.2014344},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-24},\n\tjournal = {International Journal of Health Promotion and Education},\n\tauthor = {Osei Agyemang, Richard and Bannor, Richard and Osei-Yeboah, Richard and Okyere, Paul},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {367--380},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Effect of reactive oxygen, nitrogen, and sulfur species on signaling pathways in atherosclerosis.\n \n \n \n \n\n\n \n Solanki, K.; Bezsonov, E.; Orekhov, A.; Parihar, S. P.; Vaja, S.; White, F. A.; Obukhov, A. G.; and Baig, M. S.\n\n\n \n\n\n\n Vascular Pharmacology, 154: 107282. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Effect$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{solanki_effect_2024,\n\ttitle = {Effect of reactive oxygen, nitrogen, and sulfur species on signaling pathways in atherosclerosis},\n\tvolume = {154},\n\tissn = {15371891},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1537189124000077},\n\tdoi = {10.1016/j.vph.2024.107282},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Vascular Pharmacology},\n\tauthor = {Solanki, Kundan and Bezsonov, Evgeny and Orekhov, Alexander and Parihar, Suraj P. and Vaja, Shivani and White, Fletcher A. and Obukhov, Alexander G. and Baig, Mirza S.},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {107282},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Machine Learning Demonstrates Dominance of Physical Characteristics over Particle Composition in Coal Dust Toxicity.\n \n \n \n \n\n\n \n Kamanzi, C.; Becker, M.; Von Holdt, J.; Hsu, N.; Konečný, P.; Broadhurst, J.; and Jacobs, M.\n\n\n \n\n\n\n Environmental Science & Technology, 58(3): 1636–1647. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Machine$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kamanzi_machine_2024,\n\ttitle = {Machine {Learning} {Demonstrates} {Dominance} of {Physical} {Characteristics} over {Particle} {Composition} in {Coal} {Dust} {Toxicity}},\n\tvolume = {58},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0013-936X, 1520-5851},\n\turl = {https://pubs.acs.org/doi/10.1021/acs.est.3c08732},\n\tdoi = {10.1021/acs.est.3c08732},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Environmental Science \\& Technology},\n\tauthor = {Kamanzi, Conchita and Becker, Megan and Von Holdt, Johanna and Hsu, Nai-Jen and Konečný, Petr and Broadhurst, Jennifer and Jacobs, Muazzam},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {1636--1647},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Incorporating direct molecular diagnostics in management algorithms for nontuberculous mycobacteria: Is it high time?.\n \n \n \n \n\n\n \n Opperman, C. J.; Singh, S.; Goosen, W.; Cox, H.; Warren, R.; and Esmail, A.\n\n\n \n\n\n\n IJID Regions, 10: 140–145. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Incorporating$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{opperman_incorporating_2024,\n\ttitle = {Incorporating direct molecular diagnostics in management algorithms for nontuberculous mycobacteria: {Is} it high time?},\n\tvolume = {10},\n\tissn = {27727076},\n\tshorttitle = {Incorporating direct molecular diagnostics in management algorithms for nontuberculous mycobacteria},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2772707623001303},\n\tdoi = {10.1016/j.ijregi.2023.12.003},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {IJID Regions},\n\tauthor = {Opperman, Christoffel Johannes and Singh, Sarishna and Goosen, Wynand and Cox, Helen and Warren, Rob and Esmail, Aliasgar},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {140--145},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Description of the new HIV-1 intersubtype B/C circulating recombinant form (CRF146_BC) detected in Brazil.\n \n \n \n \n\n\n \n Oliveira, R. C.; Martin, D.; De Souza, J. S. M.; Alcântara, L. C. J.; Guimarães, M. L.; Brites, C.; and Monteiro-Cunha, J. P.\n\n\n \n\n\n\n Memórias do Instituto Oswaldo Cruz, 119: e230214. 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Description$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{oliveira_description_2024,\n\ttitle = {Description of the new {HIV}-1 intersubtype {B}/{C} circulating recombinant form ({CRF146}\\_BC) detected in {Brazil}},\n\tvolume = {119},\n\tcopyright = {http://creativecommons.org/licenses/by/4.0/},\n\tissn = {1678-8060, 0074-0276},\n\turl = {http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0074-02762024000101127&tlng=en},\n\tdoi = {10.1590/0074-02760230214},\n\turldate = {2025-06-24},\n\tjournal = {Memórias do Instituto Oswaldo Cruz},\n\tauthor = {Oliveira, Rodrigo Cunha and Martin, Darren and De Souza, Juliana Sacramento Mota and Alcântara, Luiz Carlos Júnior and Guimarães, Monick Lindenmeyer and Brites, Carlos and Monteiro-Cunha, Joana Paixão},\n\tyear = {2024},\n\tpages = {e230214},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Knowledge and perceptions of blood donors of the Western Cape Blood Services, South Africa, toward vaginal sample donation for biobanking.\n \n \n \n \n\n\n \n Claassen-Weitz, S.; Kullin, B.; Du Toit, E.; Gardner-Lubbe, S.; Passmore, J. S.; Jaspan, H.; Happel, A.; Bellairs, G.; Hilton, C.; Chicken, A.; Welp, K.; Livingstone, H.; and Brink, A.\n\n\n \n\n\n\n Frontiers in Reproductive Health, 6: 1446809. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Knowledge$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{claassen-weitz_knowledge_2024,\n\ttitle = {Knowledge and perceptions of blood donors of the {Western} {Cape} {Blood} {Services}, {South} {Africa}, toward vaginal sample donation for biobanking},\n\tvolume = {6},\n\tissn = {2673-3153},\n\turl = {https://www.frontiersin.org/articles/10.3389/frph.2024.1446809/full},\n\tdoi = {10.3389/frph.2024.1446809},\n\tabstract = {Introduction \n               \n                Depletion of \n                Lactobacillus \n                species and an overgrowth of anaerobes in the vaginal tract bacterial vaginosis (BV)], is associated with non-optimal reproductive health outcomes, and increased susceptibility to sexually transmitted infections (STIs). BV is currently treated with antibiotics, although these provide suboptimal cure levels and high recurrence rates. Vaginal microbiota transplantation (VMT), the transfer of vaginal fluid from healthy donors with an optimal vaginal microbiota to a recipient with BV, has been proposed as an alternative treatment strategy. \n               \n             \n             \n              Methods \n              Here, we investigated knowledge and perceptions of blood donors to the concept of an optimal vaginal microbiome and VMT via the Western Cape Blood Service (WCBS) clinics in Cape Town, South Africa, by a self-administered questionnaire. \n             \n             \n              Results \\&amp; discussion \n               \n                Analysis of responses from 106 eligible women showed that 86\\% (91/106) would consider donating samples. Responses significantly associated with willingness to donate vaginal samples included: (1) belief that helping others outweighs the inconvenience of donating vaginal sample ( \n                p \n                = 1.093e \n                −05 \n                ) and (2) prior knowledge of the concept of a healthy vaginal microbiome ( \n                p \n                 = 0.001). Most potential donors (59/91; 65\\%) were willing to receive a VMT themselves if needed. Participants who were unwilling to donate vaginal samples (15/106; 14\\%) indicated that vaginal sample collection would be unpleasant and/or embarrassing. The benefits of a collaboration with WCBS for this project include the naturally altruistic nature of blood donors, the constant in-flow of donors to WCBS clinics, and the infrastructure and logistical aspects in place. Data from this observational study highlight factors affecting the willingness of blood donors to become vaginal sample donors.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Reproductive Health},\n\tauthor = {Claassen-Weitz, Shantelle and Kullin, Brian and Du Toit, Elloise and Gardner-Lubbe, Sugnet and Passmore, Jo-Ann S. and Jaspan, Heather and Happel, Anna-Ursula and Bellairs, Greg and Hilton, Caroline and Chicken, Anika and Welp, Kirsten and Livingstone, Hannah and Brink, Adrian},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {1446809},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Therapeutic targeting of nuclear export and import receptors in cancer and their potential in combination chemotherapy.\n \n \n \n \n\n\n \n Newell, S.; Van Der Watt, P. J.; and Leaner, V. D.\n\n\n \n\n\n\n IUBMB Life, 76(1): 4–25. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Therapeutic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{newell_therapeutic_2024,\n\ttitle = {Therapeutic targeting of nuclear export and import receptors in cancer and their potential in combination chemotherapy},\n\tvolume = {76},\n\tissn = {1521-6543, 1521-6551},\n\turl = {https://iubmb.onlinelibrary.wiley.com/doi/10.1002/iub.2773},\n\tdoi = {10.1002/iub.2773},\n\tabstract = {Abstract \n            Systemic modalities are crucial in the management of disseminated malignancies and liquid tumours. However, patient responses and tolerability to treatment are generally poor and those that enter remission often return with refractory disease. Combination therapies provide a methodology to overcome chemoresistance mechanisms and address dose‐limiting toxicities. A deeper understanding of tumorigenic processes at the molecular level has brought a targeted therapy approach to the forefront of cancer research, and novel cancer biomarkers are being identified at a rapid rate, with some showing potential therapeutic benefits. The Karyopherin superfamily of proteins is soluble receptors that mediate nucleocytoplasmic shuttling of proteins and RNAs, and recently, nuclear transport receptors have been recognized as novel anticancer targets. Inhibitors against nuclear export have been approved for clinical use against certain cancer types, whereas inhibitors against nuclear import are in preclinical stages of investigation. Mechanistically, targeting nucleocytoplasmic shuttling has shown to abrogate oncogenic signalling and restore tumour suppressor functions through nuclear sequestration of relevant proteins and mRNAs. Hence, nuclear transport inhibitors display broad spectrum anticancer activity and harbour potential to engage in synergistic interactions with a wide array of cytotoxic agents and other targeted agents. This review is focussed on the most researched nuclear transport receptors in the context of cancer, XPO1 and KPNB1, and highlights how inhibitors targeting these receptors can enhance the therapeutic efficacy of standard of care therapies and novel targeted agents in a combination therapy approach. Furthermore, an updated review on the therapeutic targeting of lesser characterized karyopherin proteins is provided and resistance to clinically approved nuclear export inhibitors is discussed.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {IUBMB Life},\n\tauthor = {Newell, Stella and Van Der Watt, Pauline J. and Leaner, Virna D.},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {4--25},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Virome release of an invasive exotic plant species in southern France.\n \n \n \n \n\n\n \n Moubset, O.; Filloux, D.; Fontes, H.; Julian, C.; Fernandez, E.; Galzi, S.; Blondin, L.; Chehida, S. B.; Lett, J.; Mesléard, F.; Kraberger, S.; Custer, J. M; Salywon, A.; Makings, E.; Marais, A.; Chiroleu, F.; Lefeuvre, P.; Martin, D. P; Candresse, T.; Varsani, A.; Ravigné, V.; and Roumagnac, P.\n\n\n \n\n\n\n Virus Evolution, 10(1): veae025. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Virome$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{moubset_virome_2024,\n\ttitle = {Virome release of an invasive exotic plant species in southern {France}},\n\tvolume = {10},\n\tcopyright = {https://creativecommons.org/licenses/by-nc/4.0/},\n\tissn = {2057-1577},\n\turl = {https://academic.oup.com/ve/article/doi/10.1093/ve/veae025/7624785},\n\tdoi = {10.1093/ve/veae025},\n\tabstract = {Abstract \n            The increase in human-mediated introduction of plant species to new regions has resulted in a rise of invasive exotic plant species (IEPS) that has had significant effects on biodiversity and ecosystem processes. One commonly accepted mechanism of invasions is that proposed by the enemy release hypothesis (ERH), which states that IEPS free from their native herbivores and natural enemies in new environments can outcompete indigenous species and become invasive. We here propose the virome release hypothesis (VRH) as a virus-centered variant of the conventional ERH that is only focused on enemies. The VRH predicts that vertically transmitted plant-associated viruses (PAV, encompassing phytoviruses and mycoviruses) should be co-introduced during the dissemination of the IEPS, while horizontally transmitted PAV of IEPS should be left behind or should not be locally transmitted in the introduced area due to a maladaptation of local vectors. To document the VRH, virome richness and composition as well as PAV prevalence, co-infection, host range, and transmission modes were compared between indigenous plant species and an invasive grass, cane bluestem (Bothriochloa barbinodis), in both its introduced range (southern France) and one area of its native range (Sonoran Desert, Arizona, USA). Contrary to the VRH, we show that invasive populations of B. barbinodis in France were not associated with a lower PAV prevalence or richness than native populations of B. barbinodis from the USA. However, comparison of virome compositions and network analyses further revealed more diverse and complex plant–virus interactions in the French ecosystem, with a significant richness of mycoviruses. Setting mycoviruses apart, only one putatively vertically transmitted phytovirus (belonging to the Amalgaviridae family) and one putatively horizontally transmitted phytovirus (belonging to the Geminiviridae family) were identified from B. barbinodis plants in the introduced area. Collectively, these characteristics of the B. barbinodis-associated PAV community in southern France suggest that a virome release phase may have immediately followed the introduction of B. barbinodis to France in the 1960s or 1970s, and that, since then, the invasive populations of this IEPS have already transitioned out of this virome release phase, and have started interacting with several local mycoviruses and a few local plant viruses.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Virus Evolution},\n\tauthor = {Moubset, Oumaima and Filloux, Denis and Fontes, Hugo and Julian, Charlotte and Fernandez, Emmanuel and Galzi, Serge and Blondin, Laurence and Chehida, Sélim Ben and Lett, Jean-Michel and Mesléard, François and Kraberger, Simona and Custer, Joy M and Salywon, Andrew and Makings, Elizabeth and Marais, Armelle and Chiroleu, Frédéric and Lefeuvre, Pierre and Martin, Darren P and Candresse, Thierry and Varsani, Arvind and Ravigné, Virginie and Roumagnac, Philippe},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {veae025},\n}\n\n\n\n

\n

\n\n\n

\n Abstract The increase in human-mediated introduction of plant species to new regions has resulted in a rise of invasive exotic plant species (IEPS) that has had significant effects on biodiversity and ecosystem processes. One commonly accepted mechanism of invasions is that proposed by the enemy release hypothesis (ERH), which states that IEPS free from their native herbivores and natural enemies in new environments can outcompete indigenous species and become invasive. We here propose the virome release hypothesis (VRH) as a virus-centered variant of the conventional ERH that is only focused on enemies. The VRH predicts that vertically transmitted plant-associated viruses (PAV, encompassing phytoviruses and mycoviruses) should be co-introduced during the dissemination of the IEPS, while horizontally transmitted PAV of IEPS should be left behind or should not be locally transmitted in the introduced area due to a maladaptation of local vectors. To document the VRH, virome richness and composition as well as PAV prevalence, co-infection, host range, and transmission modes were compared between indigenous plant species and an invasive grass, cane bluestem (Bothriochloa barbinodis), in both its introduced range (southern France) and one area of its native range (Sonoran Desert, Arizona, USA). Contrary to the VRH, we show that invasive populations of B. barbinodis in France were not associated with a lower PAV prevalence or richness than native populations of B. barbinodis from the USA. However, comparison of virome compositions and network analyses further revealed more diverse and complex plant–virus interactions in the French ecosystem, with a significant richness of mycoviruses. Setting mycoviruses apart, only one putatively vertically transmitted phytovirus (belonging to the Amalgaviridae family) and one putatively horizontally transmitted phytovirus (belonging to the Geminiviridae family) were identified from B. barbinodis plants in the introduced area. Collectively, these characteristics of the B. barbinodis-associated PAV community in southern France suggest that a virome release phase may have immediately followed the introduction of B. barbinodis to France in the 1960s or 1970s, and that, since then, the invasive populations of this IEPS have already transitioned out of this virome release phase, and have started interacting with several local mycoviruses and a few local plant viruses.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Changes in the Vaginal Microbiome During Pregnancy and the Postpartum Period in South African Women: a Longitudinal Study.\n \n \n \n \n\n\n \n Li, K. T; Li, F.; Jaspan, H.; Nyemba, D.; Myer, L.; Aldrovandi, G.; and Joseph-Davey, D.\n\n\n \n\n\n\n Reproductive Sciences, 31(1): 275–287. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Changes$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{li_changes_2024,\n\ttitle = {Changes in the {Vaginal} {Microbiome} {During} {Pregnancy} and the {Postpartum} {Period} in {South} {African} {Women}: a {Longitudinal} {Study}},\n\tvolume = {31},\n\tissn = {1933-7191, 1933-7205},\n\tshorttitle = {Changes in the {Vaginal} {Microbiome} {During} {Pregnancy} and the {Postpartum} {Period} in {South} {African} {Women}},\n\turl = {https://link.springer.com/10.1007/s43032-023-01351-4},\n\tdoi = {10.1007/s43032-023-01351-4},\n\tabstract = {Abstract \n             \n              Pregnant women in sub-Saharan Africa have high rates of maternal morbidity. There is interest in the impact of the vaginal microbiome on maternal health, including HIV and sexually transmitted infection (STI) acquisition. We characterized the vaginal microbiota of South African women ≥ 18 years with and without HIV in a longitudinal cohort over two visits during pregnancy and one visit postpartum. At each visit, we obtained HIV testing and self-collected vaginal swabs for point-of-care testing for STIs and microbiota sequencing. We categorized microbial communities and evaluated changes over pregnancy and associations with HIV status and STI diagnosis. Across 242 women (mean age 29, 44\\% living with HIV, 33\\% diagnosed with STIs), we identified four main community state types (CSTs): two lactobacillus-dominant CSTs (dominated by \n              Lactobacillus crispatus \n              and \n              Lactobacillus iners \n              respectively) and two diverse, non-lactobacillus-dominant CSTs (one dominated by \n              Gardnerella vaginalis \n              and one by diverse facultative anaerobes). From the first antenatal visit to the third trimester (24–36 weeks gestation), 60\\% of women in the \n              Gardnerella \n              -dominant CST shifted to lactobacillus-dominant CSTs. From the third trimester to postpartum (mean 17 days post-delivery), 80\\% of women in lactobacillus-dominant CSTs shifted to non-lactobacillus-dominant CSTs with a large proportion in the facultative anaerobe-dominant CST. Microbial composition differed by STI diagnosis (PERMANOVA \n              R \n              2 \n              = 0.002, \n              p \n              = 0.004), and women diagnosed with an STI were more likely to be categorized as  \n              L. iners \n              -dominant or \n              Gardnerella \n              -dominant CSTs. Overall, we found a shift toward lactobacillus dominance during pregnancy and the emergence of a distinct, highly diverse anaerobe-dominant microbiota profile in the postpartum period.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Reproductive Sciences},\n\tauthor = {Li, Katherine T and Li, Fan and Jaspan, Heather and Nyemba, Dorothy and Myer, Landon and Aldrovandi, Grace and Joseph-Davey, Dvora},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {275--287},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Healthcare Utilization 12 Months Prior to Fatal and Non-fatal Suicidal Behaviour in Cape Town, South Africa.\n \n \n \n \n\n\n \n Kootbodien, T.; Bantjes, J.; Joska, J.; Asmal, L.; Chiliza, B.; Stallones, L.; Holtman, Z.; Martin, L. J.; Ramesar, R. S.; and London, L.\n\n\n \n\n\n\n Archives of Suicide Research, 28(1): 216–230. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Healthcare$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{kootbodien_healthcare_2024,\n\ttitle = {Healthcare {Utilization} 12 {Months} {Prior} to {Fatal} and {Non}-fatal {Suicidal} {Behaviour} in {Cape} {Town}, {South} {Africa}},\n\tvolume = {28},\n\tissn = {1381-1118, 1543-6136},\n\turl = {https://www.tandfonline.com/doi/full/10.1080/13811118.2022.2152767},\n\tdoi = {10.1080/13811118.2022.2152767},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Archives of Suicide Research},\n\tauthor = {Kootbodien, Tahira and Bantjes, Jason and Joska, John and Asmal, Laila and Chiliza, Bonginkosi and Stallones, Lorann and Holtman, Zelda and Martin, Lorna J. and Ramesar, Raj S. and London, Leslie},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {216--230},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Co-regulation of innate and adaptive immune responses induced by ID93+GLA-SE vaccination in humans.\n \n \n \n \n\n\n \n Fiore-Gartland, A.; Srivastava, H.; Seese, A.; Day, T.; Penn-Nicholson, A.; Luabeya, A. K. K.; Du Plessis, N.; Loxton, A. G.; Bekker, L.; Diacon, A.; Walzl, G.; Sagawa, Z. K.; Reed, S. G.; Scriba, T. J.; Hatherill, M.; and Coler, R.\n\n\n \n\n\n\n Frontiers in Immunology, 15: 1441944. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Co-regulation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{fiore-gartland_co-regulation_2024,\n\ttitle = {Co-regulation of innate and adaptive immune responses induced by {ID93}+{GLA}-{SE} vaccination in humans},\n\tvolume = {15},\n\tissn = {1664-3224},\n\turl = {https://www.frontiersin.org/articles/10.3389/fimmu.2024.1441944/full},\n\tdoi = {10.3389/fimmu.2024.1441944},\n\tabstract = {Introduction \n              Development of an effective vaccine against tuberculosis is a critical step towards reducing the global burden of disease. A therapeutic vaccine might also reduce the high rate of TB recurrence and help address the challenges of drug-resistant strains. ID93+GLA-SE is a candidate subunit vaccine that will soon be evaluated in a phase 2b efficacy trial for prevention of recurrent TB among patients undergoing TB treatment. ID93+GLA-SE vaccination was shown to elicit robust CD4+ T cell and IgG antibody responses among recently treated TB patients in the TBVPX-203 Phase 2a study (NCT02465216), but the mechanisms underlying these responses are not well understood. \n             \n             \n              Methods \n              In this study we used specimens from TBVPX-203 participants to describe the changes in peripheral blood gene expression that occur after ID93+GLA-SE vaccination. \n             \n             \n              Results \n              Analyses revealed several distinct modules of co-varying genes that were either up- or down-regulated after vaccination, including genes associated with innate immune pathways at 3 days post-vaccination and genes associated with lymphocyte expansion and B cell activation at 7 days post-vaccination. Notably, the regulation of these gene modules was affected by the dose schedule and by participant sex, and early innate gene signatures were correlated with the ID93-specific CD4+ T cell response. \n             \n             \n              Discussion \n              The results provide insight into the complex interplay of the innate and adaptive arms of the immune system in developing responses to vaccination with ID93+GLA-SE and demonstrate how dosing and schedule can affect vaccine responses.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Immunology},\n\tauthor = {Fiore-Gartland, Andrew and Srivastava, Himangi and Seese, Aaron and Day, Tracey and Penn-Nicholson, Adam and Luabeya, Angelique Kany Kany and Du Plessis, Nelita and Loxton, Andre G. and Bekker, Linda-Gail and Diacon, Andreas and Walzl, Gerhard and Sagawa, Zachary K. and Reed, Steven G. and Scriba, Thomas J. and Hatherill, Mark and Coler, Rhea},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {1441944},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A Myeloid-Specific Lack of IL-4Rα Prevents the Development of Alternatively Activated Macrophages and Enhances Immunity to Experimental Cysticercosis.\n \n \n \n \n\n\n \n Olguín, J. E.; Corano-Arredondo, E.; Hernández-Gómez, V.; Rivera-Montoya, I.; Rodríguez, M. A.; Medina-Andrade, I.; Arendse, B.; Brombacher, F.; and Terrazas, L. I.\n\n\n \n\n\n\n Pathogens, 13(2): 169. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{olguin_myeloid-specific_2024,\n\ttitle = {A {Myeloid}-{Specific} {Lack} of {IL}-{4Rα} {Prevents} the {Development} of {Alternatively} {Activated} {Macrophages} and {Enhances} {Immunity} to {Experimental} {Cysticercosis}},\n\tvolume = {13},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2076-0817},\n\turl = {https://www.mdpi.com/2076-0817/13/2/169},\n\tdoi = {10.3390/pathogens13020169},\n\tabstract = {To determine the role that the IL-4/IL13 receptor plays in the development of alternatively activated macrophages (AAM or M2) and their role in the regulation of immunity to the extraintestinal phase of the helminth parasite Taenia crassiceps, we followed the infection in a mouse strain lacking the IL-4Rα gene (IL-4Rα−/−) and in the macrophage/neutrophil-specific IL-4Rα-deficient mouse strain (LysMcreIL-4Rα−/lox or cre/LoxP). While 100\\% of T. crassiceps-infected IL-4Rα+/+ (WT) mice harbored large parasite loads, more than 50\\% of th eIL-4Rα−/− mice resolved the infection. Approximately 88\\% of the LysMcreIL-4Rα−/lox mice displayed a sterilizing immunity to the infection. The remaining few infected cre/LoxP mice displayed the lowest number of larvae in their peritoneal cavity. The inability of the WT mice to control the infection was associated with antigen-specific Th2-type responses with higher levels of IgG1, IL-4, IL-13, and total IgE, reduced NO production, and increased arginase activity. In contrast, IL-4Rα−/− semi-resistant mice showed a Th1/Th2 combined response. Furthermore, macrophages from the WT mice displayed higher transcripts for Arginase-1 and RELM-α, as well as increased expression of PD-L2 with robust suppressive activity over anti-CD3/CD28 stimulated T cells; all of these features are associated with the AAM or M2 macrophage phenotype. In contrast, both the IL-4Rα−/− and LysMcreIL-4Rα−/lox mice did not fully develop AAM or display suppressive activity over CD3/CD28 stimulated T cells, reducing PDL2 expression. Additionally, T-CD8+ but no T-CD4+ cells showed a suppressive phenotype with increased Tim-3 and PD1 expression in WT and IL-4Rα−/−, which were absent in T. crassiceps-infected LysMcreIL-4Rα−/lox mice. These findings demonstrate a critical role for the IL-4 signaling pathway in sustaining AAM and its suppressive activity during cysticercosis, suggesting a pivotal role for AAM in favoring susceptibility to T. crassiceps infection. Thus, the absence of these suppressor cells is one of the leading mechanisms to control experimental cysticercosis successfully.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {Pathogens},\n\tauthor = {Olguín, Jonadab E. and Corano-Arredondo, Edmundo and Hernández-Gómez, Victoria and Rivera-Montoya, Irma and Rodríguez, Mario A. and Medina-Andrade, Itzel and Arendse, Berenice and Brombacher, Frank and Terrazas, Luis I.},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {169},\n}\n\n\n\n

\n

\n\n\n

\n To determine the role that the IL-4/IL13 receptor plays in the development of alternatively activated macrophages (AAM or M2) and their role in the regulation of immunity to the extraintestinal phase of the helminth parasite Taenia crassiceps, we followed the infection in a mouse strain lacking the IL-4Rα gene (IL-4Rα−/−) and in the macrophage/neutrophil-specific IL-4Rα-deficient mouse strain (LysMcreIL-4Rα−/lox or cre/LoxP). While 100% of T. crassiceps-infected IL-4Rα+/+ (WT) mice harbored large parasite loads, more than 50% of th eIL-4Rα−/− mice resolved the infection. Approximately 88% of the LysMcreIL-4Rα−/lox mice displayed a sterilizing immunity to the infection. The remaining few infected cre/LoxP mice displayed the lowest number of larvae in their peritoneal cavity. The inability of the WT mice to control the infection was associated with antigen-specific Th2-type responses with higher levels of IgG1, IL-4, IL-13, and total IgE, reduced NO production, and increased arginase activity. In contrast, IL-4Rα−/− semi-resistant mice showed a Th1/Th2 combined response. Furthermore, macrophages from the WT mice displayed higher transcripts for Arginase-1 and RELM-α, as well as increased expression of PD-L2 with robust suppressive activity over anti-CD3/CD28 stimulated T cells; all of these features are associated with the AAM or M2 macrophage phenotype. In contrast, both the IL-4Rα−/− and LysMcreIL-4Rα−/lox mice did not fully develop AAM or display suppressive activity over CD3/CD28 stimulated T cells, reducing PDL2 expression. Additionally, T-CD8+ but no T-CD4+ cells showed a suppressive phenotype with increased Tim-3 and PD1 expression in WT and IL-4Rα−/−, which were absent in T. crassiceps-infected LysMcreIL-4Rα−/lox mice. These findings demonstrate a critical role for the IL-4 signaling pathway in sustaining AAM and its suppressive activity during cysticercosis, suggesting a pivotal role for AAM in favoring susceptibility to T. crassiceps infection. Thus, the absence of these suppressor cells is one of the leading mechanisms to control experimental cysticercosis successfully.\n

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\n \n\n \n \n \n \n \n \n New azaaurone derivatives as potential multitarget agents in HIV‐TB coinfection.\n \n \n \n \n\n\n \n Leite, D. I.; Campaniço, A.; Costa, P. A. G.; Correa, I. A.; Da Costa, L. J.; Bastos, M. M.; Moreira, R.; Lopes, F.; Jordaan, A.; Warner, D. F.; and Boechat, N.\n\n\n \n\n\n\n Archiv der Pharmazie, 357(2): 2300560. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"New$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{leite_new_2024,\n\ttitle = {New azaaurone derivatives as potential multitarget agents in {HIV}‐{TB} coinfection},\n\tvolume = {357},\n\tissn = {0365-6233, 1521-4184},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/ardp.202300560},\n\tdoi = {10.1002/ardp.202300560},\n\tabstract = {Abstract \n             \n              Tuberculosis (TB) disease, caused by \n              Mycobacterium tuberculosis \n              ( \n              Mtb \n              ) is the leading cause of death among people with human immunodeficiency virus (HIV) infection. No dual‐target drug is currently being used to simultaneously treat both infections. This work aimed to obtain new multitarget HIV‐TB agents, with the goal of optimizing treatments and preventing this coinfection. These compounds incorporate the structural features of azaaurones as anti‐ \n              Mtb \n              and zidovudine (AZT) as the antiretroviral moiety. The azaaurone scaffold displayed submicromolar activities against \n              Mtb \n              , and AZT is a potent antiretroviral drug. Six derivatives were synthetically generated, and five were evaluated against both infective agents. Evaluations of anti‐HIV activity were carried out in HIV‐1‐infected MT‐4 cells and on endogenous HIV‐1 reverse transcriptase (RT) activity. The H37Rv strain was used for anti‐ \n              Mtb \n              assessments. Most compounds displayed potent antitubercular and moderate anti‐HIV activity. ( \n              E \n              )‐ \n              12 \n              exhibited a promising multitarget profile with an MIC \n              90 \n              of 2.82 µM and an IC \n              50 \n              of 1.98 µM in HIV‐1‐infected T lymphocyte cells, with an 84\\% inhibition of RT activity. Therefore, ( \n              E \n              )‐ \n              12 \n              could be the first promising compound from a family of multitarget agents used to treat HIV‐TB coinfection. In addition, the compound could offer a prototype for the development of new strategies in scientific research to treat this global health issue.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {Archiv der Pharmazie},\n\tauthor = {Leite, Debora I. and Campaniço, Andre and Costa, Pedro A. G. and Correa, Isadora A. and Da Costa, Luciana J. and Bastos, Monica M. and Moreira, Rui and Lopes, Francisca and Jordaan, Audrey and Warner, Digby F. and Boechat, Nubia},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {2300560},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Intra- and inter-subtype HIV diversity between 1994 and 2018 in southern Uganda: a longitudinal population-based study.\n \n \n \n \n\n\n \n Kim, S.; Kigozi, G.; Martin, M. A; Galiwango, R. M; Quinn, T. C; Redd, A. D; Ssekubugu, R.; Bonsall, D.; Ssemwanga, D.; Rambaut, A.; Herbeck, J. T; Reynolds, S. J; Foley, B.; Abeler-Dörner, L.; Fraser, C.; Ratmann, O.; Kagaayi, J.; Laeyendecker, O.; and Grabowski, M. K\n\n\n \n\n\n\n Virus Evolution, 10(1): veae065. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Intra-$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{kim_intra-_2024,\n\ttitle = {Intra- and inter-subtype {HIV} diversity between 1994 and 2018 in southern {Uganda}: a longitudinal population-based study},\n\tvolume = {10},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2057-1577},\n\tshorttitle = {Intra- and inter-subtype {HIV} diversity between 1994 and 2018 in southern {Uganda}},\n\turl = {https://academic.oup.com/ve/article/doi/10.1093/ve/veae065/7741203},\n\tdoi = {10.1093/ve/veae065},\n\tabstract = {Abstract \n            There is limited data on human immunodeficiency virus (HIV) evolutionary trends in African populations. We evaluated changes in HIV viral diversity and genetic divergence in southern Uganda over a 24-year period spanning the introduction and scale-up of HIV prevention and treatment programs using HIV sequence and survey data from the Rakai Community Cohort Study, an open longitudinal population-based HIV surveillance cohort. Gag (p24) and env (gp41) HIV data were generated from people living with HIV (PLHIV) in 31 inland semi-urban trading and agrarian communities (1994–2018) and four hyperendemic Lake Victoria fishing communities (2011–2018) under continuous surveillance. HIV subtype was assigned using the Recombination Identification Program with phylogenetic confirmation. Inter-subtype diversity was evaluated using the Shannon diversity index, and intra-subtype diversity with the nucleotide diversity and pairwise TN93 genetic distance. Genetic divergence was measured using root-to-tip distance and pairwise TN93 genetic distance analyses. Demographic history of HIV was inferred using a coalescent-based Bayesian Skygrid model. Evolutionary dynamics were assessed among demographic and behavioral population subgroups, including by migration status. 9931 HIV sequences were available from 4999 PLHIV, including 3060 and 1939 persons residing in inland and fishing communities, respectively. In inland communities, subtype A1 viruses proportionately increased from 14.3\\% in 1995 to 25.9\\% in 2017 (P \\&lt; .001), while those of subtype D declined from 73.2\\% in 1995 to 28.2\\% in 2017 (P \\&lt; .001). The proportion of viruses classified as recombinants significantly increased by nearly four-fold from 12.2\\% in 1995 to 44.8\\% in 2017. Inter-subtype HIV diversity has generally increased. While intra-subtype p24 genetic diversity and divergence leveled off after 2014, intra-subtype gp41 diversity, effective population size, and divergence increased through 2017. Intra- and inter-subtype viral diversity increased across all demographic and behavioral population subgroups, including among individuals with no recent migration history or extra-community sexual partners. This study provides insights into population-level HIV evolutionary dynamics following the scale-up of HIV prevention and treatment programs. Continued molecular surveillance may provide a better understanding of the dynamics driving population HIV evolution and yield important insights for epidemic control and vaccine development.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Virus Evolution},\n\tauthor = {Kim, Seungwon and Kigozi, Godfrey and Martin, Michael A and Galiwango, Ronald M and Quinn, Thomas C and Redd, Andrew D and Ssekubugu, Robert and Bonsall, David and Ssemwanga, Deogratius and Rambaut, Andrew and Herbeck, Joshua T and Reynolds, Steven J and Foley, Brian and Abeler-Dörner, Lucie and Fraser, Christophe and Ratmann, Oliver and Kagaayi, Joseph and Laeyendecker, Oliver and Grabowski, Mary K},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {veae065},\n}\n\n\n\n

\n

\n\n\n

\n Abstract There is limited data on human immunodeficiency virus (HIV) evolutionary trends in African populations. We evaluated changes in HIV viral diversity and genetic divergence in southern Uganda over a 24-year period spanning the introduction and scale-up of HIV prevention and treatment programs using HIV sequence and survey data from the Rakai Community Cohort Study, an open longitudinal population-based HIV surveillance cohort. Gag (p24) and env (gp41) HIV data were generated from people living with HIV (PLHIV) in 31 inland semi-urban trading and agrarian communities (1994–2018) and four hyperendemic Lake Victoria fishing communities (2011–2018) under continuous surveillance. HIV subtype was assigned using the Recombination Identification Program with phylogenetic confirmation. Inter-subtype diversity was evaluated using the Shannon diversity index, and intra-subtype diversity with the nucleotide diversity and pairwise TN93 genetic distance. Genetic divergence was measured using root-to-tip distance and pairwise TN93 genetic distance analyses. Demographic history of HIV was inferred using a coalescent-based Bayesian Skygrid model. Evolutionary dynamics were assessed among demographic and behavioral population subgroups, including by migration status. 9931 HIV sequences were available from 4999 PLHIV, including 3060 and 1939 persons residing in inland and fishing communities, respectively. In inland communities, subtype A1 viruses proportionately increased from 14.3% in 1995 to 25.9% in 2017 (P < .001), while those of subtype D declined from 73.2% in 1995 to 28.2% in 2017 (P < .001). The proportion of viruses classified as recombinants significantly increased by nearly four-fold from 12.2% in 1995 to 44.8% in 2017. Inter-subtype HIV diversity has generally increased. While intra-subtype p24 genetic diversity and divergence leveled off after 2014, intra-subtype gp41 diversity, effective population size, and divergence increased through 2017. Intra- and inter-subtype viral diversity increased across all demographic and behavioral population subgroups, including among individuals with no recent migration history or extra-community sexual partners. This study provides insights into population-level HIV evolutionary dynamics following the scale-up of HIV prevention and treatment programs. Continued molecular surveillance may provide a better understanding of the dynamics driving population HIV evolution and yield important insights for epidemic control and vaccine development.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Pharmacogenetics of tamoxifen in breast cancer patients of African descent: Lack of data.\n \n \n \n \n\n\n \n Kruger, B.; Shamley, D.; Soko, N. D.; and Dandara, C.\n\n\n \n\n\n\n Clinical and Translational Science, 17(3): e13761. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Pharmacogenetics$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{kruger_pharmacogenetics_2024,\n\ttitle = {Pharmacogenetics of tamoxifen in breast cancer patients of {African} descent: {Lack} of data},\n\tvolume = {17},\n\tissn = {1752-8054, 1752-8062},\n\tshorttitle = {Pharmacogenetics of tamoxifen in breast cancer patients of {African} descent},\n\turl = {https://ascpt.onlinelibrary.wiley.com/doi/10.1111/cts.13761},\n\tdoi = {10.1111/cts.13761},\n\tabstract = {Abstract \n            Tamoxifen, a selective estrogen receptor modulator, is used to treat hormone receptor‐positive breast cancer. Tamoxifen acts as a prodrug, with its primary therapeutic effect mediated by its principal metabolite, endoxifen. However, tamoxifen has complex pharmacokinetics involving several drug‐metabolizing enzymes and transporters influencing its disposition. Genes encoding enzymes involved in tamoxifen disposition exhibit genetic polymorphisms which vary widely across world populations. This review highlights the lack of data on tamoxifen pharmacogenetics among African populations. Gaps in data are described in this study with the purpose that future research can address this dearth of research on the pharmacogenetics of tamoxifen among African breast cancer patients. Initiatives such as the African Pharmacogenomics Network (APN) are crucial in promoting comprehensive pharmacogenetics studies to pinpoint important variants in pharmacogenes that could be used to reduce toxicity and improve efficacy.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Clinical and Translational Science},\n\tauthor = {Kruger, Bianca and Shamley, Delva and Soko, Nyarai Desiree and Dandara, Collet},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {e13761},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Longitudinal gut microbiota composition of South African and Nigerian infants in relation to tetanus vaccine responses.\n \n \n \n \n\n\n \n Iwase, S. C.; Osawe, S.; Happel, A.; Gray, C. M.; Holmes, S. P.; Blackburn, J. M.; Abimiku, A.; and Jaspan, H. B.\n\n\n \n\n\n\n Microbiology Spectrum, 12(2): e03190–23. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Longitudinal$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{iwase_longitudinal_2024,\n\ttitle = {Longitudinal gut microbiota composition of {South} {African} and {Nigerian} infants in relation to tetanus vaccine responses},\n\tvolume = {12},\n\tissn = {2165-0497},\n\turl = {https://journals.asm.org/doi/10.1128/spectrum.03190-23},\n\tdoi = {10.1128/spectrum.03190-23},\n\tabstract = {ABSTRACT \n             \n              Infants who are exposed to HIV but uninfected (iHEU) have higher risk of infectious morbidity than infants who are HIV-unexposed and uninfected (iHUU), possibly due to altered immunity. As infant gut microbiota may influence immune development, we evaluated the effects of HIV exposure on infant gut microbiota and its association with tetanus toxoid vaccine responses. We evaluated the gut microbiota of 82 South African (61 iHEU and 21 iHUU) and 196 Nigerian (141 iHEU and 55 iHUU) infants at {\\textless}1 and 15 weeks of life by 16S rRNA gene sequencing. Anti-tetanus antibodies were measured by enzyme-linked immunosorbent assay at matched time points. Gut microbiota in the 278 included infants and its succession were more strongly influenced by geographical location and age than by HIV exposure. Microbiota of Nigerian infants, who were exclusively breastfed, drastically changed over 15 weeks, becoming dominated by \n              Bifidobacterium longum \n              subspecies \n              infantis \n              . This change was not observed among South African infants, even when limiting the analysis to exclusively breastfed infants. The Least Absolute Shrinkage and Selection Operator regression suggested that HIV exposure and gut microbiota were independently associated with tetanus titers at week 15, and that high passively transferred antibody levels, as seen in the Nigerian cohort, may mitigate these effects. In conclusion, in two African cohorts, HIV exposure minimally altered the infant gut microbiota compared to age and setting, but both specific gut microbes and HIV exposure independently predicted humoral tetanus vaccine responses. \n             \n             \n              IMPORTANCE \n              Gut microbiota plays an essential role in immune system development. Since infants HIV-exposed and uninfected (iHEU) are more vulnerable to infectious diseases than unexposed infants, we explored the impact of HIV exposure on gut microbiota and its association with vaccine responses. This study was conducted in two African countries with rapidly increasing numbers of iHEU. Infant HIV exposure did not substantially affect gut microbial succession, but geographic location had a strong effect. However, both the relative abundance of specific gut microbes and HIV exposure were independently associated with tetanus titers, which were also influenced by baseline tetanus titers (maternal transfer). Our findings provide insight into the effect of HIV exposure, passive maternal antibody, and gut microbiota on infant humoral vaccine responses. \n             \n          ,  \n            Gut microbiota plays an essential role in immune system development. Since infants HIV-exposed and uninfected (iHEU) are more vulnerable to infectious diseases than unexposed infants, we explored the impact of HIV exposure on gut microbiota and its association with vaccine responses. This study was conducted in two African countries with rapidly increasing numbers of iHEU. Infant HIV exposure did not substantially affect gut microbial succession, but geographic location had a strong effect. However, both the relative abundance of specific gut microbes and HIV exposure were independently associated with tetanus titers, which were also influenced by baseline tetanus titers (maternal transfer). Our findings provide insight into the effect of HIV exposure, passive maternal antibody, and gut microbiota on infant humoral vaccine responses.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {Microbiology Spectrum},\n\tauthor = {Iwase, Saori C. and Osawe, Sophia and Happel, Anna-Ursula and Gray, Clive M. and Holmes, Susan P. and Blackburn, Jonathan M. and Abimiku, Alash'le and Jaspan, Heather B.},\n\teditor = {Yeruva, Laxmi},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {e03190--23},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Infants who are exposed to HIV but uninfected (iHEU) have higher risk of infectious morbidity than infants who are HIV-unexposed and uninfected (iHUU), possibly due to altered immunity. As infant gut microbiota may influence immune development, we evaluated the effects of HIV exposure on infant gut microbiota and its association with tetanus toxoid vaccine responses. We evaluated the gut microbiota of 82 South African (61 iHEU and 21 iHUU) and 196 Nigerian (141 iHEU and 55 iHUU) infants at \\textless1 and 15 weeks of life by 16S rRNA gene sequencing. Anti-tetanus antibodies were measured by enzyme-linked immunosorbent assay at matched time points. Gut microbiota in the 278 included infants and its succession were more strongly influenced by geographical location and age than by HIV exposure. Microbiota of Nigerian infants, who were exclusively breastfed, drastically changed over 15 weeks, becoming dominated by Bifidobacterium longum subspecies infantis . This change was not observed among South African infants, even when limiting the analysis to exclusively breastfed infants. The Least Absolute Shrinkage and Selection Operator regression suggested that HIV exposure and gut microbiota were independently associated with tetanus titers at week 15, and that high passively transferred antibody levels, as seen in the Nigerian cohort, may mitigate these effects. In conclusion, in two African cohorts, HIV exposure minimally altered the infant gut microbiota compared to age and setting, but both specific gut microbes and HIV exposure independently predicted humoral tetanus vaccine responses. IMPORTANCE Gut microbiota plays an essential role in immune system development. Since infants HIV-exposed and uninfected (iHEU) are more vulnerable to infectious diseases than unexposed infants, we explored the impact of HIV exposure on gut microbiota and its association with vaccine responses. This study was conducted in two African countries with rapidly increasing numbers of iHEU. Infant HIV exposure did not substantially affect gut microbial succession, but geographic location had a strong effect. However, both the relative abundance of specific gut microbes and HIV exposure were independently associated with tetanus titers, which were also influenced by baseline tetanus titers (maternal transfer). Our findings provide insight into the effect of HIV exposure, passive maternal antibody, and gut microbiota on infant humoral vaccine responses. , Gut microbiota plays an essential role in immune system development. Since infants HIV-exposed and uninfected (iHEU) are more vulnerable to infectious diseases than unexposed infants, we explored the impact of HIV exposure on gut microbiota and its association with vaccine responses. This study was conducted in two African countries with rapidly increasing numbers of iHEU. Infant HIV exposure did not substantially affect gut microbial succession, but geographic location had a strong effect. However, both the relative abundance of specific gut microbes and HIV exposure were independently associated with tetanus titers, which were also influenced by baseline tetanus titers (maternal transfer). Our findings provide insight into the effect of HIV exposure, passive maternal antibody, and gut microbiota on infant humoral vaccine responses.\n

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\n \n\n \n \n \n \n \n \n Increase of niche filling with increase of host richness for plant-infecting mastreviruses.\n \n \n \n \n\n\n \n Ben Chéhida, S.; Devi Bunwaree, H.; Hoareau, M.; Moubset, O.; Julian, C.; Blondin, L.; Filloux, D.; Lavergne, C.; Roumagnac, P.; Varsani, A.; Martin, D. P; Lett, J.; and Lefeuvre, P.\n\n\n \n\n\n\n Virus Evolution, 10(1): veae107. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Increase$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{ben_chehida_increase_2024,\n\ttitle = {Increase of niche filling with increase of host richness for plant-infecting mastreviruses},\n\tvolume = {10},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2057-1577},\n\turl = {https://academic.oup.com/ve/article/doi/10.1093/ve/veae107/7923423},\n\tdoi = {10.1093/ve/veae107},\n\tabstract = {Abstract \n            Now that it has been realized that viruses are ubiquitous, questions have been raised on factors influencing their diversity and distribution. For phytoviruses, understanding the interplay between plant diversity and virus species richness and prevalence remains cardinal. As both the amplification and the dilution of viral species richness due to increasing host diversity have been theorized and observed, a deeper understanding of how plants and viruses interact in natural environments is needed to explore how host availability conditions viral diversity and distributions. From a unique dataset, this study explores interactions of Mastrevirus species (family Geminiviridae) with Poales order hosts across 10 sites from three contrasting ecosystems on La Réunion. Among 273 plant pools, representing 61 Poales species, 15 Mastrevirus species were characterized from 22 hosts. The analysis revealed a strong association of mastreviruses with hosts from agroecosystems, the rare presence of viruses in coastal grasslands, and the absence of mastreviruses in subalpine areas, areas dominated by native plants. This suggests that detected mastreviruses were introduced through anthropogenic activities, emphasizing the role of humans in shaping the global pathobiome. By reconstructing the realized host–virus infection network, besides revealing a pattern of increasing viral richness with increasing host richness, we observed increasing viral niche occupancies with increasing host species richness, implying that virus realized richness at any given site is conditioned on the global capacity of the plant populations to host diverse mastreviruses. Whether this tendency is driven by synergy between viruses or by an interplay between vector population and plant richness remains to be established.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Virus Evolution},\n\tauthor = {Ben Chéhida, Sélim and Devi Bunwaree, Heemee and Hoareau, Murielle and Moubset, Oumaima and Julian, Charlotte and Blondin, Laurence and Filloux, Denis and Lavergne, Christophe and Roumagnac, Philippe and Varsani, Arvind and Martin, Darren P and Lett, Jean-Michel and Lefeuvre, Pierre},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {veae107},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Another decade of antimalarial drug discovery: New targets, tools and molecules.\n \n \n \n \n\n\n \n Woodland, J. G.; Horatscheck, A.; Soares De Melo, C.; Dziwornu, G. A.; and Taylor, D.\n\n\n \n\n\n\n In Progress in Medicinal Chemistry, volume 63, pages 161–234. Elsevier, 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Another$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@incollection{woodland_another_2024,\n\ttitle = {Another decade of antimalarial drug discovery: {New} targets, tools and molecules},\n\tvolume = {63},\n\tcopyright = {https://www.elsevier.com/tdm/userlicense/1.0/},\n\tisbn = {9780443297809},\n\tshorttitle = {Another decade of antimalarial drug discovery},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0079646824000031},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tbooktitle = {Progress in {Medicinal} {Chemistry}},\n\tpublisher = {Elsevier},\n\tauthor = {Woodland, John G. and Horatscheck, André and Soares De Melo, Candice and Dziwornu, Godwin A. and Taylor, Dale},\n\tyear = {2024},\n\tdoi = {10.1016/bs.pmch.2024.08.001},\n\tpages = {161--234},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Modelling the Cost-Effectiveness of Hepatitis A in South Africa.\n \n \n \n \n\n\n \n Patterson, J.; Cleary, S.; Norman, J.; Van Zyl, H.; Awine, T.; Mayet, S.; Kagina, B.; Muloiwa, R.; Hussey, G.; and Silal, S.\n\n\n \n\n\n\n Vaccines, 12(2): 116. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Modelling$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{patterson_modelling_2024,\n\ttitle = {Modelling the {Cost}-{Effectiveness} of {Hepatitis} {A} in {South} {Africa}},\n\tvolume = {12},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2076-393X},\n\turl = {https://www.mdpi.com/2076-393X/12/2/116},\n\tdoi = {10.3390/vaccines12020116},\n\tabstract = {The World Health Organization (WHO) recommends the consideration of introducing routine hepatitis A vaccination into national immunization schedules for children ≥ 1 years old in countries with intermediate HAV endemicity. Recent data suggest that South Africa is transitioning from high to intermediate HAV endemicity, thus it is important to consider the impact and cost of potential routine hepatitis A vaccination strategies in the country. An age-structured compartmental model of hepatitis A transmission was calibrated with available data from South Africa, incorporating direct costs of hepatitis A treatment and vaccination. We used the calibrated model to evaluate the impact and costs of several childhood hepatitis A vaccination scenarios from 2023 to 2030. We assessed how each scenario impacted the burden of hepatitis A (symptomatic hepatitis A cases and mortality) as well as calculated the incremental cost per DALY averted as compared to the South African cost-effectiveness threshold. All costs and outcomes were discounted at 5\\%. For the modelled scenarios, the median estimated cost of the different vaccination strategies ranged from USD 1.71 billion to USD 2.85 billion over the period of 2023 to 2030, with the cost increasing for each successive scenario and approximately 39–52\\% of costs being due to vaccination. Scenario 1, which represented the administration of one dose of the hepatitis A vaccine in children {\\textless} 2 years old, requires approximately 5.3 million vaccine doses over 2023–2030 and is projected to avert a total of 136,042 symptomatic cases [IQR: 88,842–221,483] and 31,106 [IQR: 22,975–36,742] deaths due to hepatitis A over the period of 2023 to 2030. The model projects that Scenario 1 would avert 8741 DALYs over the period of 2023 to 2030; however, it is not cost-effective against the South African cost-effectiveness threshold with an ICER per DALY averted of USD 21,006. While Scenario 3 and 4 included the administration of more vaccine doses and averted more symptomatic cases of hepatitis A, these scenarios were absolutely dominated owing to the population being infected before vaccination through the mass campaigns at older ages. The model was highly sensitive to variation of access to liver transplant in South Africa. When increasing the access to liver transplant to 100\\% for the baseline and Scenario 1, the ICER for Scenario 1 becomes cost-effective against the CET (ICER = USD 2425). Given these findings, we recommend further research is conducted to understand the access to liver transplants in South Africa and better estimate the cost of liver transplant care for hepatitis A patients. The modelling presented in this paper has been used to develop a user-friendly application for vaccine policy makers to further interrogate the model outcomes and consider the costs and benefits of introducing routine hepatitis A vaccination in South Africa.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {Vaccines},\n\tauthor = {Patterson, Jenna and Cleary, Susan and Norman, Jared and Van Zyl, Heiletjé and Awine, Timothy and Mayet, Saadiyah and Kagina, Benjamin and Muloiwa, Rudzani and Hussey, Gregory and Silal, Sheetal},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {116},\n}\n\n\n\n

\n

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\n The World Health Organization (WHO) recommends the consideration of introducing routine hepatitis A vaccination into national immunization schedules for children ≥ 1 years old in countries with intermediate HAV endemicity. Recent data suggest that South Africa is transitioning from high to intermediate HAV endemicity, thus it is important to consider the impact and cost of potential routine hepatitis A vaccination strategies in the country. An age-structured compartmental model of hepatitis A transmission was calibrated with available data from South Africa, incorporating direct costs of hepatitis A treatment and vaccination. We used the calibrated model to evaluate the impact and costs of several childhood hepatitis A vaccination scenarios from 2023 to 2030. We assessed how each scenario impacted the burden of hepatitis A (symptomatic hepatitis A cases and mortality) as well as calculated the incremental cost per DALY averted as compared to the South African cost-effectiveness threshold. All costs and outcomes were discounted at 5%. For the modelled scenarios, the median estimated cost of the different vaccination strategies ranged from USD 1.71 billion to USD 2.85 billion over the period of 2023 to 2030, with the cost increasing for each successive scenario and approximately 39–52% of costs being due to vaccination. Scenario 1, which represented the administration of one dose of the hepatitis A vaccine in children \\textless 2 years old, requires approximately 5.3 million vaccine doses over 2023–2030 and is projected to avert a total of 136,042 symptomatic cases [IQR: 88,842–221,483] and 31,106 [IQR: 22,975–36,742] deaths due to hepatitis A over the period of 2023 to 2030. The model projects that Scenario 1 would avert 8741 DALYs over the period of 2023 to 2030; however, it is not cost-effective against the South African cost-effectiveness threshold with an ICER per DALY averted of USD 21,006. While Scenario 3 and 4 included the administration of more vaccine doses and averted more symptomatic cases of hepatitis A, these scenarios were absolutely dominated owing to the population being infected before vaccination through the mass campaigns at older ages. The model was highly sensitive to variation of access to liver transplant in South Africa. When increasing the access to liver transplant to 100% for the baseline and Scenario 1, the ICER for Scenario 1 becomes cost-effective against the CET (ICER = USD 2425). Given these findings, we recommend further research is conducted to understand the access to liver transplants in South Africa and better estimate the cost of liver transplant care for hepatitis A patients. The modelling presented in this paper has been used to develop a user-friendly application for vaccine policy makers to further interrogate the model outcomes and consider the costs and benefits of introducing routine hepatitis A vaccination in South Africa.\n

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\n \n\n \n \n \n \n \n \n Airborne transmission risks of tuberculosis and COVID-19 in schools in South Africa, Switzerland, and Tanzania: Modeling of environmental data.\n \n \n \n \n\n\n \n Banholzer, N.; Schmutz, R.; Middelkoop, K.; Hella, J.; Egger, M.; Wood, R.; and Fenner, L.\n\n\n \n\n\n\n PLOS Global Public Health, 4(1): e0002800. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Airborne$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{banholzer_airborne_2024,\n\ttitle = {Airborne transmission risks of tuberculosis and {COVID}-19 in schools in {South} {Africa}, {Switzerland}, and {Tanzania}: {Modeling} of environmental data},\n\tvolume = {4},\n\tissn = {2767-3375},\n\tshorttitle = {Airborne transmission risks of tuberculosis and {COVID}-19 in schools in {South} {Africa}, {Switzerland}, and {Tanzania}},\n\turl = {https://dx.plos.org/10.1371/journal.pgph.0002800},\n\tdoi = {10.1371/journal.pgph.0002800},\n\tabstract = {The COVID-19 pandemic renewed interest in airborne transmission of respiratory infections, particularly in congregate indoor settings, such as schools. We modeled transmission risks of tuberculosis (caused by \n              Mycobacterium tuberculosis \n              , \n              Mtb \n              ) and COVID-19 (caused by SARS-CoV-2) in South African, Swiss and Tanzanian secondary schools. We estimated the risks of infection with the Wells-Riley equation, expressed as the median with 2.5\\% and 97.5\\% quantiles (credible interval [CrI]), based on the ventilation rate and the duration of exposure to infectious doses (so-called quanta). We computed the air change rate (ventilation) using carbon dioxide (CO \n              2 \n              ) as a tracer gas and modeled the quanta generation rate based on reported estimates from the literature. The share of infectious students in the classroom is determined by country-specific estimates of pulmonary TB. For SARS-CoV-2, the number of infectious students was estimated based on excess mortality to mitigate the bias from country-specific reporting and testing. Average CO \n              2 \n              concentration (parts per million [ppm]) was 1,610 ppm in South Africa, 1,757 ppm in Switzerland, and 648 ppm in Tanzania. The annual risk of infection for \n              Mtb \n              was 22.1\\% (interquartile range [IQR] 2.7\\%-89.5\\%) in South Africa, 0.7\\% (IQR 0.1\\%-6.4\\%) in Switzerland, and 0.5\\% (IQR 0.0\\%-3.9\\%) in Tanzania. For SARS-CoV-2, the monthly risk of infection was 6.8\\% (IQR 0.8\\%-43.8\\%) in South Africa, 1.2\\% (IQR 0.1\\%-8.8\\%) in Switzerland, and 0.9\\% (IQR 0.1\\%-6.6\\%) in Tanzania. The differences in transmission risks primarily reflect a higher incidence of SARS-CoV-2 and particularly prevalence of TB in South Africa, but also higher air change rates due to better natural ventilation of the classrooms in Tanzania. Global comparisons of the modeled risk of infectious disease transmission in classrooms can provide high-level information for policy-making regarding appropriate infection control strategies.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Global Public Health},\n\tauthor = {Banholzer, Nicolas and Schmutz, Remo and Middelkoop, Keren and Hella, Jerry and Egger, Matthias and Wood, Robin and Fenner, Lukas},\n\teditor = {Finger, Flavio},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {e0002800},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Phylogenetic evidence of extensive spatial mixing of diverse HIV-1 group M lineages within Cameroon but not between its neighbours.\n \n \n \n \n\n\n \n Godwe, C.; Goni, O. H; San, J. E; Sonela, N.; Tchakoute, M.; Nanfack, A.; Koro, F. K; Butel, C.; Vidal, N.; Duerr, R.; Martin, D. P; De Oliveira, T.; Peeters, M.; Altfeld, M.; Ayouba, A.; Ndung’u, T.; and Tongo, M.\n\n\n \n\n\n\n Virus Evolution, 10(1): veae070. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Phylogenetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{godwe_phylogenetic_2024,\n\ttitle = {Phylogenetic evidence of extensive spatial mixing of diverse {HIV}-1 group {M} lineages within {Cameroon} but not between its neighbours},\n\tvolume = {10},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2057-1577},\n\turl = {https://academic.oup.com/ve/article/doi/10.1093/ve/veae070/7747406},\n\tdoi = {10.1093/ve/veae070},\n\tabstract = {Abstract \n            From the perspective of developing relevant interventions for treating HIV and controlling its spread, it is particularly important to comprehensively understand the underlying diversity of the virus, especially in countries where the virus has been present and evolving since the cross-species transmission event that triggered the global pandemic. Here, we generate and phylogenetically analyse sequences derived from the gag-protease (2010 bp; n = 115), partial integrase (345 bp; n = 36), and nef (719 bp; n = 321) genes of HIV-1 group M (HIV-1M) isolates sampled between 2000 and 2022 from two cosmopolitan cities and 40 remote villages of Cameroon. While 52.4\\% of all sequenced viruses belonged to circulating recombinant form (CRF) 02\\_AG (CRF02\\_AG), the remainder were highly diverse, collectively representing seven subtypes and sub-subtypes, eight CRFs, and 36 highly divergent lineages that fall outside the established HIV-1M classification. Additionally, in 77 samples for which at least two genes were typed, 31\\% of the studied viruses apparently had fragments from viruses belonging to different clades. Furthermore, we found that the distribution of HIV-1M populations is similar between different regions of Cameroon. In contrast, HIV-1M demographics in Cameroon differ significantly from those in its neighbouring countries in the Congo Basin (CB). In phylogenetic trees, viral sequences cluster according to the countries where they were sampled, suggesting that while there are minimal geographical or social barriers to viral dissemination throughout Cameroon, there is strongly impeded dispersal of HIV-1M lineages between Cameroon and other locations of the CB. This suggests that the apparent stability of highly diverse Cameroonian HIV-1M populations may be attributable to the extensive mixing of human populations within the country and the concomitant trans-national movements of major lineages with very similar degrees of fitness; coupled with the relatively infrequent inter-national transmission of these lineages from neighbouring countries in the CB.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Virus Evolution},\n\tauthor = {Godwe, Célestin and Goni, Oumarou H and San, James E and Sonela, Nelson and Tchakoute, Mérimé and Nanfack, Aubin and Koro, Francioli K and Butel, Christelle and Vidal, Nicole and Duerr, Ralf and Martin, Darren P and De Oliveira, Tulio and Peeters, Martine and Altfeld, Marcus and Ayouba, Ahidjo and Ndung’u, Thumbi and Tongo, Marcel},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {veae070},\n}\n\n\n\n

\n

\n\n\n

\n Abstract From the perspective of developing relevant interventions for treating HIV and controlling its spread, it is particularly important to comprehensively understand the underlying diversity of the virus, especially in countries where the virus has been present and evolving since the cross-species transmission event that triggered the global pandemic. Here, we generate and phylogenetically analyse sequences derived from the gag-protease (2010 bp; n = 115), partial integrase (345 bp; n = 36), and nef (719 bp; n = 321) genes of HIV-1 group M (HIV-1M) isolates sampled between 2000 and 2022 from two cosmopolitan cities and 40 remote villages of Cameroon. While 52.4% of all sequenced viruses belonged to circulating recombinant form (CRF) 02_AG (CRF02_AG), the remainder were highly diverse, collectively representing seven subtypes and sub-subtypes, eight CRFs, and 36 highly divergent lineages that fall outside the established HIV-1M classification. Additionally, in 77 samples for which at least two genes were typed, 31% of the studied viruses apparently had fragments from viruses belonging to different clades. Furthermore, we found that the distribution of HIV-1M populations is similar between different regions of Cameroon. In contrast, HIV-1M demographics in Cameroon differ significantly from those in its neighbouring countries in the Congo Basin (CB). In phylogenetic trees, viral sequences cluster according to the countries where they were sampled, suggesting that while there are minimal geographical or social barriers to viral dissemination throughout Cameroon, there is strongly impeded dispersal of HIV-1M lineages between Cameroon and other locations of the CB. This suggests that the apparent stability of highly diverse Cameroonian HIV-1M populations may be attributable to the extensive mixing of human populations within the country and the concomitant trans-national movements of major lineages with very similar degrees of fitness; coupled with the relatively infrequent inter-national transmission of these lineages from neighbouring countries in the CB.\n

\n\n\n

\n \n\n \n \n \n \n \n \n What is next for BCG revaccination to prevent tuberculosis?.\n \n \n \n \n\n\n \n White, R. G; Fiore-Gartland, A. J; Hanekom, W. A; Vekemans, J.; Garcia-Basteiro, A. L; Churchyard, G.; Rangaka, M. X; Frick, M.; Behr, M. A; Hill, P. C; and Mave, V.\n\n\n \n\n\n\n The Lancet Respiratory Medicine, 12(3): e7–e8. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"What$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{white_what_2024,\n\ttitle = {What is next for {BCG} revaccination to prevent tuberculosis?},\n\tvolume = {12},\n\tissn = {22132600},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2213260024000092},\n\tdoi = {10.1016/S2213-2600(24)00009-2},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Respiratory Medicine},\n\tauthor = {White, Richard G and Fiore-Gartland, Andrew J and Hanekom, Willem A and Vekemans, Johan and Garcia-Basteiro, Alberto L and Churchyard, Gavin and Rangaka, Molebogeng X and Frick, Mike and Behr, Marcel A and Hill, Philip C and Mave, Vidya},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {e7--e8},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Investigating genomic diversity of Staphylococcus aureus associated with pediatric atopic dermatitis in South Africa.\n \n \n \n \n\n\n \n Ndhlovu, G. O. N.; Javkar, K. G.; Matuvhunye, T.; Ngondoh, F.; Jamrozy, D.; Bentley, S.; Shittu, A. O.; and Dube, F. S.\n\n\n \n\n\n\n Frontiers in Microbiology, 15: 1422902. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Investigating$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{ndhlovu_investigating_2024,\n\ttitle = {Investigating genomic diversity of {Staphylococcus} aureus associated with pediatric atopic dermatitis in {South} {Africa}},\n\tvolume = {15},\n\tissn = {1664-302X},\n\turl = {https://www.frontiersin.org/articles/10.3389/fmicb.2024.1422902/full},\n\tdoi = {10.3389/fmicb.2024.1422902},\n\tabstract = {Importance \n               \n                Staphylococcus aureus \n                frequently colonizes the skin and nose of patients with atopic dermatitis (AD), a disease associated with skin barrier dysfunction and chronic cutaneous inflammation. Published genomic studies on AD-associated \n                S. aureus \n                in pediatric populations in sub-Saharan Africa are limited. \n               \n             \n             \n              Objectives \n               \n                To investigate the phenotypic and genomic diversity of \n                S. aureus \n                in children with and without AD during early childhood. \n               \n             \n             \n              Data, setting and participants \n              A cross-sectional study of 220 children (aged 9–38 months) with AD (cases) and without AD (controls) from Cape Town and Umtata, South Africa. \n             \n             \n              Main outcomes and measures \n               \n                S. aureus \n                phenotypic and genomic diversity were investigated using whole-genome sequencing, antibiotic susceptibility testing and biofilm microtiter assay. \n               \n             \n             \n              Results \n               \n                Of the 124 \n                S. aureus \n                isolates recovered from 220 children, 96 isolates (79 cases and 17 controls) with high-quality sequences were analyzed. Isolates from cases showed greater phenotypic resistance to gentamicin (10\\%), rifampicin (4\\%), chloramphenicol (4\\%), and exhibited multidrug resistance (9\\%) than in controls. Furthermore, the isolates from cases formed stronger biofilms than those from controls (76\\% vs. 35\\%, \n                p \n                 = 0.001), but showed no dominance of any virulence factor gene or mobile genetic elements. There was no significant difference in the distribution of immune evasion cluster types between cases and controls. However, IEC type G was identified only among cases. \n               \n             \n             \n              Conclusion and relevance \n               \n                AD-associated \n                S. aureus \n                has phenotypic and genetic features that are important for successful pathogenic colonization and survival. Further studies are needed to assess the pathological implications of colonization of various \n                S. aureus \n                lineages \n                in vivo \n                to elucidate their pathological contribution to AD pathogenesis and pathophysiology.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Microbiology},\n\tauthor = {Ndhlovu, Gillian O. N. and Javkar, Kiran G. and Matuvhunye, Takudzwa and Ngondoh, Froodia and Jamrozy, Dorota and Bentley, Stephen and Shittu, Adebayo O. and Dube, Felix S.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {1422902},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Distinct T cell polyfunctional profile in SARS-CoV-2 seronegative children associated with endemic human coronavirus cross-reactivity.\n \n \n \n \n\n\n \n Benede, N.; Tincho, M. B.; Walters, A.; Subbiah, V.; Ngomti, A.; Baguma, R.; Butters, C.; Hahnle, L.; Mennen, M.; Skelem, S.; Adriaanse, M.; Facey-Thomas, H.; Scott, C.; Day, J.; Spracklen, T. F.; Van Graan, S.; Balla, S. R.; Moyo-Gwete, T.; Moore, P. L.; MacGinty, R.; Botha, M.; Workman, L.; Johnson, M.; Goldblatt, D.; Zar, H. J.; Ntusi, N. A.; Zühlke, L.; Webb, K.; Riou, C.; Burgers, W. A.; and Keeton, R. S.\n\n\n \n\n\n\n iScience, 27(1): 108728. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Distinct$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{benede_distinct_2024,\n\ttitle = {Distinct {T} cell polyfunctional profile in {SARS}-{CoV}-2 seronegative children associated with endemic human coronavirus cross-reactivity},\n\tvolume = {27},\n\tissn = {25890042},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2589004223028055},\n\tdoi = {10.1016/j.isci.2023.108728},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {iScience},\n\tauthor = {Benede, Ntombi and Tincho, Marius B. and Walters, Avril and Subbiah, Vennesa and Ngomti, Amkele and Baguma, Richard and Butters, Claire and Hahnle, Lina and Mennen, Mathilda and Skelem, Sango and Adriaanse, Marguerite and Facey-Thomas, Heidi and Scott, Christiaan and Day, Jonathan and Spracklen, Timothy F. and Van Graan, Strauss and Balla, Sashkia R. and Moyo-Gwete, Thandeka and Moore, Penny L. and MacGinty, Rae and Botha, Maresa and Workman, Lesley and Johnson, Marina and Goldblatt, David and Zar, Heather J. and Ntusi, Ntobeko A.B. and Zühlke, Liesl and Webb, Kate and Riou, Catherine and Burgers, Wendy A. and Keeton, Roanne S.},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {108728},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n The pathogenesis of experimental Emergomycosis in mice.\n \n \n \n \n\n\n \n Höft, M. A.; Duvenage, L.; Salie, S.; Keeton, R.; Botha, A.; Schwartz, I. S.; Govender, N. P.; Brown, G. D.; and Hoving, J. C.\n\n\n \n\n\n\n PLOS Neglected Tropical Diseases, 18(1): e0011850. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{hoft_pathogenesis_2024,\n\ttitle = {The pathogenesis of experimental {Emergomycosis} in mice},\n\tvolume = {18},\n\tissn = {1935-2735},\n\turl = {https://dx.plos.org/10.1371/journal.pntd.0011850},\n\tdoi = {10.1371/journal.pntd.0011850},\n\tabstract = {Emergomyces africanus \n              is a recently identified thermally-dimorphic fungal pathogen that causes disseminated infection in people living with advanced HIV disease. Known as emergomycosis, this disseminated disease is associated with very high case fatality rates. Over the last decade, improved diagnostics and fungal identification in South Africa resulted in a dramatic increase in the number of reported cases. Although the true burden of disease is still unknown, emergomycosis is among the most frequently diagnosed dimorphic fungal infections in Southern Africa; and additional species in the genus have been identified on four continents. Little is known about the pathogenesis and the host’s immune response to this emerging pathogen. Therefore, we established a murine model of pulmonary infection using a clinical isolate, \n              E \n              . \n              africanus \n              (CBS 136260). Both conidia and yeast forms caused pulmonary and disseminated infection in mice with organisms isolated in culture from lung, spleen, liver, and kidney. Wild-type C57BL/6 mice demonstrated a drop in body weight at two weeks post-infection, corresponding to a peak in fungal burden in the lung, spleen, liver, and kidney. An increase in pro-inflammatory cytokine production was detected in homogenized lung supernatants including IFN-γ, IL-1β, IL-6, IL12-p40 and IL-17 at three- and four-weeks post-infection. No significant differences in TNF, IL-12p70 and IL-10 were observed in wild-type mice between one and four-weeks post-infection. Rag-1-deficient mice, lacking mature T-and B-cells, had an increased fungal burden associated with reduced IFN-γ production. Together our data support a protective T-helper type-1 immune response to \n              E \n              . \n              africanus \n              infection. This may provide a possible explanation for the susceptibility of only a subset of people living with advanced HIV disease despite hypothesized widespread environmental exposure. In summary, we have established a novel murine model of \n              E \n              . \n              africanus \n              disease providing critical insights into the host immune components required for eliminating the infection.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Neglected Tropical Diseases},\n\tauthor = {Höft, Maxine A. and Duvenage, Lucian and Salie, Sumayah and Keeton, Roanne and Botha, Alfred and Schwartz, Ilan S. and Govender, Nelesh P. and Brown, Gordon D. and Hoving, Jennifer Claire},\n\teditor = {Fahal, Ahmed Hassan},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {e0011850},\n}\n\n\n\n

\n

\n\n\n

\n Emergomyces africanus is a recently identified thermally-dimorphic fungal pathogen that causes disseminated infection in people living with advanced HIV disease. Known as emergomycosis, this disseminated disease is associated with very high case fatality rates. Over the last decade, improved diagnostics and fungal identification in South Africa resulted in a dramatic increase in the number of reported cases. Although the true burden of disease is still unknown, emergomycosis is among the most frequently diagnosed dimorphic fungal infections in Southern Africa; and additional species in the genus have been identified on four continents. Little is known about the pathogenesis and the host’s immune response to this emerging pathogen. Therefore, we established a murine model of pulmonary infection using a clinical isolate, E . africanus (CBS 136260). Both conidia and yeast forms caused pulmonary and disseminated infection in mice with organisms isolated in culture from lung, spleen, liver, and kidney. Wild-type C57BL/6 mice demonstrated a drop in body weight at two weeks post-infection, corresponding to a peak in fungal burden in the lung, spleen, liver, and kidney. An increase in pro-inflammatory cytokine production was detected in homogenized lung supernatants including IFN-γ, IL-1β, IL-6, IL12-p40 and IL-17 at three- and four-weeks post-infection. No significant differences in TNF, IL-12p70 and IL-10 were observed in wild-type mice between one and four-weeks post-infection. Rag-1-deficient mice, lacking mature T-and B-cells, had an increased fungal burden associated with reduced IFN-γ production. Together our data support a protective T-helper type-1 immune response to E . africanus infection. This may provide a possible explanation for the susceptibility of only a subset of people living with advanced HIV disease despite hypothesized widespread environmental exposure. In summary, we have established a novel murine model of E . africanus disease providing critical insights into the host immune components required for eliminating the infection.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Clinical exome sequencing elucidates underlying cause of death in sudden unexpected death of infants: two case reports.\n \n \n \n \n\n\n \n Heathfield, L. J.; Martin, L. J.; Van Der Heyde, Y.; Molefe, I.; and Ramesar, R.\n\n\n \n\n\n\n International Journal of Legal Medicine, 138(2): 693–700. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Clinical$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{heathfield_clinical_2024,\n\ttitle = {Clinical exome sequencing elucidates underlying cause of death in sudden unexpected death of infants: two case reports},\n\tvolume = {138},\n\tissn = {0937-9827, 1437-1596},\n\tshorttitle = {Clinical exome sequencing elucidates underlying cause of death in sudden unexpected death of infants},\n\turl = {https://link.springer.com/10.1007/s00414-023-03065-3},\n\tdoi = {10.1007/s00414-023-03065-3},\n\tabstract = {Abstract \n             \n              Sudden unexpected death in infants (SUDI) is a traumatic event for families, and unfortunately its occurrence remains high in many parts of the world. Whilst cause of death is resolved for most cases, others remain undetermined following postmortem investigations. There has been a recognition of the role of genetic testing in unexplained cases, where previous studies have demonstrated the resolution of cases through DNA analyses. Here we present two case reports of SUDI cases admitted to Salt River Mortuary, South Africa, and show that underlying causes of death were determined for both infants using clinical exome sequencing. The first infant was heterozygous for a variant (rs148175795) in \n              COL6A3 \n              , which suggested a bronchopulmonary dysplasia phenotype. This hypothesis led to finding of a second candidate variant in \n              DMP1 \n              (rs142880465), which may contribute towards a digenic/polygenic mechanism of a more severe phenotype. Histological analysis of retained tissue sections showed an asphyxial mechanism of death, where bronchiolar muscle weakness from an underlying bronchopulmonary dysplasia may have contributed to the asphyxia by affecting respiration. In the second infant, a homozygous variant (rs201340753) was identified in \n              MASP1 \n              , which was heterozygous in each parent, highlighting the value of including parental DNA in genetic studies. Whilst mannose-binding lectin deficiency could not be assessed, it is plausible that this variant may have acted in combination with other risk factors within the triple-risk model to result in sudden death. These results may have genetic implications for family members, and represent possible new candidate variants for molecular autopsies.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {International Journal of Legal Medicine},\n\tauthor = {Heathfield, Laura Jane and Martin, Lorna Jean and Van Der Heyde, Yolande and Molefe, Itumeleng and Ramesar, Raj},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {693--700},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Structural insights into the inhibitory mechanism of angiotensin‐I‐converting enzyme by the lactotripeptides IPP and VPP.\n \n \n \n \n\n\n \n Gregory, K. S.; Cozier, G. E.; Schwager, S. L. U.; Sturrock, E. D.; and Acharya, K. R.\n\n\n \n\n\n\n FEBS Letters, 598(2): 242–251. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Structural$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{gregory_structural_2024,\n\ttitle = {Structural insights into the inhibitory mechanism of angiotensin‐{I}‐converting enzyme by the lactotripeptides {IPP} and {VPP}},\n\tvolume = {598},\n\tissn = {0014-5793, 1873-3468},\n\turl = {https://febs.onlinelibrary.wiley.com/doi/10.1002/1873-3468.14768},\n\tdoi = {10.1002/1873-3468.14768},\n\tabstract = {Human somatic angiotensin‐1‐converting enzyme (sACE) is composed of a catalytic N‐(nACE) and C‐domain (cACE) of similar size with different substrate specificities. It is involved in the regulation of blood pressure by converting angiotensin I to the vasoconstrictor angiotensin II and has been a major focus in the development of therapeutics for hypertension. Bioactive peptides from various sources, including milk, have been identified as natural ACE inhibitors. We report the structural basis for the role of two lacototripeptides, Val‐Pro‐Pro and Ile‐Pro‐Pro, in domain‐specific inhibition of ACE using X‐ray crystallography and kinetic analysis. The lactotripeptides have preference for nACE due to altered polar interactions distal to the catalytic zinc ion. Elucidating the mechanism of binding and domain selectivity of these peptides also provides important insights into the functional roles of ACE.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {FEBS Letters},\n\tauthor = {Gregory, Kyle S. and Cozier, Gyles E. and Schwager, Sylva L. U. and Sturrock, Edward D. and Acharya, K. Ravi},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {242--251},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Two-step evolution of HIV-1 budding system leading to pandemic in the human population.\n \n \n \n \n\n\n \n Konno, Y.; Uriu, K.; Chikata, T.; Takada, T.; Kurita, J.; Ueda, M. T.; Islam, S.; Yang Tan, B. J.; Ito, J.; Aso, H.; Kumata, R.; Williamson, C.; Iwami, S.; Takiguchi, M.; Nishimura, Y.; Morita, E.; Satou, Y.; Nakagawa, S.; Koyanagi, Y.; and Sato, K.\n\n\n \n\n\n\n Cell Reports, 43(2): 113697. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Two-step$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{konno_two-step_2024,\n\ttitle = {Two-step evolution of {HIV}-1 budding system leading to pandemic in the human population},\n\tvolume = {43},\n\tissn = {22111247},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2211124724000251},\n\tdoi = {10.1016/j.celrep.2024.113697},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {Cell Reports},\n\tauthor = {Konno, Yoriyuki and Uriu, Keiya and Chikata, Takayuki and Takada, Toru and Kurita, Jun-ichi and Ueda, Mahoko Takahashi and Islam, Saiful and Yang Tan, Benjy Jek and Ito, Jumpei and Aso, Hirofumi and Kumata, Ryuichi and Williamson, Carolyn and Iwami, Shingo and Takiguchi, Masafumi and Nishimura, Yoshifumi and Morita, Eiji and Satou, Yorifumi and Nakagawa, So and Koyanagi, Yoshio and Sato, Kei},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {113697},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Network-based integrative multi-omics approach reveals biosignatures specific to COVID-19 disease phases.\n \n \n \n \n\n\n \n Agamah, F. E.; Ederveen, T. H. A.; Skelton, M.; Martin, D. P.; Chimusa, E. R.; and ’T Hoen, P. A. C.\n\n\n \n\n\n\n Frontiers in Molecular Biosciences, 11: 1393240. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Network-based$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{agamah_network-based_2024,\n\ttitle = {Network-based integrative multi-omics approach reveals biosignatures specific to {COVID}-19 disease phases},\n\tvolume = {11},\n\tissn = {2296-889X},\n\turl = {https://www.frontiersin.org/articles/10.3389/fmolb.2024.1393240/full},\n\tdoi = {10.3389/fmolb.2024.1393240},\n\tabstract = {Background \n COVID-19 disease is characterized by a spectrum of disease phases (mild, moderate, and severe). Each disease phase is marked by changes in omics profiles with corresponding changes in the expression of features (biosignatures). However, integrative analysis of multiple omics data from different experiments across studies to investigate biosignatures at various disease phases is limited. Exploring an integrative multi-omics profile analysis through a network approach could be used to determine biosignatures associated with specific disease phases and enable the examination of the relationships between the biosignatures. \n \n \n Aim \n To identify and characterize biosignatures underlying various COVID-19 disease phases in an integrative multi-omics data analysis. \n \n \n Method \n We leveraged a multi-omics network-based approach to integrate transcriptomics, metabolomics, proteomics, and lipidomics data. The World Health Organization Ordinal Scale WHO Ordinal Scale was used as a disease severity reference to harmonize COVID-19 patient metadata across two studies with independent data. A unified COVID-19 knowledge graph was constructed by assembling a disease-specific interactome from the literature and databases. Disease-state specific omics-graphs were constructed by integrating multi-omics data with the unified COVID-19 knowledge graph. We expanded on the network layers of multiXrank, a random walk with restart on multilayer network algorithm, to explore disease state omics-specific graphs and perform enrichment analysis. \n \n \n Results \n \n Network analysis revealed the biosignatures involved in inducing chemokines and inflammatory responses as hubs in the severe and moderate disease phases. We observed distinct biosignatures between severe and moderate disease phases as compared to mild-moderate and mild-severe disease phases. Mild COVID-19 cases were characterized by a unique biosignature comprising C-C Motif Chemokine Ligand 4 ( \n CCL4 \n ), and Interferon Regulatory Factor 1 ( \n IRF1 \n ). Hepatocyte Growth Factor (HGF), Matrix Metallopeptidase 12 ( \n MMP12 \n ), Interleukin 10 ( \n IL10 \n ), Nuclear Factor Kappa B Subunit 1 ( \n NFKB1 \n ), and suberoylcarnitine form hubs in the omics network that characterizes the moderate disease state. The severe cases were marked by biosignatures such as Signal Transducer and Activator of Transcription 1 ( \n STAT1 \n ), Superoxide Dismutase 2 ( \n SOD2 \n ), \n HGF, \n taurine, lysophosphatidylcholine, diacylglycerol, triglycerides, and sphingomyelin that characterize the disease state. \n \n \n \n Conclusion \n This study identified both biosignatures of different omics types enriched in disease-related pathways and their associated interactions (such as protein-protein, protein-transcript, protein-metabolite, transcript-metabolite, and lipid-lipid interactions) that are unique to mild, moderate, and severe COVID-19 disease states. These biosignatures include molecular features that underlie the observed clinical heterogeneity of COVID-19 and emphasize the need for disease-phase-specific treatment strategies. The approach implemented here can be used to find associations between transcripts, proteins, lipids, and metabolites in other diseases.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Molecular Biosciences},\n\tauthor = {Agamah, Francis E. and Ederveen, Thomas H. A. and Skelton, Michelle and Martin, Darren P. and Chimusa, Emile R. and ’T Hoen, Peter A. C.},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {1393240},\n}\n\n\n\n

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\n Background COVID-19 disease is characterized by a spectrum of disease phases (mild, moderate, and severe). Each disease phase is marked by changes in omics profiles with corresponding changes in the expression of features (biosignatures). However, integrative analysis of multiple omics data from different experiments across studies to investigate biosignatures at various disease phases is limited. Exploring an integrative multi-omics profile analysis through a network approach could be used to determine biosignatures associated with specific disease phases and enable the examination of the relationships between the biosignatures. Aim To identify and characterize biosignatures underlying various COVID-19 disease phases in an integrative multi-omics data analysis. Method We leveraged a multi-omics network-based approach to integrate transcriptomics, metabolomics, proteomics, and lipidomics data. The World Health Organization Ordinal Scale WHO Ordinal Scale was used as a disease severity reference to harmonize COVID-19 patient metadata across two studies with independent data. A unified COVID-19 knowledge graph was constructed by assembling a disease-specific interactome from the literature and databases. Disease-state specific omics-graphs were constructed by integrating multi-omics data with the unified COVID-19 knowledge graph. We expanded on the network layers of multiXrank, a random walk with restart on multilayer network algorithm, to explore disease state omics-specific graphs and perform enrichment analysis. Results Network analysis revealed the biosignatures involved in inducing chemokines and inflammatory responses as hubs in the severe and moderate disease phases. We observed distinct biosignatures between severe and moderate disease phases as compared to mild-moderate and mild-severe disease phases. Mild COVID-19 cases were characterized by a unique biosignature comprising C-C Motif Chemokine Ligand 4 ( CCL4 ), and Interferon Regulatory Factor 1 ( IRF1 ). Hepatocyte Growth Factor (HGF), Matrix Metallopeptidase 12 ( MMP12 ), Interleukin 10 ( IL10 ), Nuclear Factor Kappa B Subunit 1 ( NFKB1 ), and suberoylcarnitine form hubs in the omics network that characterizes the moderate disease state. The severe cases were marked by biosignatures such as Signal Transducer and Activator of Transcription 1 ( STAT1 ), Superoxide Dismutase 2 ( SOD2 ), HGF, taurine, lysophosphatidylcholine, diacylglycerol, triglycerides, and sphingomyelin that characterize the disease state. Conclusion This study identified both biosignatures of different omics types enriched in disease-related pathways and their associated interactions (such as protein-protein, protein-transcript, protein-metabolite, transcript-metabolite, and lipid-lipid interactions) that are unique to mild, moderate, and severe COVID-19 disease states. These biosignatures include molecular features that underlie the observed clinical heterogeneity of COVID-19 and emphasize the need for disease-phase-specific treatment strategies. The approach implemented here can be used to find associations between transcripts, proteins, lipids, and metabolites in other diseases.\n

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\n \n\n \n \n \n \n \n \n Comparing the immune abnormalities in MIS-C to healthy children and those with inflammatory disease reveals distinct inflammatory cytokine production and a monofunctional T cell response.\n \n \n \n \n\n\n \n Butters, C.; Benede, N.; Moyo-Gwete, T.; Richardson, S. I.; Rohlwink, U.; Shey, M.; Ayres, F.; Manamela, N. P.; Makhado, Z.; Balla, S. R.; Madzivhandila, M.; Ngomti, A.; Baguma, R.; Facey-Thomas, H.; Spracklen, T. F.; Day, J.; Van Der Ross, H.; Riou, C.; Burgers, W. A.; Scott, C.; Zühlke, L.; Moore, P. L.; Keeton, R. S.; and Webb, K.\n\n\n \n\n\n\n Clinical Immunology, 259: 109877. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Comparing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{butters_comparing_2024,\n\ttitle = {Comparing the immune abnormalities in {MIS}-{C} to healthy children and those with inflammatory disease reveals distinct inflammatory cytokine production and a monofunctional {T} cell response},\n\tvolume = {259},\n\tissn = {15216616},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1521661623006411},\n\tdoi = {10.1016/j.clim.2023.109877},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Clinical Immunology},\n\tauthor = {Butters, Claire and Benede, Ntombi and Moyo-Gwete, Thandeka and Richardson, Simone I. and Rohlwink, Ursula and Shey, Muki and Ayres, Frances and Manamela, Nelia P. and Makhado, Zanele and Balla, Sashkia R. and Madzivhandila, Mashudu and Ngomti, Amkele and Baguma, Richard and Facey-Thomas, Heidi and Spracklen, Timothy F. and Day, Jonathan and Van Der Ross, Hamza and Riou, Catherine and Burgers, Wendy A. and Scott, Christiaan and Zühlke, Liesl and Moore, Penny L. and Keeton, Roanne S. and Webb, Kate},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {109877},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The Capacity of Drug-Metabolising Enzymes in Modulating the Therapeutic Efficacy of Drugs to Treat Rhabdomyosarcoma.\n \n \n \n \n\n\n \n Picher, E. A.; Wahajuddin, M.; Barth, S.; Chisholm, J.; Shipley, J.; and Pors, K.\n\n\n \n\n\n\n Cancers, 16(5): 1012. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{picher_capacity_2024,\n\ttitle = {The {Capacity} of {Drug}-{Metabolising} {Enzymes} in {Modulating} the {Therapeutic} {Efficacy} of {Drugs} to {Treat} {Rhabdomyosarcoma}},\n\tvolume = {16},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2072-6694},\n\turl = {https://www.mdpi.com/2072-6694/16/5/1012},\n\tdoi = {10.3390/cancers16051012},\n\tabstract = {Rhabdomyosarcoma (RMS) is a rare soft tissue sarcoma (STS) that predominantly affects children and teenagers. It is the most common STS in children (40\\%) and accounts for 5–8\\% of total childhood malignancies. Apart from surgery and radiotherapy in eligible patients, standard chemotherapy is the only therapeutic option clinically available for RMS patients. While survival rates for this childhood cancer have considerably improved over the last few decades for low-risk and intermediate-risk cases, the mortality rate remains exceptionally high in high-risk RMS patients with recurrent and/or metastatic disease. The intensification of chemotherapeutic protocols in advanced-stage RMS has historically induced aggravated toxicity with only very modest therapeutic gain. In this review, we critically analyse what has been achieved so far in RMS therapy and provide insight into how a diverse group of drug-metabolising enzymes (DMEs) possess the capacity to modify the clinical efficacy of chemotherapy. We provide suggestions for new therapeutic strategies that exploit the presence of DMEs for prodrug activation, targeted chemotherapy that does not rely on DMEs, and RMS-molecular-subtype-targeted therapies that have the potential to enter clinical evaluation.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-24},\n\tjournal = {Cancers},\n\tauthor = {Picher, Enric Arasanz and Wahajuddin, Muhammad and Barth, Stefan and Chisholm, Julia and Shipley, Janet and Pors, Klaus},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {1012},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Walking a thin line between fixation and epitope binding – characterization of antigen retrieval methods suitable for eosinophil and HSV-2 staining in formalin-fixed female reproductive tissue.\n \n \n \n \n\n\n \n Wadephul, L. M.; Arndts, K.; Katawa, G.; Dietlmeier, E.; Horsnell, W.; Hoerauf, A.; and Ritter, M.\n\n\n \n\n\n\n European Journal of Histochemistry, 68(2). April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Walking$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{wadephul_walking_2024,\n\ttitle = {Walking a thin line between fixation and epitope binding – characterization of antigen retrieval methods suitable for eosinophil and {HSV}-2 staining in formalin-fixed female reproductive tissue},\n\tvolume = {68},\n\tcopyright = {https://creativecommons.org/licenses/by-nc/4.0},\n\tissn = {2038-8306, 1121-760X},\n\turl = {https://www.ejh.it/ejh/article/view/3929},\n\tdoi = {10.4081/ejh.2024.3929},\n\tabstract = {Antibody-based fluorescence analysis of female reproductive tissues in research of sexually transmitted diseases allows for an in-depth understanding of protein localization, interactions, and pathogenesis. However, in many cases, cryosectioning is not compatible with biosafety regulations; at all times, exposure of lab personnel and the public to potentially harmful pathogens from biological infectious material must be avoided; thus, formaldehyde fixation is essential. Due to formaldehyde’s cross-linking properties, protein detection with antibodies can be impeded. To allow effective epitope binding during immunofluorescence of formalin-fixed paraffin-embedded vaginal tissue, we investigated two antigen retrieval methods. We tested these methods regarding their suitability for automated image analysis, facilitating reproducible quantitative microscopic data acquisition in sexually transmitted disease research. Heat-based retrieval at 80°C in citrate buffer proved to increase antibody binding to eosinophil protein and HSV-2 visibly and tissue morphology best, and was the most efficient for sample processing and quantitative analysis.},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {European Journal of Histochemistry},\n\tauthor = {Wadephul, Lisa Marie and Arndts, Kathrin and Katawa, Gnatoulma and Dietlmeier, Eva and Horsnell, William and Hoerauf, Achim and Ritter, Manuel},\n\tmonth = apr,\n\tyear = {2024},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Advancing intercontinental collaboration in human genetics: success story of the African and European Young Investigator Forum.\n \n \n \n \n\n\n \n Alimohamed, M. Z.; Mnika, K.; Adadey, S. M.; Barbosa-Matos, R.; Avram, E.; Nevondwe, P.; Akurugu, W. A.; Mupfururirwa, W.; De Miranda Cerqueira, J. X.; Dore, R.; Săbău, I.; Kalantari, S.; Da Silva, A. R. G. F.; Anzaku, A. A.; Matimba, A.; Chauke, P. A.; Johari, M.; Nembaware, V.; and Mroczek, M.\n\n\n \n\n\n\n European Journal of Human Genetics, 32(1): 3–5. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Advancing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{alimohamed_advancing_2024,\n\ttitle = {Advancing intercontinental collaboration in human genetics: success story of the {African} and {European} {Young} {Investigator} {Forum}},\n\tvolume = {32},\n\tissn = {1018-4813, 1476-5438},\n\tshorttitle = {Advancing intercontinental collaboration in human genetics},\n\turl = {https://www.nature.com/articles/s41431-023-01487-6},\n\tdoi = {10.1038/s41431-023-01487-6},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {European Journal of Human Genetics},\n\tauthor = {Alimohamed, Mohamed Zahir and Mnika, Khuthala and Adadey, Samuel Mawuli and Barbosa-Matos, Rita and Avram, Elena and Nevondwe, Patracia and Akurugu, Wisdom A. and Mupfururirwa, Wilson and De Miranda Cerqueira, Juliana Xavier and Dore, Rhys and Săbău, Ileana-Delia and Kalantari, Silvia and Da Silva, Ana Raquel Gouveia Freitas and Anzaku, Abbas Abel and Matimba, Alice and Chauke, Paballo Abel and Johari, Mridul and Nembaware, Victoria and Mroczek, Magdalena},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {3--5},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Machine learning and bioinformatic analyses link the cell surface receptor transcript levels to the drug response of breast cancer cells and drug off-target effects.\n \n \n \n \n\n\n \n Sinkala, M.; Naran, K.; Ramamurthy, D.; Mungra, N.; Dzobo, K.; Martin, D.; and Barth, S.\n\n\n \n\n\n\n PLOS ONE, 19(2): e0296511. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Machine$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{sinkala_machine_2024,\n\ttitle = {Machine learning and bioinformatic analyses link the cell surface receptor transcript levels to the drug response of breast cancer cells and drug off-target effects},\n\tvolume = {19},\n\tissn = {1932-6203},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0296511},\n\tdoi = {10.1371/journal.pone.0296511},\n\tabstract = {Breast cancer responds variably to anticancer therapies, often leading to significant off-target effects. This study proposes that the variability in tumour responses and drug-induced adverse events is linked to the transcriptional profiles of cell surface receptors (CSRs) in breast tumours and normal tissues. We analysed multiple datasets to compare CSR expression in breast tumours with that in non-cancerous human tissues. Our findings correlate the drug responses of breast cancer cell lines with the expression levels of their targeted CSRs. Notably, we identified distinct differences in CSR expression between primary breast tumour subtypes and corresponding cell lines, which may influence drug response predictions. Additionally, we used clinical trial data to uncover associations between CSR gene expression in healthy tissues and the incidence of adverse drug reactions. This integrative approach facilitates the selection of optimal CSR targets for therapy, leveraging cell line dose-responses, CSR expression in normal tissues, and patient adverse event profiles.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Sinkala, Musalula and Naran, Krupa and Ramamurthy, Dharanidharan and Mungra, Neelakshi and Dzobo, Kevin and Martin, Darren and Barth, Stefan},\n\teditor = {Li, Pan},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {e0296511},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The timing of HIV-1 infection of cells that persist on therapy is not strongly influenced by replication competency or cellular tropism of the provirus.\n \n \n \n \n\n\n \n Joseph, S. B.; Abrahams, M.; Moeser, M.; Tyers, L.; Archin, N. M.; Council, O. D.; Sondgeroth, A.; Spielvogel, E.; Emery, A.; Zhou, S.; Doolabh, D.; Ismail, S. D.; Karim, S. A.; Margolis, D. M.; Pond, S. K.; Garrett, N.; Swanstrom, R.; and Williamson, C.\n\n\n \n\n\n\n PLOS Pathogens, 20(2): e1011974. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{joseph_timing_2024,\n\ttitle = {The timing of {HIV}-1 infection of cells that persist on therapy is not strongly influenced by replication competency or cellular tropism of the provirus},\n\tvolume = {20},\n\tissn = {1553-7374},\n\turl = {https://dx.plos.org/10.1371/journal.ppat.1011974},\n\tdoi = {10.1371/journal.ppat.1011974},\n\tabstract = {People with HIV-1 (PWH) on antiretroviral therapy (ART) can maintain undetectable virus levels, but a small pool of infected cells persists. This pool is largely comprised of defective proviruses that may produce HIV-1 proteins but are incapable of making infectious virus, with only a fraction ({\\textasciitilde}10\\%) of these cells harboring intact viral genomes, some of which produce infectious virus following ex vivo stimulation (i.e. inducible intact proviruses). A majority of the inducible proviruses that persist on ART are formed near the time of therapy initiation. Here we compared proviral DNA (assessed here as 3’ half genomes amplified from total cellular DNA) and inducible replication competent viruses in the pool of infected cells that persists during ART to determine if the original infection of these cells occurred at comparable times prior to therapy initiation. Overall, the average percent of proviruses that formed late (i.e. around the time of ART initiation, 60\\%) did not differ from the average percent of replication competent inducible viruses that formed late (69\\%), and this was also true for proviral DNA that was hypermutated (57\\%). Further, there was no evidence that entry into the long-lived infected cell pool was impeded by the ability to use the CXCR4 coreceptor, nor was the formation of long-lived infected cells enhanced during primary infection, when viral loads are exceptionally high. We observed that infection of cells that transitioned to be long-lived was enhanced among people with a lower nadir CD4 \n              + \n              T cell count. Together these data suggest that the timing of infection of cells that become long-lived is impacted more by biological processes associated with immunodeficiency before ART than the replication competency and/or cellular tropism of the infecting virus or the intactness of the provirus. Further research is needed to determine the mechanistic link between immunodeficiency and the timing of infected cells transitioning to the long-lived pool, particularly whether this is due to differences in infected cell clearance, turnover rates and/or homeostatic proliferation before and after ART.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Pathogens},\n\tauthor = {Joseph, Sarah B. and Abrahams, Melissa-Rose and Moeser, Matthew and Tyers, Lynn and Archin, Nancie M. and Council, Olivia D. and Sondgeroth, Amy and Spielvogel, Ean and Emery, Ann and Zhou, Shuntai and Doolabh, Deelan and Ismail, Sherazaan D. and Karim, Salim Abdool and Margolis, David M. and Pond, Sergei Kosakovsky and Garrett, Nigel and Swanstrom, Ronald and Williamson, Carolyn},\n\teditor = {Moore, Penny L.},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {e1011974},\n}\n\n\n\n

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\n People with HIV-1 (PWH) on antiretroviral therapy (ART) can maintain undetectable virus levels, but a small pool of infected cells persists. This pool is largely comprised of defective proviruses that may produce HIV-1 proteins but are incapable of making infectious virus, with only a fraction (~10%) of these cells harboring intact viral genomes, some of which produce infectious virus following ex vivo stimulation (i.e. inducible intact proviruses). A majority of the inducible proviruses that persist on ART are formed near the time of therapy initiation. Here we compared proviral DNA (assessed here as 3’ half genomes amplified from total cellular DNA) and inducible replication competent viruses in the pool of infected cells that persists during ART to determine if the original infection of these cells occurred at comparable times prior to therapy initiation. Overall, the average percent of proviruses that formed late (i.e. around the time of ART initiation, 60%) did not differ from the average percent of replication competent inducible viruses that formed late (69%), and this was also true for proviral DNA that was hypermutated (57%). Further, there was no evidence that entry into the long-lived infected cell pool was impeded by the ability to use the CXCR4 coreceptor, nor was the formation of long-lived infected cells enhanced during primary infection, when viral loads are exceptionally high. We observed that infection of cells that transitioned to be long-lived was enhanced among people with a lower nadir CD4 + T cell count. Together these data suggest that the timing of infection of cells that become long-lived is impacted more by biological processes associated with immunodeficiency before ART than the replication competency and/or cellular tropism of the infecting virus or the intactness of the provirus. Further research is needed to determine the mechanistic link between immunodeficiency and the timing of infected cells transitioning to the long-lived pool, particularly whether this is due to differences in infected cell clearance, turnover rates and/or homeostatic proliferation before and after ART.\n

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\n \n\n \n \n \n \n \n \n Vaccine and Non-Vaccine HPV Types Presence in Adolescents with Vertically Acquired HIV Five Years Post Gardasil Quadrivalent Vaccination: The ZIMGARD Cohort.\n \n \n \n \n\n\n \n Murahwa, A. T.; Mudzviti, T.; Mandishora, R. S. D.; Chatindo, T.; Chanetsa, P.; Pascoe, M.; Shamu, T.; Basera, W.; Luethy, R.; and Williamson, A.\n\n\n \n\n\n\n Viruses, 16(1): 162. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Vaccine$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{murahwa_vaccine_2024,\n\ttitle = {Vaccine and {Non}-{Vaccine} {HPV} {Types} {Presence} in {Adolescents} with {Vertically} {Acquired} {HIV} {Five} {Years} {Post} {Gardasil} {Quadrivalent} {Vaccination}: {The} {ZIMGARD} {Cohort}},\n\tvolume = {16},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1999-4915},\n\tshorttitle = {Vaccine and {Non}-{Vaccine} {HPV} {Types} {Presence} in {Adolescents} with {Vertically} {Acquired} {HIV} {Five} {Years} {Post} {Gardasil} {Quadrivalent} {Vaccination}},\n\turl = {https://www.mdpi.com/1999-4915/16/1/162},\n\tdoi = {10.3390/v16010162},\n\tabstract = {Background: Human papillomavirus (HPV) vaccination programs are a key intervention in protecting individuals against HPV-related disease. HIV1-infected individuals are at increased risk of HPV-associated cancers. This study was conducted to evaluate the potential role of prophylactic HPV vaccines in preventing new HPV infections among participants with perinatally acquired HIV who received the quadrivalent HPV vaccine at least five years before this study. Methods: This cross-sectional study was conducted at Newlands Clinic, Harare, Zimbabwe. The clinic provided the Gardasil quadrivalent HPV vaccine (4vHPV) to 624 adolescents living with HIV starting in December 2015. Vaginal and penile swabs were collected and tested for HPV types from the study participants who had received the 4vHPV vaccine 5–6 years before enrolment. Results: We present the results of 98 participants (44.6\\% female) vaccinated at a median age of 15 years (IQR 12–16). The mean amount of time since vaccination was 6 years (SD: ±0.4). The HPV-positive rate amongst the analyzed swabs was 69\\% (68/98). Among 30/98 (31\\%) HPV-positive participants, 13/98 (13\\%) had low-risk HPV types, and 17/98 (17\\%) had high-risk HPV types. Twelve participants tested positive for HPV18, only one participant tested positive for HPV16, and an additional four (4.3\\%) tested positive for either type 6 or 11, with respect to vaccine-preventable low-risk HPV types. Conclusion: The Gardasil quadrivalent HPV vaccine (4vHPV) was expected to protect against infection with HPV types 16, 18, 6, and 11. We demonstrated a possible waning of immunity to HPV18 in 17\\% of the participants, and an associated loss in cross-protection against HPV45. We observed a relatively high prevalence of ‘opportunistic non-vaccine HPV types’ or ‘ecological niche occupiers’ in this cohort, and suggest further research on the involvement of these types in cervical and other genital cancers. Our study is one of the few, if not the first, to report on HPV vaccine immunoprotection among people living with HIV (PLWH), thereby setting a baseline for further studies on HPV vaccine effectiveness among PLWH.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Viruses},\n\tauthor = {Murahwa, Alltalents T. and Mudzviti, Tinashe and Mandishora, Racheal S. Dube and Chatindo, Takudzwa and Chanetsa, Peace and Pascoe, Margaret and Shamu, Tinei and Basera, Wisdom and Luethy, Ruedi and Williamson, Anna-Lise},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {162},\n}\n\n\n\n

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\n Background: Human papillomavirus (HPV) vaccination programs are a key intervention in protecting individuals against HPV-related disease. HIV1-infected individuals are at increased risk of HPV-associated cancers. This study was conducted to evaluate the potential role of prophylactic HPV vaccines in preventing new HPV infections among participants with perinatally acquired HIV who received the quadrivalent HPV vaccine at least five years before this study. Methods: This cross-sectional study was conducted at Newlands Clinic, Harare, Zimbabwe. The clinic provided the Gardasil quadrivalent HPV vaccine (4vHPV) to 624 adolescents living with HIV starting in December 2015. Vaginal and penile swabs were collected and tested for HPV types from the study participants who had received the 4vHPV vaccine 5–6 years before enrolment. Results: We present the results of 98 participants (44.6% female) vaccinated at a median age of 15 years (IQR 12–16). The mean amount of time since vaccination was 6 years (SD: ±0.4). The HPV-positive rate amongst the analyzed swabs was 69% (68/98). Among 30/98 (31%) HPV-positive participants, 13/98 (13%) had low-risk HPV types, and 17/98 (17%) had high-risk HPV types. Twelve participants tested positive for HPV18, only one participant tested positive for HPV16, and an additional four (4.3%) tested positive for either type 6 or 11, with respect to vaccine-preventable low-risk HPV types. Conclusion: The Gardasil quadrivalent HPV vaccine (4vHPV) was expected to protect against infection with HPV types 16, 18, 6, and 11. We demonstrated a possible waning of immunity to HPV18 in 17% of the participants, and an associated loss in cross-protection against HPV45. We observed a relatively high prevalence of ‘opportunistic non-vaccine HPV types’ or ‘ecological niche occupiers’ in this cohort, and suggest further research on the involvement of these types in cervical and other genital cancers. Our study is one of the few, if not the first, to report on HPV vaccine immunoprotection among people living with HIV (PLWH), thereby setting a baseline for further studies on HPV vaccine effectiveness among PLWH.\n

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\n \n\n \n \n \n \n \n \n Reactivation of Kaposi’s sarcoma-associated herpesvirus (KSHV) by SARS-CoV-2 in non-hospitalised HIV-infected patients.\n \n \n \n \n\n\n \n Lambarey, H.; Blumenthal, M. J.; Chetram, A.; Joyimbana, W.; Jennings, L.; Orrell, C.; and Schäfer, G.\n\n\n \n\n\n\n eBioMedicine, 100: 104986. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Reactivation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{lambarey_reactivation_2024,\n\ttitle = {Reactivation of {Kaposi}’s sarcoma-associated herpesvirus ({KSHV}) by {SARS}-{CoV}-2 in non-hospitalised {HIV}-infected patients},\n\tvolume = {100},\n\tissn = {23523964},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352396424000215},\n\tdoi = {10.1016/j.ebiom.2024.104986},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {eBioMedicine},\n\tauthor = {Lambarey, Humaira and Blumenthal, Melissa J. and Chetram, Abeen and Joyimbana, Wendy and Jennings, Lauren and Orrell, Catherine and Schäfer, Georgia},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {104986},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Emergence of Omicron FN.1 a descendent of BQ.1.1 in Botswana.\n \n \n \n \n\n\n \n Choga, W. T; Gustani-Buss, E.; Tegally, H.; Maruapula, D.; Yu, X.; Moir, M.; Zuze, B. J L; James, S. E.; Ndlovu, N. S; Seru, K.; Motshosi, P.; Blenkinsop, A.; Gobe, I.; Baxter, C.; Manasa, J.; Lockman, S.; Shapiro, R.; Makhema, J.; Wilkinson, E.; Blackard, J. T; Lemey, P.; Lessells, R. J; Martin, D. P; De Oliveira, T.; Gaseitsiwe, S.; and Moyo, S.\n\n\n \n\n\n\n Virus Evolution, 10(1): veae095. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Emergence$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{choga_emergence_2024,\n\ttitle = {Emergence of {Omicron} {FN}.1 a descendent of {BQ}.1.1 in {Botswana}},\n\tvolume = {10},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2057-1577},\n\turl = {https://academic.oup.com/ve/article/doi/10.1093/ve/veae095/7906938},\n\tdoi = {10.1093/ve/veae095},\n\tabstract = {Abstract \n            Botswana, like the rest of the world, has been significantly impacted by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In December 2022, we detected a monophyletic cluster of genomes comprising a sublineage of the Omicron variant of concern (VOC) designated as B.1.1.529.5.3.1.1.1.1.1.1.74.1 (alias FN.1, clade 22E). These genomes were sourced from both epidemiologically linked and unlinked samples collected in three close locations within the district of Greater Gaborone. In this study, we assessed the worldwide prevalence of the FN.1 lineage, evaluated its mutational profile, and conducted a phylogeographic analysis to reveal its global dispersal dynamics. Among approximately 16 million publicly available SARS-CoV-2 sequences generated by 30 September 2023, only 87 were of the FN.1 lineage, including 22 from Botswana, 6 from South Africa, and 59 from the UK. The estimated time to the most recent common ancestor of the 87 FN.1 sequences was 22 October 2022 [95\\% highest posterior density: 2 September 2022—24 November 2022], with the earliest of the 22 Botswana sequences having been sampled on 7 December 2022. Discrete trait reconstruction of FN.1 identified Botswana as the most probable place of origin. The FN.1 lineage is derived from the BQ.1.1 lineage and carries two missense variants in the spike protein, S:K182E in NTD and S:T478R in RDB. Among the over 90 SARS-CoV-2 lineages circulating in Botswana between September 2020 and July 2023, FN.1 was most closely related to BQ.1.1.74 based on maximum likelihood phylogenetic inference, differing only by the S:K182E mutation found in FN.1. Given the early detection of numerous novel variants from Botswana and its neighbouring countries, our study underscores the necessity of continuous surveillance to monitor the emergence of potential VOCs, integrating molecular and spatial data to identify dissemination patterns enhancing preparedness efforts.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Virus Evolution},\n\tauthor = {Choga, Wonderful T and Gustani-Buss, Emanuele and Tegally, Houriiyah and Maruapula, Dorcas and Yu, Xiaoyu and Moir, Monika and Zuze, Boitumelo J L and James, San Emmanuel and Ndlovu, Nokuthula S and Seru, Kedumetse and Motshosi, Patience and Blenkinsop, Alexandra and Gobe, Irene and Baxter, Cheryl and Manasa, Justen and Lockman, Shahin and Shapiro, Roger and Makhema, Joseph and Wilkinson, Eduan and Blackard, Jason T and Lemey, Phillipe and Lessells, Richard J and Martin, Darren P and De Oliveira, Tulio and Gaseitsiwe, Simani and Moyo, Sikhulile},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {veae095},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Emergomyces africanus poses an emerging threat.\n \n \n \n \n\n\n \n Hoving, J. C.\n\n\n \n\n\n\n Nature Microbiology, 9(1): 4–5. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Emergomyces$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{hoving_emergomyces_2024,\n\ttitle = {Emergomyces africanus poses an emerging threat},\n\tvolume = {9},\n\tissn = {2058-5276},\n\turl = {https://www.nature.com/articles/s41564-023-01565-x},\n\tdoi = {10.1038/s41564-023-01565-x},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Microbiology},\n\tauthor = {Hoving, Jennifer Claire},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {4--5},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n γδ T cell antigen receptor polyspecificity enables T cell responses to a broad range of immune challenges.\n \n \n \n \n\n\n \n Guo, J.; Chowdhury, R. R.; Mallajosyula, V.; Xie, J.; Dubey, M.; Liu, Y.; Li, J.; Wei, Y.; Palanski, B. A.; Wang, C.; Qiu, L.; Ohanyan, M.; Kask, O.; Sola, E.; Kamalyan, L.; Lewis, D. B.; Scriba, T. J.; Davis, M. M.; Dodd, D.; Zeng, X.; and Chien, Y.\n\n\n \n\n\n\n Proceedings of the National Academy of Sciences, 121(4): e2315592121. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"γδ$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{guo__2024,\n\ttitle = {γδ {T} cell antigen receptor polyspecificity enables {T} cell responses to a broad range of immune challenges},\n\tvolume = {121},\n\tissn = {0027-8424, 1091-6490},\n\turl = {https://pnas.org/doi/10.1073/pnas.2315592121},\n\tdoi = {10.1073/pnas.2315592121},\n\tabstract = {γδ T cells are essential for immune defense and modulating physiological processes. While they have the potential to recognize large numbers of antigens through somatic gene rearrangement, the antigens which trigger most γδ T cell response remain unidentified, and the role of antigen recognition in γδ T cell function is contentious. Here, we show that some γδ T cell receptors (TCRs) exhibit polyspecificity, recognizing multiple ligands of diverse molecular nature. These ligands include haptens, metabolites, neurotransmitters, posttranslational modifications, as well as peptides and proteins of microbial and host origin. Polyspecific γδ T cells are enriched among activated cells in naive mice and the responding population in infection. They express diverse TCR sequences, have different functional potentials, and include the innate-like γδ T cells, such as the major IL-17 responders in various pathological/physiological conditions. We demonstrate that encountering their antigenic microbiome metabolite maintains their homeostasis and functional response, indicating that their ability to recognize multiple ligands is essential for their function. Human γδ T cells with similar polyspecificity also respond to various immune challenges. This study demonstrates that polyspecificity is a prevalent feature of γδ T cell antigen recognition, which enables rapid and robust T cell responses to a wide range of challenges, highlighting a unique function of γδ T cells.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {Proceedings of the National Academy of Sciences},\n\tauthor = {Guo, Jing and Chowdhury, Roshni Roy and Mallajosyula, Vamsee and Xie, Jianming and Dubey, Megha and Liu, Yuanyuan and Li, Jing and Wei, Yu-ling and Palanski, Brad A. and Wang, Conghua and Qiu, Lingfeng and Ohanyan, Mané and Kask, Oliver and Sola, Elsa and Kamalyan, Lilit and Lewis, David B. and Scriba, Thomas J. and Davis, Mark M. and Dodd, Dylan and Zeng, Xun and Chien, Yueh-hsiu},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {e2315592121},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Humoral immunoprofiling identifies novel biomarkers and an immune suppressive autoantibody phenotype at the site of disease in pancreatic ductal adenocarcinoma.\n \n \n \n \n\n\n \n Maimela, P. W. M.; Smith, M.; Nel, A. J. M.; Bernam, S. D. P.; Jonas, E. G.; and Blackburn, J. M.\n\n\n \n\n\n\n Frontiers in Oncology, 14: 1330419. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Humoral$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{maimela_humoral_2024,\n\ttitle = {Humoral immunoprofiling identifies novel biomarkers and an immune suppressive autoantibody phenotype at the site of disease in pancreatic ductal adenocarcinoma},\n\tvolume = {14},\n\tissn = {2234-943X},\n\turl = {https://www.frontiersin.org/articles/10.3389/fonc.2024.1330419/full},\n\tdoi = {10.3389/fonc.2024.1330419},\n\tabstract = {Pancreatic ductal adenocarcinoma (PDAC) is a heterogeneous cancer, with minimal response to therapeutic intervention and with 85\\% of cases diagnosed at an advanced stage due to lack of early symptoms, highlighting the importance of understanding PDAC immunology in greater detail. Here, we applied an immunoproteomic approach to investigate autoantibody responses against cancer-testis and tumor-associated antigens in PDAC using a high-throughput multiplexed protein microarray platform, comparing humoral immune responses in serum and at the site of disease in order to shed new light on immune responses in the tumor microenvironment. We simultaneously quantified serum or tissue IgG and IgA antibody isotypes and subclasses in a cohort of PDAC, disease control and healthy patients, observing inter alia that subclass utilization in tumor tissue samples was predominantly immune suppressive IgG4 and inflammatory IgA2, contrasting with predominant IgG3 and IgA1 subclass utilization in matched sera and implying local autoantibody production at the site of disease in an immune-tolerant environment. By comparison, serum autoantibody subclass profiling for the disease controls identified IgG4, IgG1, and IgA1 as the abundant subclasses. Combinatorial analysis of serum autoantibody responses identified panels of candidate biomarkers. The top IgG panel included ACVR2B, GAGE1, LEMD1, MAGEB1 and PAGE1 (sensitivity, specificity and AUC values of 0.933, 0.767 and 0.906). Conversely, the top IgA panel included AURKA, GAGE1, MAGEA10, PLEKHA5 and XAGE3aV1 (sensitivity, specificity, and AUC values of 1.000, 0.800, and 0.954). Assessment of antigen-specific serum autoantibody glycoforms revealed abundant sialylation on IgA in PDAC, consistent with an immune suppressive IgA response to disease.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Oncology},\n\tauthor = {Maimela, Pamela Winnie M. and Smith, Muneerah and Nel, Andrew J. M. and Bernam, Suba Dharshanan P. and Jonas, Eduard G. and Blackburn, Jonathan M.},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {1330419},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Ecology meets reproductive medicine in HIV prevention: the case for geography-informed approaches for bacterial vaginosis in Africa.\n \n \n \n \n\n\n \n Passmore, J. S.; Ngcapu, S.; Gitome, S.; Kullin, B. R.; Welp, K.; Martin, D. P.; Potloane, D.; Manhanzva, M. T.; Obimbo, M. M.; Gill, K.; Fevre, M. L.; Happel, A.; Jaspan, H. B.; Kasaro, M.; and Bukusi, E. A.\n\n\n \n\n\n\n Frontiers in Reproductive Health, 6: 1431306. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Ecology$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{passmore_ecology_2024,\n\ttitle = {Ecology meets reproductive medicine in {HIV} prevention: the case for geography-informed approaches for bacterial vaginosis in {Africa}},\n\tvolume = {6},\n\tissn = {2673-3153},\n\tshorttitle = {Ecology meets reproductive medicine in {HIV} prevention},\n\turl = {https://www.frontiersin.org/articles/10.3389/frph.2024.1431306/full},\n\tdoi = {10.3389/frph.2024.1431306},\n\tabstract = {Purpose of review \n              Women in Africa bear the burden of the HIV epidemic, which has been associated with the high prevalence of bacterial vaginosis (BV) in the region. However, little progress has been made in finding an effective cure for BV. Drawing on advances in microbiome-directed therapies for gastrointestinal disorders, similar live-biotherapeutic based approaches for BV treatment are being evaluated. Here, we summarize current knowledge regarding vaginal microbiota in BV, explore geographical differences in vaginal microbiota, and argue that novel BV therapeutics should be tailored specifically to meet the needs of African women. \n             \n             \n              Recent findings \n               \n                Cervicovaginal microbiota dominated by \n                Lactobacillus crispatus \n                are optimal, although these are uncommon in African women. Besides socio-behavioural and environmental influences on the vaginal microbiota, host and microbial genetic traits should be considered, particularly those relating to glycogen metabolism. Novel microbiome-directed approaches being developed to treat BV should employ transfers of multiple microbial strains to ensure sustained colonization and BV cure. \n               \n             \n             \n              Summary \n              Improving the efficacy and durability of BV treatment with microbiome-directed therapies by appropriately accounting for host and microbial genetic factors, could potentially reduce the risk of HIV infection in African women.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Reproductive Health},\n\tauthor = {Passmore, Jo-Ann S. and Ngcapu, Sinaye and Gitome, Serah and Kullin, Brian R. and Welp, Kirsten and Martin, Darren P. and Potloane, Disebo and Manhanzva, Monalisa T. and Obimbo, Moses M. and Gill, Katherine and Fevre, Mellissa Le and Happel, Anna-Ursula and Jaspan, Heather B. and Kasaro, Margaret and Bukusi, Elizabeth A.},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {1431306},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Genotype–Phenotype Characterization of Serial Mycobacterium tuberculosis Isolates in Bedaquiline-Resistant Tuberculosis.\n \n \n \n \n\n\n \n Brown, T. S; Tang, L.; Omar, S. V.; Joseph, L.; Meintjes, G.; Maartens, G.; Wasserman, S.; Shah, N S.; Farhat, M. R; Gandhi, N. R; Ismail, N.; Brust, J. C M; and Mathema, B.\n\n\n \n\n\n\n Clinical Infectious Diseases, 78(2): 269–276. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Genotype–Phenotype$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{brown_genotypephenotype_2024,\n\ttitle = {Genotype–{Phenotype} {Characterization} of {Serial} \\textit{{Mycobacterium} tuberculosis} {Isolates} in {Bedaquiline}-{Resistant} {Tuberculosis}},\n\tvolume = {78},\n\tcopyright = {https://academic.oup.com/pages/standard-publication-reuse-rights},\n\tissn = {1058-4838, 1537-6591},\n\turl = {https://academic.oup.com/cid/article/78/2/269/7326309},\n\tdoi = {10.1093/cid/ciad596},\n\tabstract = {Abstract \n             \n              Background \n              Emerging resistance to bedaquiline (BDQ) threatens to undermine advances in the treatment of drug-resistant tuberculosis (DRTB). Characterizing serial Mycobacterium tuberculosis (Mtb) isolates collected during BDQ-based treatment can provide insights into the etiologies of BDQ resistance in this important group of DRTB patients. \n             \n             \n              Methods \n              We measured mycobacteria growth indicator tube (MGIT)–based BDQ minimum inhibitory concentrations (MICs) of Mtb isolates collected from 195 individuals with no prior BDQ exposure who were receiving BDQ-based treatment for DRTB. We conducted whole-genome sequencing on serial Mtb isolates from all participants who had any isolate with a BDQ MIC \\&gt;1 collected before or after starting treatment (95 total Mtb isolates from 24 participants). \n             \n             \n              Results \n              Sixteen of 24 participants had BDQ-resistant TB (MGIT MIC ≥4 µg/mL) and 8 had BDQ-intermediate infections (MGIT MIC = 2 µg/mL). Participants with pre-existing resistance outnumbered those with resistance acquired during treatment, and 8 of 24 participants had polyclonal infections. BDQ resistance was observed across multiple Mtb strain types and involved a diverse catalog of mmpR5 (Rv0678) mutations, but no mutations in atpE or pepQ. Nine pairs of participants shared genetically similar isolates separated by \\&lt;5 single nucleotide polymorphisms, concerning for potential transmitted BDQ resistance. \n             \n             \n              Conclusions \n              BDQ-resistant TB can arise via multiple, overlapping processes, including transmission of strains with pre-existing resistance. Capturing the within-host diversity of these infections could potentially improve clinical diagnosis, population-level surveillance, and molecular diagnostic test development.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {Clinical Infectious Diseases},\n\tauthor = {Brown, Tyler S and Tang, Linrui and Omar, Shaheed Vally and Joseph, Lavania and Meintjes, Graeme and Maartens, Gary and Wasserman, Sean and Shah, N Sarita and Farhat, Maha R and Gandhi, Neel R and Ismail, Nazir and Brust, James C M and Mathema, Barun},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {269--276},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The divergent outcome of IL-4Rα signalling on Foxp3 T regulatory cells in listeriosis and tuberculosis.\n \n \n \n \n\n\n \n Chia, J. E.; Rousseau, R. P.; Ozturk, M.; Poswayo, S. K. L.; Lucas, R.; Brombacher, F.; and Parihar, S. P.\n\n\n \n\n\n\n Frontiers in Immunology, 15: 1427055. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{chia_divergent_2024,\n\ttitle = {The divergent outcome of {IL}-{4Rα} signalling on {Foxp3} {T} regulatory cells in listeriosis and tuberculosis},\n\tvolume = {15},\n\tissn = {1664-3224},\n\turl = {https://www.frontiersin.org/articles/10.3389/fimmu.2024.1427055/full},\n\tdoi = {10.3389/fimmu.2024.1427055},\n\tabstract = {Introduction \n              Forkhead box P3 (Foxp3) T regulatory cells are critical for maintaining self-tolerance, immune homeostasis, and regulating the immune system. \n             \n             \n              Methods \n               \n                We investigated interleukin-4 receptor alpha (IL-4Rα) signalling on T regulatory cells (Tregs) during \n                Listeria monocytogenes \n                ( \n                L. monocytogenes \n                ) infection using a mouse model on a BALB/c background, specifically with IL-4Rα knockdown in Tregs (Foxp3 \n                cre \n                IL-4Rα \n                −/lox \n                ). \n               \n             \n             \n              Results \n               \n                We showed an impairment of Treg responses, along with a decreased bacterial burden and diminished tissue pathology in the liver and spleen, which translated into better survival. Mechanistically, we observed an enhancement of the Th1 signature, characterised by increased expression of the T-bet transcription factor and a greater number of effector T cells producing IFN-γ, IL-2 following \n                ex-vivo \n                stimulation with heat-killed \n                L. monocytogenes \n                in Foxp3 \n                cre \n                IL-4Rα \n                -/lox \n                mice. Furthermore, CD8 T cells from Foxp3 \n                cre \n                IL-4Rα \n                -/lox \n                mice displayed increased cytotoxicity (Granzyme-B) with higher proliferation capacity (Ki-67), better survival (Bcl-2) with concomitant reduced apoptosis (activated caspase 3). In contrast to \n                L. monocytogenes \n                , Foxp3 \n                cre \n                IL-4Rα \n                -/lox \n                mice displayed similar bacterial burdens, lung pathology and survival during \n                Mycobacterium tuberculosis \n                ( \n                M. tuberculosis \n                ) infection, despite increased T cell numbers and IFN-γ, TNF and IL-17 production. \n               \n             \n             \n              Conclusion \n              Our results demonstrated that the diminished IL-4Rα signalling on Foxp3+ T regulatory cells resulted in a loss of their functionality, leading to survival benefits in listeriosis but not in tuberculosis.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Immunology},\n\tauthor = {Chia, Julius E. and Rousseau, Robert P. and Ozturk, Mumin and Poswayo, Sibongiseni K. L. and Lucas, Rodney and Brombacher, Frank and Parihar, Suraj P.},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {1427055},\n}\n\n\n\n

\n

\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Post-pandemic memory T cell response to SARS-CoV-2 is durable, broadly targeted, and cross-reactive to the hypermutated BA.2.86 variant.\n \n \n \n \n\n\n \n Nesamari, R.; Omondi, M. A.; Baguma, R.; Höft, M. A.; Ngomti, A.; Nkayi, A. A.; Besethi, A. S.; Magugu, S. F.; Mosala, P.; Walters, A.; Clark, G. M.; Mennen, M.; Skelem, S.; Adriaanse, M.; Grifoni, A.; Sette, A.; Keeton, R. S.; Ntusi, N. A.; Riou, C.; and Burgers, W. A.\n\n\n \n\n\n\n Cell Host & Microbe, 32(2): 162–169.e3. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Post-pandemic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{nesamari_post-pandemic_2024,\n\ttitle = {Post-pandemic memory {T} cell response to {SARS}-{CoV}-2 is durable, broadly targeted, and cross-reactive to the hypermutated {BA}.2.86 variant},\n\tvolume = {32},\n\tissn = {19313128},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1931312823004985},\n\tdoi = {10.1016/j.chom.2023.12.003},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {Cell Host \\& Microbe},\n\tauthor = {Nesamari, Rofhiwa and Omondi, Millicent A. and Baguma, Richard and Höft, Maxine A. and Ngomti, Amkele and Nkayi, Anathi A. and Besethi, Asiphe S. and Magugu, Siyabulela F.J. and Mosala, Paballo and Walters, Avril and Clark, Gesina M. and Mennen, Mathilda and Skelem, Sango and Adriaanse, Marguerite and Grifoni, Alba and Sette, Alessandro and Keeton, Roanne S. and Ntusi, Ntobeko A.B. and Riou, Catherine and Burgers, Wendy A.},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {162--169.e3},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Global Globin Network and adopting genomic variant database requirements for thalassemia.\n \n \n \n \n\n\n \n Halim-Fikri, H.; Zulkipli, N. N.; Alauddin, H.; Bento, C.; Lederer, C. W; Kountouris, P.; Kleanthous, M.; Hernaningsih, Y.; Thong, M.; Mahmood, M. H.; Mohd Yasin, N.; Esa, E.; Elion, J.; Coviello, D.; Raja-Sabudin, R.; El-Kamah, G.; Burn, J.; Mohd Yusoff, N.; Ramesar, R.; and Zilfalil, B. A.\n\n\n \n\n\n\n Database, 2024: baae080. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Global$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{halim-fikri_global_2024,\n\ttitle = {Global {Globin} {Network} and adopting genomic variant database requirements for thalassemia},\n\tvolume = {2024},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1758-0463},\n\turl = {https://academic.oup.com/database/article/doi/10.1093/database/baae080/7749354},\n\tdoi = {10.1093/database/baae080},\n\tabstract = {Abstract \n            Thalassemia is one of the most prevalent monogenic disorders in low- and middle-income countries (LMICs). There are an estimated 270 million carriers of hemoglobinopathies (abnormal hemoglobins and/or thalassemia) worldwide, necessitating global methods and solutions for effective and optimal therapy. LMICs are disproportionately impacted by thalassemia, and due to disparities in genomics awareness and diagnostic resources, certain LMICs lag behind high-income countries (HICs). This spurred the establishment of the Global Globin Network (GGN) in 2015 at UNESCO, Paris, as a project-wide endeavor within the Human Variome Project (HVP). Primarily aimed at enhancing thalassemia clinical services, research, and genomic diagnostic capabilities with a focus on LMIC needs, GGN aims to foster data collection in a shared database by all affected nations, thus improving data sharing and thalassemia management. In this paper, we propose a minimum requirement for establishing a genomic database in thalassemia based on the HVP database guidelines. We suggest using an existing platform recommended by HVP, the Leiden Open Variation Database (LOVD) (https://www.lovd.nl/). Adoption of our proposed criteria will assist in improving or supplementing the existing databases, allowing for better-quality services for individuals with thalassemia. \n            Database URL: https://www.lovd.nl/},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Database},\n\tauthor = {Halim-Fikri, Hashim and Zulkipli, Ninie Nadia and Alauddin, Hafiza and Bento, Celeste and Lederer, Carsten W and Kountouris, Petros and Kleanthous, Marina and Hernaningsih, Yetti and Thong, Meow-Keong and Mahmood, Muhammad Hamdi and Mohd Yasin, Norafiza and Esa, Ezalia and Elion, Jacques and Coviello, Domenico and Raja-Sabudin, Raja-Zahratul-Azma and El-Kamah, Ghada and Burn, John and Mohd Yusoff, Narazah and Ramesar, Raj and Zilfalil, Bin Alwi},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {baae080},\n}\n\n\n\n

\n

\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Unlocking Opportunities for Mycobacterium leprae and Mycobacterium ulcerans.\n \n \n \n \n\n\n \n Shyam, M.; Kumar, S.; and Singh, V.\n\n\n \n\n\n\n ACS Infectious Diseases, 10(2): 251–269. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Unlocking$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{shyam_unlocking_2024,\n\ttitle = {Unlocking {Opportunities} for \\textit{{Mycobacterium} leprae} and \\textit{{Mycobacterium} ulcerans}},\n\tvolume = {10},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2373-8227, 2373-8227},\n\turl = {https://pubs.acs.org/doi/10.1021/acsinfecdis.3c00371},\n\tdoi = {10.1021/acsinfecdis.3c00371},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {ACS Infectious Diseases},\n\tauthor = {Shyam, Mousumi and Kumar, Sumit and Singh, Vinayak},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {251--269},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Virologic outcomes with tenofovir-lamivudine-dolutegravir in adults failing PI-based second-line ART.\n \n \n \n \n\n\n \n Zhao, Y.; Voget, J.; Singini, I.; Omar, Z.; Mudaly, V.; Boulle, A.; Maartens, G.; and Meintjes, G.\n\n\n \n\n\n\n Southern African Journal of HIV Medicine, 25(1). April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Virologic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{zhao_virologic_2024,\n\ttitle = {Virologic outcomes with tenofovir-lamivudine-dolutegravir in adults failing {PI}-based second-line {ART}},\n\tvolume = {25},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0},\n\tissn = {2078-6751, 1608-9693},\n\turl = {http://www.sajhivmed.org.za/index.php/HIVMED/article/view/1567},\n\tdoi = {10.4102/sajhivmed.v25i1.1567},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Southern African Journal of HIV Medicine},\n\tauthor = {Zhao, Ying and Voget, Jacqueline and Singini, Isaac and Omar, Zaayid and Mudaly, Vanessa and Boulle, Andrew and Maartens, Gary and Meintjes, Graeme},\n\tmonth = apr,\n\tyear = {2024},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Advancing microbiome research through standardized data and metadata collection: introducing the Microbiome Research Data Toolkit.\n \n \n \n \n\n\n \n Zass, L.; Mwapagha, L. M; Louis-Jacques, A. F; Allali, I.; Mulindwa, J.; Kiran, A.; Hanachi, M.; Souiai, O.; Mulder, N.; and Oduaran, O. H\n\n\n \n\n\n\n Database, 2024: baae062. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Advancing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{zass_advancing_2024,\n\ttitle = {Advancing microbiome research through standardized data and metadata collection: introducing the {Microbiome} {Research} {Data} {Toolkit}},\n\tvolume = {2024},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1758-0463},\n\tshorttitle = {Advancing microbiome research through standardized data and metadata collection},\n\turl = {https://academic.oup.com/database/article/doi/10.1093/database/baae062/7738174},\n\tdoi = {10.1093/database/baae062},\n\tabstract = {Abstract \n            Microbiome research has made significant gains with the evolution of sequencing technologies. Ensuring comparability between studies and enhancing the findability, accessibility, interoperability and reproducibility of microbiome data are crucial for maximizing the value of this growing body of research. Addressing the challenges of standardized metadata reporting, collection and curation, the Microbiome Working Group of the Human Hereditary and Health in Africa (H3Africa) consortium aimed to develop a comprehensive solution. In this paper, we present the Microbiome Research Data Toolkit, a versatile tool designed to standardize microbiome research metadata, facilitate MIxS-MIMS and PhenX reporting, standardize prospective collection of participant biological and lifestyle data, and retrospectively harmonize such data. This toolkit enables past, present and future microbiome research endeavors to collaborate effectively, fostering novel collaborations and accelerating knowledge discovery in the field. \n            Database URL: https://doi.org/10.25375/uct.24218999.v2},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Database},\n\tauthor = {Zass, Lyndon and Mwapagha, Lamech M and Louis-Jacques, Adetola F and Allali, Imane and Mulindwa, Julius and Kiran, Anmol and Hanachi, Mariem and Souiai, Oussama and Mulder, Nicola and Oduaran, Ovokeraye H},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {baae062},\n}\n\n\n\n

\n

\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Cysteinyl leukotriene receptor-1 as a potential target for host-directed therapy during chronic schistosomiasis in murine model.\n \n \n \n \n\n\n \n Mosala, P.; Mpotje, T.; Abdel Aziz, N.; Ndlovu, H.; Musaigwa, F.; Nono, J. K.; and Brombacher, F.\n\n\n \n\n\n\n Frontiers in Immunology, 15: 1279043. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Cysteinyl$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{mosala_cysteinyl_2024,\n\ttitle = {Cysteinyl leukotriene receptor-1 as a potential target for host-directed therapy during chronic schistosomiasis in murine model},\n\tvolume = {15},\n\tissn = {1664-3224},\n\turl = {https://www.frontiersin.org/articles/10.3389/fimmu.2024.1279043/full},\n\tdoi = {10.3389/fimmu.2024.1279043},\n\tabstract = {Schistosomiasis remains the most devastating neglected tropical disease, affecting over 240 million people world-wide. The disease is caused by the eggs laid by mature female worms that are trapped in host’s tissues, resulting in chronic Th2 driven fibrogranulmatous pathology. Although the disease can be treated with a relatively inexpensive drug, praziquantel (PZQ), re-infections remain a major problem in endemic areas. There is a need for new therapeutic drugs and alternative drug treatments for schistosomiasis. The current study hypothesized that cysteinyl leukotrienes (cysLTs) could mediate fibroproliferative pathology during schistosomiasis. Cysteinyl leukotrienes (cysLTs) are potent lipid mediators that are known to be key players in inflammatory diseases, such as asthma and allergic rhinitis. The present study aimed to investigate the role of cysLTR1 during experimental acute and chronic schistosomiasis using cysLTR1 \n              -/- \n              mice, as well as the use of cysLTR1 inhibitor (Montelukast) to assess immune responses during chronic \n              Schistosoma mansoni \n              infection. Mice deficient of cysLTR1 and littermate control mice were infected with either high or low dose of \n              Schistosoma mansoni \n              to achieve chronic or acute schistosomiasis, respectively. Hepatic granulomatous inflammation, hepatic fibrosis and IL-4 production in the liver was significantly reduced in mice lacking cysLTR1 during chronic schistosomiasis, while reduced liver pathology was observed during acute schistosomiasis. Pharmacological blockade of cysLTR1 using montelukast in combination with PZQ reduced hepatic inflammation and parasite egg burden in chronically infected mice. Combination therapy led to the expansion of Tregs in chronically infected mice. We show that the disruption of cysLTR1 is dispensable for host survival during schistosomiasis, suggesting an important role cysLTR1 may play during early immunity against schistosomiasis. Our findings revealed that the combination of montelukast and PZQ could be a potential prophylactic treatment for chronic schistosomiasis by reducing fibrogranulomatous pathology in mice. In conclusion, the present study demonstrated that cysLTR1 is a potential target for host-directed therapy to ameliorate fibrogranulomatous pathology in the liver during chronic and acute schistosomiasis in mice.},\n\turldate = {2025-06-24},\n\tjournal = {Frontiers in Immunology},\n\tauthor = {Mosala, Paballo and Mpotje, Thabo and Abdel Aziz, Nada and Ndlovu, Hlumani and Musaigwa, Fungai and Nono, Justin Komguep and Brombacher, Frank},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {1279043},\n}\n\n\n\n

\n

\n\n\n

\n Schistosomiasis remains the most devastating neglected tropical disease, affecting over 240 million people world-wide. The disease is caused by the eggs laid by mature female worms that are trapped in host’s tissues, resulting in chronic Th2 driven fibrogranulmatous pathology. Although the disease can be treated with a relatively inexpensive drug, praziquantel (PZQ), re-infections remain a major problem in endemic areas. There is a need for new therapeutic drugs and alternative drug treatments for schistosomiasis. The current study hypothesized that cysteinyl leukotrienes (cysLTs) could mediate fibroproliferative pathology during schistosomiasis. Cysteinyl leukotrienes (cysLTs) are potent lipid mediators that are known to be key players in inflammatory diseases, such as asthma and allergic rhinitis. The present study aimed to investigate the role of cysLTR1 during experimental acute and chronic schistosomiasis using cysLTR1 -/- mice, as well as the use of cysLTR1 inhibitor (Montelukast) to assess immune responses during chronic Schistosoma mansoni infection. Mice deficient of cysLTR1 and littermate control mice were infected with either high or low dose of Schistosoma mansoni to achieve chronic or acute schistosomiasis, respectively. Hepatic granulomatous inflammation, hepatic fibrosis and IL-4 production in the liver was significantly reduced in mice lacking cysLTR1 during chronic schistosomiasis, while reduced liver pathology was observed during acute schistosomiasis. Pharmacological blockade of cysLTR1 using montelukast in combination with PZQ reduced hepatic inflammation and parasite egg burden in chronically infected mice. Combination therapy led to the expansion of Tregs in chronically infected mice. We show that the disruption of cysLTR1 is dispensable for host survival during schistosomiasis, suggesting an important role cysLTR1 may play during early immunity against schistosomiasis. Our findings revealed that the combination of montelukast and PZQ could be a potential prophylactic treatment for chronic schistosomiasis by reducing fibrogranulomatous pathology in mice. In conclusion, the present study demonstrated that cysLTR1 is a potential target for host-directed therapy to ameliorate fibrogranulomatous pathology in the liver during chronic and acute schistosomiasis in mice.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Clinical Significance of Elevated KSHV Viral Load in HIV-Related Kaposi’s Sarcoma Patients in South Africa.\n \n \n \n \n\n\n \n Tibenderana, R. M.; Blumenthal, M. J.; Bukajumbe, E.; Schäfer, G.; and Mohamed, Z.\n\n\n \n\n\n\n Viruses, 16(2): 189. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Clinical$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{tibenderana_clinical_2024,\n\ttitle = {Clinical {Significance} of {Elevated} {KSHV} {Viral} {Load} in {HIV}-{Related} {Kaposi}’s {Sarcoma} {Patients} in {South} {Africa}},\n\tvolume = {16},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1999-4915},\n\turl = {https://www.mdpi.com/1999-4915/16/2/189},\n\tdoi = {10.3390/v16020189},\n\tabstract = {Kaposi’s sarcoma (KS) is an AIDS-defining illness caused by Kaposi’s sarcoma-associated herpesvirus (KSHV) predominantly in the context of HIV-related immune suppression. We aimed to explore the usefulness of KSHV DNA viral load (VL) measurement in predicting the severity, response to treatment and outcome of KS. We retrospectively assessed a cohort of KS patients (n = 94) receiving treatment at Groote Schuur Hospital, Cape Town, South Africa. Demographic and clinical data, KS staging and response to treatment were extracted from patient files, while long-term survival was ascertained from hospital records. KSHV serology and VL and hIL-6 were determined empirically from patients’ blood. All patients were HIV-positive adults, the majority of whom were on HAART at the time of recruitment. KSHV VL was detectable in 65 patients’ blood (median: 280.5/106 cells (IQR: 69.7–1727.3)) and was highest in patients with S1 HIV-related systemic disease (median 1066.9/106 cells, IQR: 70.5–11,269.6). KSHV VL was associated with the S1 stage in a binomial regression controlling for confounders (adjusted odds ratio 5.55, 95\\% CI: 1.28–24.14, p = 0.022). A subset of six patients identified to have extremely high KSHV VLs was predominantly T1 stage with pulmonary KS, and most had died at follow-up. In our cohort, elevated KSHV VL is associated with systemic HIV-related illness in KS disease. Extremely high KSHV VLs warrant further investigation for patients potentially requiring intensive treatment and investigation for progression or diagnosis of concurrent KSHV lytic syndromes.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {Viruses},\n\tauthor = {Tibenderana, Rebecca Monica and Blumenthal, Melissa Jayne and Bukajumbe, Emmanuel and Schäfer, Georgia and Mohamed, Zainab},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {189},\n}\n\n\n\n

\n

\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n SARS-CoV-2 seroepidemiology in Cape Town, South Africa, and implications for future outbreaks in low-income communities.\n \n \n \n \n\n\n \n Hussey, H.; Vreede, H.; Davies, M.; Heekes, A.; Kalk, E.; Hardie, D.; Van Zyl, G.; Naidoo, M.; Morden, E.; Bam, J.; Zinyakatira, N.; Centner, C. M.; Maritz, J.; Opie, J.; Chapanduka, Z.; Mahomed, H.; Smith, M.; Cois, A.; Pienaar, D.; Redd, A. D.; Preiser, W.; Wilkinson, R.; Boulle, A.; and Hsiao, N.\n\n\n \n\n\n\n PLOS Global Public Health, 4(8): e0003554. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"SARS-CoV-2$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{hussey_sars-cov-2_2024,\n\ttitle = {{SARS}-{CoV}-2 seroepidemiology in {Cape} {Town}, {South} {Africa}, and implications for future outbreaks in low-income communities},\n\tvolume = {4},\n\tissn = {2767-3375},\n\turl = {https://dx.plos.org/10.1371/journal.pgph.0003554},\n\tdoi = {10.1371/journal.pgph.0003554},\n\tabstract = {In low- and middle-income countries where SARS-CoV-2 testing is limited, seroprevalence studies can help describe and characterise the extent of the pandemic, as well as elucidate protection conferred by prior exposure. We conducted repeated cross-sectional serosurveys (July 2020 –November 2021) using residual samples from patients from Cape Town, South Africa, sent for routine laboratory studies for non-COVID-19 conditions. SARS-CoV-2 anti-nucleocapsid antibodies and linked clinical information were used to investigate: (1) seroprevalence over time and risk factors associated with seropositivity, (2) ecological comparison of seroprevalence between subdistricts, (3) case ascertainment rates, and (4) the relative protection against COVID-19 associated with seropositivity and vaccination statuses. Among the subset sampled, seroprevalence of SARS-CoV-2 in Cape Town increased from 39.19\\% (95\\% confidence interval [CI] 37.23–41.19) in July 2020 to 67.8\\% (95\\%CI 66.31–69.25) in November 2021. Poorer communities had both higher seroprevalence and COVID-19 mortality. Only 10\\% of seropositive individuals had a recorded positive SARS-CoV-2 test. Using COVID-19 hospital admission and death data at the Provincial Health Data Centre, antibody positivity before the start of the Omicron BA.1 wave (28 November 2021) was strongly protective for severe disease (adjusted odds ratio [aOR] 0.15; 95\\%CI 0.05–0.46), with additional benefit in those who were also vaccinated (aOR 0.07, 95\\%CI 0.01–0.35). The high population seroprevalence in Cape Town was attained at the cost of substantial COVID-19 mortality. At the individual level, seropositivity was highly protective against subsequent infections and severe COVID-19 disease. In low-income communities, where diagnostic testing capacity is often limited, surveillance systems dependent on them will underestimate the true extent of an outbreak. Rapidly conducted seroprevalence studies can play an important role in addressing this.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Global Public Health},\n\tauthor = {Hussey, Hannah and Vreede, Helena and Davies, Mary-Ann and Heekes, Alexa and Kalk, Emma and Hardie, Diana and Van Zyl, Gert and Naidoo, Michelle and Morden, Erna and Bam, Jamy-Lee and Zinyakatira, Nesbert and Centner, Chad M. and Maritz, Jean and Opie, Jessica and Chapanduka, Zivanai and Mahomed, Hassan and Smith, Mariette and Cois, Annibale and Pienaar, David and Redd, Andrew D. and Preiser, Wolfgang and Wilkinson, Robert and Boulle, Andrew and Hsiao, Nei-yuan},\n\teditor = {Inbaraj, Leeberk Raja},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {e0003554},\n}\n\n\n\n

\n

\n\n\n

\n In low- and middle-income countries where SARS-CoV-2 testing is limited, seroprevalence studies can help describe and characterise the extent of the pandemic, as well as elucidate protection conferred by prior exposure. We conducted repeated cross-sectional serosurveys (July 2020 –November 2021) using residual samples from patients from Cape Town, South Africa, sent for routine laboratory studies for non-COVID-19 conditions. SARS-CoV-2 anti-nucleocapsid antibodies and linked clinical information were used to investigate: (1) seroprevalence over time and risk factors associated with seropositivity, (2) ecological comparison of seroprevalence between subdistricts, (3) case ascertainment rates, and (4) the relative protection against COVID-19 associated with seropositivity and vaccination statuses. Among the subset sampled, seroprevalence of SARS-CoV-2 in Cape Town increased from 39.19% (95% confidence interval [CI] 37.23–41.19) in July 2020 to 67.8% (95%CI 66.31–69.25) in November 2021. Poorer communities had both higher seroprevalence and COVID-19 mortality. Only 10% of seropositive individuals had a recorded positive SARS-CoV-2 test. Using COVID-19 hospital admission and death data at the Provincial Health Data Centre, antibody positivity before the start of the Omicron BA.1 wave (28 November 2021) was strongly protective for severe disease (adjusted odds ratio [aOR] 0.15; 95%CI 0.05–0.46), with additional benefit in those who were also vaccinated (aOR 0.07, 95%CI 0.01–0.35). The high population seroprevalence in Cape Town was attained at the cost of substantial COVID-19 mortality. At the individual level, seropositivity was highly protective against subsequent infections and severe COVID-19 disease. In low-income communities, where diagnostic testing capacity is often limited, surveillance systems dependent on them will underestimate the true extent of an outbreak. Rapidly conducted seroprevalence studies can play an important role in addressing this.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Doubling down on dual systems: A cerebellum–amygdala route towards action- and outcome-based social and affective behavior.\n \n \n \n \n\n\n \n Terburg, D.; Van Honk, J.; and Schutter, D. J.\n\n\n \n\n\n\n Cortex, 173: 175–186. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Doubling$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{terburg_doubling_2024,\n\ttitle = {Doubling down on dual systems: {A} cerebellum–amygdala route towards action- and outcome-based social and affective behavior},\n\tvolume = {173},\n\tissn = {00109452},\n\tshorttitle = {Doubling down on dual systems},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S001094522400039X},\n\tdoi = {10.1016/j.cortex.2024.02.002},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Cortex},\n\tauthor = {Terburg, David and Van Honk, Jack and Schutter, Dennis J.L.G.},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {175--186},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n High-flow nasal oxygen in resource-constrained, non-intensive, high-care wards for COVID-19 acute hypoxaemic respiratory failure: Comparing outcomes of the first v. third waves at a tertiary centre in South Africa.\n \n \n \n \n\n\n \n Audley, G; Raubenheimer, P; Symons, G; Mendelson, M; Meintjes, G; Ntusi, N A B; Wasserman, S; Dlamini, S; Dheda, K; Van Zyl-Smit, R; and Calligaro, G\n\n\n \n\n\n\n African Journal of Thoracic and Critical Care Medicine, 30(1): e1151. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"High-flow$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{audley_high-flow_2024,\n\ttitle = {High-flow nasal oxygen in resource-constrained, non-intensive, high-care wards for {COVID}-19 acute hypoxaemic respiratory failure: {Comparing} outcomes of the first v. third waves at a tertiary centre in {South} {Africa}},\n\tvolume = {30},\n\tcopyright = {https://creativecommons.org/licenses/by-nc/4.0},\n\tissn = {2617-0205, 2617-0191},\n\tshorttitle = {High-flow nasal oxygen in resource-constrained, non-intensive, high-care wards for {COVID}-19 acute hypoxaemic respiratory failure},\n\turl = {https://samajournals.co.za/index.php/ajtccm/article/view/1151},\n\tdoi = {10.7196/AJTCCM.2024.v30i1.1151},\n\tabstract = {Background. High-flow nasal oxygen (HFNO) is an accepted treatment for severe COVID-19-related acute hypoxaemic respiratory failure (AHRF). \nObjectives. To determine whether treatment outcomes at Groote Schuur Hospital, Cape Town, South Africa, during the third COVID-19 wave would be affected by increased institutional experience and capacity for HNFO and more restrictive admission criteria for respiratory high-care wards and intensive care units. \nMethods. We included consecutive patients with COVID-19-related AHRF treated with HFNO during the first and third COVID-19 waves. The primary endpoint was comparison of HFNO failure (composite of the need for intubation or death while on HFNO) between waves. \nResults. A total of 744 patients were included: 343 in the first COVID-19 wave and 401 in the third. Patients treated with HFNO in the first wave were older (median (interquartile range) age 53 (46 - 61) years v. 47 (40 - 56) years; p{\\textless}0.001), and had higher prevalences of diabetes (46.9\\% v. 36.9\\%; p=0.006), hypertension (51.0\\% v. 35.2\\%; p{\\textless}0.001), obesity (33.5\\% v. 26.2\\%; p=0.029) and HIV infection (12.5\\% v. 5.5\\%; p{\\textless}0.001). The partial pressure of arterial oxygen to fraction of inspired oxygen (PaO2/FiO2) ratio at HFNO initiation and the ratio of oxygen saturation/FiO2 to respiratory rate within 6 hours (ROX-6 score) after HFNO commencement were lower in the first wave compared with the third (median 57.9 (47.3 - 74.3) mmHg v. 64.3 (51.2 - 79.0) mmHg; p=0.005 and 3.19 (2.37 - 3.77) v. 3.43 (2.93 - 4.00); p{\\textless}0.001, respectively). The likelihood of HFNO failure (57.1\\% v. 59.6\\%; p=0.498) and mortality (46.9\\% v. 52.1\\%; p=0.159) did not differ significantly between the first and third waves. \nConclusion. Despite differences in patient characteristics, circulating viral variant and institutional experience with HFNO, treatment outcomes were very similar in the first and third COVID-19 waves. We conclude that once AHRF is established in COVID-19 pneumonia, the comorbidity profile and HFNO provider experience do not appear to affect outcome.},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {African Journal of Thoracic and Critical Care Medicine},\n\tauthor = {Audley, G and Raubenheimer, P and Symons, G and Mendelson, M and Meintjes, G and Ntusi, N A B and Wasserman, S and Dlamini, S and Dheda, K and Van Zyl-Smit, R and Calligaro, G},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {e1151},\n}\n\n\n\n

\n

\n\n\n

\n Background. High-flow nasal oxygen (HFNO) is an accepted treatment for severe COVID-19-related acute hypoxaemic respiratory failure (AHRF). Objectives. To determine whether treatment outcomes at Groote Schuur Hospital, Cape Town, South Africa, during the third COVID-19 wave would be affected by increased institutional experience and capacity for HNFO and more restrictive admission criteria for respiratory high-care wards and intensive care units. Methods. We included consecutive patients with COVID-19-related AHRF treated with HFNO during the first and third COVID-19 waves. The primary endpoint was comparison of HFNO failure (composite of the need for intubation or death while on HFNO) between waves. Results. A total of 744 patients were included: 343 in the first COVID-19 wave and 401 in the third. Patients treated with HFNO in the first wave were older (median (interquartile range) age 53 (46 - 61) years v. 47 (40 - 56) years; p\\textless0.001), and had higher prevalences of diabetes (46.9% v. 36.9%; p=0.006), hypertension (51.0% v. 35.2%; p\\textless0.001), obesity (33.5% v. 26.2%; p=0.029) and HIV infection (12.5% v. 5.5%; p\\textless0.001). The partial pressure of arterial oxygen to fraction of inspired oxygen (PaO2/FiO2) ratio at HFNO initiation and the ratio of oxygen saturation/FiO2 to respiratory rate within 6 hours (ROX-6 score) after HFNO commencement were lower in the first wave compared with the third (median 57.9 (47.3 - 74.3) mmHg v. 64.3 (51.2 - 79.0) mmHg; p=0.005 and 3.19 (2.37 - 3.77) v. 3.43 (2.93 - 4.00); p\\textless0.001, respectively). The likelihood of HFNO failure (57.1% v. 59.6%; p=0.498) and mortality (46.9% v. 52.1%; p=0.159) did not differ significantly between the first and third waves. Conclusion. Despite differences in patient characteristics, circulating viral variant and institutional experience with HFNO, treatment outcomes were very similar in the first and third COVID-19 waves. We conclude that once AHRF is established in COVID-19 pneumonia, the comorbidity profile and HFNO provider experience do not appear to affect outcome.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Genetic Variation in ABCB1, ADRB1, CYP3A4, CYP3A5, NEDD4L and NR3C2 Confers Differential Susceptibility to Resistant Hypertension among South Africans.\n \n \n \n \n\n\n \n Katsukunya, J. N.; Jones, E.; Soko, N. D.; Blom, D.; Sinxadi, P.; Rayner, B.; and Dandara, C.\n\n\n \n\n\n\n Journal of Personalized Medicine, 14(7): 664. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{katsukunya_genetic_2024,\n\ttitle = {Genetic {Variation} in {ABCB1}, {ADRB1}, {CYP3A4}, {CYP3A5}, {NEDD4L} and {NR3C2} {Confers} {Differential} {Susceptibility} to {Resistant} {Hypertension} among {South} {Africans}},\n\tvolume = {14},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2075-4426},\n\turl = {https://www.mdpi.com/2075-4426/14/7/664},\n\tdoi = {10.3390/jpm14070664},\n\tabstract = {Resistant hypertension (RHTN) prevalence ranges from 4 to 19\\% in Africa. There is a paucity of data on the role of genetic variation on RHTN among Africans. We set out to investigate the role of polymorphisms in ABCB1, ADRB1, CYP3A4, CYP3A5, NEDD4L, and NR3C2, on RHTN susceptibility among South Africans. Using a retrospective matched case–control study, 190 RHTN patients (cases: blood pressure (BP) ≥ 140/90 mmHg on ≥3 anti-hypertensives or BP {\\textless} 140/90 mmHg on {\\textgreater}3 anti-hypertensives) and 189 non-RHTN patients (controls: {\\textless}3 anti-hypertensives, BP {\\textless} 140/90 or ≥140/90 mmHg), 12 single nucleotide polymorphisms were genotyped using polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP), quantitative PCR and Sanger sequencing. Genetic association analyses were conducted using the additive model and multivariable logistic regression. Homozygosity for CYP3A5 rs776746C/C genotype (p = 0.02; OR: 0.44; CI: 0.22–0.89) was associated with reduced risk for RHTN. Homozygous ADRB1 rs1801252G/G (p = 0.02; OR: 3.30; CI: 1.17–10.03) and NEDD4L rs4149601A/A genotypes (p = 0.001; OR: 3.82; CI: 1.67–9.07) were associated with increased risk for RHTN. Carriers of the of ADRB1 rs1801252—rs1801253 G–C haplotype had 2.83-fold odds of presenting with RHTN (p = 0.04; OR: 2.83; CI: 1.05–8.20). These variants that are associated with RHTN may have clinical utility in the selection of antihypertensive drugs in our population.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Personalized Medicine},\n\tauthor = {Katsukunya, Jonathan N. and Jones, Erika and Soko, Nyarai D. and Blom, Dirk and Sinxadi, Phumla and Rayner, Brian and Dandara, Collet},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {664},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Prospective multicentre accuracy evaluation of the FUJIFILM SILVAMP TB LAM test for the diagnosis of tuberculosis in people living with HIV demonstrates lot-to-lot variability.\n \n \n \n \n\n\n \n Székely, R.; Sossen, B.; Mukoka, M.; Muyoyeta, M.; Nakabugo, E.; Hella, J.; Nguyen, H. V.; Ubolyam, S.; Chikamatsu, K.; Macé, A.; Vermeulen, M.; Centner, C. M.; Nyangu, S.; Sanjase, N.; Sasamalo, M.; Dinh, H. T.; Ngo, T. A.; Manosuthi, W.; Jirajariyavej, S.; Mitarai, S.; Nguyen, N. V.; Avihingsanon, A.; Reither, K.; Nakiyingi, L.; Kerkhoff, A. D.; MacPherson, P.; Meintjes, G.; Denkinger, C. M.; Ruhwald, M.; and FujiLAM Study Consortium\n\n\n \n\n\n\n PLOS ONE, 19(5): e0303846. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Prospective$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{szekely_prospective_2024,\n\ttitle = {Prospective multicentre accuracy evaluation of the {FUJIFILM} {SILVAMP} {TB} {LAM} test for the diagnosis of tuberculosis in people living with {HIV} demonstrates lot-to-lot variability},\n\tvolume = {19},\n\tissn = {1932-6203},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0303846},\n\tdoi = {10.1371/journal.pone.0303846},\n\tabstract = {There is an urgent need for rapid, non-sputum point-of-care diagnostics to detect tuberculosis. This prospective trial in seven high tuberculosis burden countries evaluated the diagnostic accuracy of the point-of-care urine-based lipoarabinomannan assay FUJIFILM SILVAMP TB LAM (FujiLAM) among inpatients and outpatients living with HIV. Diagnostic performance of FujiLAM was assessed against a mycobacterial reference standard (sputum culture, blood culture, and Xpert Ultra from urine and sputum at enrollment, and additional sputum culture ≤7 days from enrollment), an extended mycobacterial reference standard (eMRS), and a composite reference standard including clinical evaluation. Of 1637 participants considered for the analysis, 296 (18\\%) were tuberculosis positive by eMRS. Median age was 40 years, median CD4 cell count was 369 cells/ul, and 52\\% were female. Overall FujiLAM sensitivity was 54·4\\% (95\\% CI: 48·7–60·0), overall specificity was 85·2\\% (83·2–87·0) against eMRS. Sensitivity and specificity estimates varied between sites, ranging from 26·5\\% (95\\% CI: 17·4\\%–38·0\\%) to 73·2\\% (60·4\\%–83·0\\%), and 75·0 (65·0\\%–82·9\\%) to 96·5 (92·1\\%–98·5\\%), respectively. Post-hoc exploratory analysis identified significant variability in the performance of the six FujiLAM lots used in this study. Lot variability limited interpretation of FujiLAM test performance. Although results with the current version of FujiLAM are too variable for clinical decision-making, the lipoarabinomannan biomarker still holds promise for tuberculosis diagnostics. The trial is registered at clinicaltrials.gov (NCT04089423).},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Székely, Rita and Sossen, Bianca and Mukoka, Madalo and Muyoyeta, Monde and Nakabugo, Elizabeth and Hella, Jerry and Nguyen, Hung Van and Ubolyam, Sasiwimol and Chikamatsu, Kinuyo and Macé, Aurélien and Vermeulen, Marcia and Centner, Chad M. and Nyangu, Sarah and Sanjase, Nsala and Sasamalo, Mohamed and Dinh, Huong Thi and Ngo, The Anh and Manosuthi, Weerawat and Jirajariyavej, Supunnee and Mitarai, Satoshi and Nguyen, Nhung Viet and Avihingsanon, Anchalee and Reither, Klaus and Nakiyingi, Lydia and Kerkhoff, Andrew D. and MacPherson, Peter and Meintjes, Graeme and Denkinger, Claudia M. and Ruhwald, Morten and {FujiLAM Study Consortium}},\n\teditor = {Pham, Minh Duc},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {e0303846},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Interactions between Zoliflodacin and Neisseria gonorrhoeae Gyrase and Topoisomerase IV: Enzymological Basis for Cellular Targeting.\n \n \n \n \n\n\n \n Collins, J. A.; Basarab, G. S.; Chibale, K.; and Osheroff, N.\n\n\n \n\n\n\n ACS Infectious Diseases, 10(8): 3071–3082. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Interactions$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{collins_interactions_2024,\n\ttitle = {Interactions between {Zoliflodacin} and \\textit{{Neisseria} gonorrhoeae} {Gyrase} and {Topoisomerase} {IV}: {Enzymological} {Basis} for {Cellular} {Targeting}},\n\tvolume = {10},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2373-8227, 2373-8227},\n\tshorttitle = {Interactions between {Zoliflodacin} and \\textit{{Neisseria} gonorrhoeae} {Gyrase} and {Topoisomerase} {IV}},\n\turl = {https://pubs.acs.org/doi/10.1021/acsinfecdis.4c00438},\n\tdoi = {10.1021/acsinfecdis.4c00438},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {ACS Infectious Diseases},\n\tauthor = {Collins, Jessica A. and Basarab, Gregory S. and Chibale, Kelly and Osheroff, Neil},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {3071--3082},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Leveraging human–mouse studies to advance the genetics of hearing impairment in Africa.\n \n \n \n \n\n\n \n James, K.; and Oluwole, O. G.\n\n\n \n\n\n\n The Journal of Gene Medicine, 26(7): e3714. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Leveraging$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{james_leveraging_2024,\n\ttitle = {Leveraging human–mouse studies to advance the genetics of hearing impairment in {Africa}},\n\tvolume = {26},\n\tissn = {1099-498X, 1521-2254},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/jgm.3714},\n\tdoi = {10.1002/jgm.3714},\n\tabstract = {Abstract \n            Mouse models are used extensively to understand human pathobiology and mechanistic functions of disease‐associated loci. However, in this review, we investigate the potential of using genetic mouse models to identify genetic markers that can disrupt hearing thresholds in mice and then target the hearing‐enriched orthologues and loci in humans. Currently, little is known about the real prevalence of genes that cause hearing impairment (HI) in Africa. Pre‐screening mouse cell lines to identify orthologues of interest has the potential to improve the genetic diagnosis for HI in Africa to a significant percentage, for example, 10–20\\%. Furthermore, the functionality of a candidate gene derived from mouse screening with heterogeneous genetic backgrounds and multi‐omic approaches can shed light on the molecular, genetic heterogeneity and plausible mode of inheritance of a gene in hearing‐impaired individuals especially in the absence of large families to investigate.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {The Journal of Gene Medicine},\n\tauthor = {James, Kili and Oluwole, Oluwafemi G.},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {e3714},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Tips for Getting Your Manuscript Accepted into ACS Medicinal Chemistry Letters.\n \n \n \n \n\n\n \n Woodland, J. G.; and Chibale, K.\n\n\n \n\n\n\n ACS Medicinal Chemistry Letters, 15(3): 316–317. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Tips$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{woodland_tips_2024,\n\ttitle = {Tips for {Getting} {Your} {Manuscript} {Accepted} into \\textit{{ACS} {Medicinal} {Chemistry} {Letters}}},\n\tvolume = {15},\n\tcopyright = {https://doi.org/10.15223/policy-001},\n\tissn = {1948-5875, 1948-5875},\n\turl = {https://pubs.acs.org/doi/10.1021/acsmedchemlett.4c00059},\n\tdoi = {10.1021/acsmedchemlett.4c00059},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {ACS Medicinal Chemistry Letters},\n\tauthor = {Woodland, John G. and Chibale, Kelly},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {316--317},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n SARS-CoV-2 Viral Replication Persists in the Human Lung for Several Weeks after Symptom Onset.\n \n \n \n \n\n\n \n Tomasicchio, M.; Jaumdally, S.; Wilson, L.; Kotze, A.; Semple, L.; Meier, S.; Pooran, A.; Esmail, A.; Pillay, K.; Roberts, R.; Kriel, R.; Meldau, R.; Oelofse, S.; Mandviwala, C.; Burns, J.; Londt, R.; Davids, M.; Van Der Merwe, C.; Roomaney, A.; Kühn, L.; Perumal, T.; Scott, A. J.; Hale, M. J.; Baillie, V.; Mahtab, S.; Williamson, C.; Joseph, R.; Sigal, A.; Joubert, I.; Piercy, J.; Thomson, D.; Fredericks, D. L.; Miller, M. G. A.; Nunes, M. C.; Madhi, S. A.; and Dheda, K.\n\n\n \n\n\n\n American Journal of Respiratory and Critical Care Medicine, 209(7): 840–851. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"SARS-CoV-2$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{tomasicchio_sars-cov-2_2024,\n\ttitle = {{SARS}-{CoV}-2 {Viral} {Replication} {Persists} in the {Human} {Lung} for {Several} {Weeks} after {Symptom} {Onset}},\n\tvolume = {209},\n\tissn = {1073-449X, 1535-4970},\n\turl = {https://www.atsjournals.org/doi/10.1164/rccm.202308-1438OC},\n\tdoi = {10.1164/rccm.202308-1438OC},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {American Journal of Respiratory and Critical Care Medicine},\n\tauthor = {Tomasicchio, Michele and Jaumdally, Shameem and Wilson, Lindsay and Kotze, Andrea and Semple, Lynn and Meier, Stuart and Pooran, Anil and Esmail, Aliasgar and Pillay, Komala and Roberts, Riyaadh and Kriel, Raymond and Meldau, Richard and Oelofse, Suzette and Mandviwala, Carley and Burns, Jessica and Londt, Rolanda and Davids, Malika and Van Der Merwe, Charnay and Roomaney, Aqeedah and Kühn, Louié and Perumal, Tahlia and Scott, Alex J. and Hale, Martin J. and Baillie, Vicky and Mahtab, Sana and Williamson, Carolyn and Joseph, Rageema and Sigal, Alex and Joubert, Ivan and Piercy, Jenna and Thomson, David and Fredericks, David L. and Miller, Malcolm G. A. and Nunes, Marta C. and Madhi, Shabir A. and Dheda, Keertan},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {840--851},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Brief Report: Inflammatory Markers in Pregnancy Are Associated With Postpartum Weight in South African Women Living With HIV on Antiretroviral Therapy.\n \n \n \n \n\n\n \n Madlala, H. P.; Myer, L.; Geffen, H.; Rusch, J.; Shey, M. S.; Meyer, D.; Goedecke, J. H.; Malaba, T. R.; Gray, C. M.; Newell, M.; and Jao, J.\n\n\n \n\n\n\n JAIDS Journal of Acquired Immune Deficiency Syndromes, 96(2): 161–165. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Brief$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{madlala_brief_2024,\n\ttitle = {Brief {Report}: {Inflammatory} {Markers} in {Pregnancy} {Are} {Associated} {With} {Postpartum} {Weight} in {South} {African} {Women} {Living} {With} {HIV} on {Antiretroviral} {Therapy}},\n\tvolume = {96},\n\tissn = {1525-4135},\n\tshorttitle = {Brief {Report}},\n\turl = {https://journals.lww.com/10.1097/QAI.0000000000003406},\n\tdoi = {10.1097/QAI.0000000000003406},\n\tabstract = {Background: \n              Postpartum weight (PPW) contributes to long-term obesity, a growing concern in persons with HIV (PWHs). We investigated whether inflammatory markers in pregnancy may be involved in postpartum (PP) obesity in PWHs. \n             \n             \n              Setting: \n              A total of 57 pregnant PWHs enrolled at ≤14 weeks gestation (T1) in Gugulethu antenatal care clinic in Cape Town and followed through 48 weeks PP were included. \n             \n             \n              Methods: \n              Plasma soluble (s) CD14, sCD163, leptin, tumor necrosis factor receptor 1, resistin, adiponectin, and interleukin-6 (IL-6) were assayed in duplicate using the Luminex platform. We considered each inflammatory marker at T1 (n = 57) and T3 (29–36 weeks gestation, n = 31) as a separate exposure of interest. Linear mixed-effects models were fit to examine whether each exposure was associated with average PPW and PPW trajectories; linear regression was used for associations with PPW change between T1 and 48 weeks. \n             \n             \n              Results: \n               \n                The median age was 32 years (interquartile range [IQR], 29–35), 98\\% were multigravida, and 49\\% had a BMI ≥30 kg/m \n                2 \n                . Higher T1 sCD14 levels were associated with higher average weight through 48 weeks PP (ß = 0.002, \n                P \n                = 0.04) and T3 sCD14 with higher PPW gain (ß = 0.007, \n                P \n                = 0.04). Leptin (ß = 0.414, \n                P \n                {\\textless} 0.01), tumor necrosis factor receptor 1 (ß = 11.048, \n                P \n                {\\textless} 0.01), and resistin (ß = 0.714, \n                P \n                = 0.01) at T3 were associated with higher average PPW and IL-6 (ß = 2.266, \n                P \n                = 0.02) with PPW gain. \n               \n             \n             \n              Conclusions: \n              These findings suggest that low-grade inflammation in pregnancy may play a role in PP obesity, pointing to potential mechanisms with implications for long-term cardiometabolic health in PWH.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},\n\tauthor = {Madlala, Hlengiwe P. and Myer, Landon and Geffen, Hayli and Rusch, Jody and Shey, Muki S. and Meyer, Demi and Goedecke, Julia H. and Malaba, Thokozile R. and Gray, Clive M. and Newell, Marie-Louise and Jao, Jennifer},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {161--165},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Neighbourhood factors and tuberculosis incidence in Cape Town: A negative binomial regression and spatial analysis.\n \n \n \n \n\n\n \n Molemans, M.; Kayaert, L.; Olislagers, Q.; Abrahams, S.; Berkowitz, N.; Mohr‐Holland, E.; McKelly, D.; Wood, R.; Van Leth, F.; and Hermans, S.\n\n\n \n\n\n\n Tropical Medicine & International Health, 29(7): 599–611. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Neighbourhood$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{molemans_neighbourhood_2024,\n\ttitle = {Neighbourhood factors and tuberculosis incidence in {Cape} {Town}: {A} negative binomial regression and spatial analysis},\n\tvolume = {29},\n\tissn = {1360-2276, 1365-3156},\n\tshorttitle = {Neighbourhood factors and tuberculosis incidence in {Cape} {Town}},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/tmi.14001},\n\tdoi = {10.1111/tmi.14001},\n\tabstract = {Abstract \n             \n              Objectives \n              Although the link between poverty and tuberculosis (TB) is widely recognised, limited studies have investigated the association between neighbourhood factors and TB incidence. Since the factors influencing different episodes of TB might be different, this study focused on the first episode of TB disease (first‐episode TB). \n             \n             \n              Methods \n               \n                All first episodes in previously linked and geocoded TB notification data from 2007 to 2015 in Cape Town, South Africa, were aggregated at the neighbourhood level and merged with the 2011 census data. We conducted an ecological study to assess the association between neighbourhood incidence of first‐episode TB and neighbourhood factors (total TB burden [all episodes] in the previous year, socioeconomic index, mean household size, mean age, and percentage males) using a negative binomial regression. We also examined the presence of hotspots in neighbourhood TB incidence with the Global Moran's \n                I \n                statistic and assessed spatial dependency in the association between neighbourhood factors and TB incidence using a spatial lag model. \n               \n             \n             \n              Results \n              The study included 684 neighbourhoods with a median first‐episode TB incidence rate of 114 (IQR: 0–345) per 100,000 people. We found lower neighbourhood socioeconomic index (SEI), higher neighbourhood total TB burden, lower neighbourhood mean household size, and lower neighbourhood mean age were associated with increased neighbourhood first‐episode TB incidence. Our findings revealed a hotspot of first‐episode TB incidence in Cape Town and evidence of spatial dependency in the association between neighbourhood factors and TB incidence. \n             \n             \n              Conclusion \n              Neighbourhood TB burden and SEI were associated with first‐episode TB incidence, and there was spatial dependency in this association. Our findings can inform targeted interventions to reduce TB in high‐risk neighbourhoods, thereby reducing health disparities and promoting health equity.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {Tropical Medicine \\& International Health},\n\tauthor = {Molemans, M. and Kayaert, L. and Olislagers, Q. and Abrahams, S. and Berkowitz, N. and Mohr‐Holland, E. and McKelly, D. and Wood, R. and Van Leth, F. and Hermans, S.},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {599--611},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Generation of Multicellular 3D Liver Organoids From Induced Pluripotent Stem Cells as a Tool for Modelling Liver Diseases.\n \n \n \n \n\n\n \n Maepa, S.; Marakalala, M.; and Ndlovu, H.\n\n\n \n\n\n\n BIO-PROTOCOL, 14(1350). 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Generation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{maepa_generation_2024,\n\ttitle = {Generation of {Multicellular} {3D} {Liver} {Organoids} {From} {Induced} {Pluripotent} {Stem} {Cells} as a {Tool} for {Modelling} {Liver} {Diseases}},\n\tvolume = {14},\n\tissn = {2331-8325},\n\turl = {https://bio-protocol.org/en/bpdetail?id=5042&type=0},\n\tdoi = {10.21769/BioProtoc.5042},\n\tlanguage = {en},\n\tnumber = {1350},\n\turldate = {2025-06-24},\n\tjournal = {BIO-PROTOCOL},\n\tauthor = {Maepa, Setjie and Marakalala, Mohlopheni and Ndlovu, Hlumani},\n\tyear = {2024},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Xpert MTB/RIF Ultra versus mycobacterial growth indicator tube liquid culture for detection of Mycobacterium tuberculosis in symptomatic adults: a diagnostic accuracy study.\n \n \n \n \n\n\n \n Xie, Y. L; Eichberg, C.; Hapeela, N.; Nakabugo, E.; Anyango, I.; Arora, K.; Korte, J. E; Odero, R.; Van Heerden, J.; Zemanay, W.; Kennedy, S.; Nabeta, P.; Hanif, M.; Rodrigues, C.; Skrahina, A.; Stevens, W.; Dietze, R.; Liu, X.; Ellner, J. J; Alland, D.; Joloba, M. L; Schumacher, S. G; McCarthy, K. D; Nakiyingi, L.; and Dorman, S. E\n\n\n \n\n\n\n The Lancet Microbe, 5(6): e520–e528. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Xpert$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{xie_xpert_2024,\n\ttitle = {Xpert {MTB}/{RIF} {Ultra} versus mycobacterial growth indicator tube liquid culture for detection of {Mycobacterium} tuberculosis in symptomatic adults: a diagnostic accuracy study},\n\tvolume = {5},\n\tissn = {26665247},\n\tshorttitle = {Xpert {MTB}/{RIF} {Ultra} versus mycobacterial growth indicator tube liquid culture for detection of {Mycobacterium} tuberculosis in symptomatic adults},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524724000016},\n\tdoi = {10.1016/S2666-5247(24)00001-6},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Xie, Yingda L and Eichberg, Christie and Hapeela, Nchimunya and Nakabugo, Elizabeth and Anyango, Irene and Arora, Kiranjot and Korte, Jeffrey E and Odero, Ronald and Van Heerden, Judi and Zemanay, Widaad and Kennedy, Samuel and Nabeta, Pamela and Hanif, Mahmud and Rodrigues, Camilla and Skrahina, Alena and Stevens, Wendy and Dietze, Reynaldo and Liu, Xin and Ellner, Jerrold J and Alland, David and Joloba, Moses L and Schumacher, Samuel G and McCarthy, Kimberly D and Nakiyingi, Lydia and Dorman, Susan E},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {e520--e528},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Corrigendum to ‘Would you? “Effects of oxytocin on moral choices in forensic psychopathic patients” [Compr. Psychoneuroendocrinology (2024) 100245].\n \n \n \n \n\n\n \n Rijnders, R. J.; Van Den Hoogen, S.; Van Honk, J.; Terburg, D.; and Kempes, M. M.\n\n\n \n\n\n\n Comprehensive Psychoneuroendocrinology, 19: 100252. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Corrigendum$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{rijnders_corrigendum_2024,\n\ttitle = {Corrigendum to ‘{Would} you? “{Effects} of oxytocin on moral choices in forensic psychopathic patients” [{Compr}. {Psychoneuroendocrinology} (2024) 100245]},\n\tvolume = {19},\n\tissn = {26664976},\n\tshorttitle = {Corrigendum to ‘{Would} you?},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666497624000286},\n\tdoi = {10.1016/j.cpnec.2024.100252},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Comprehensive Psychoneuroendocrinology},\n\tauthor = {Rijnders, Ronald J.P. and Van Den Hoogen, Sophie and Van Honk, Jack and Terburg, David and Kempes, Maaike M.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {100252},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Human Leukocyte Antigen-Allelic Variations May Influence the Age at Cancer Diagnosis in Lynch Syndrome.\n \n \n \n \n\n\n \n Ndou, L.; Chambuso, R.; Valley-Omar, Z.; Rebello, G.; Algar, U.; Goldberg, P.; Boutall, A.; and Ramesar, R.\n\n\n \n\n\n\n Journal of Personalized Medicine, 14(6): 575. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Human$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{ndou_human_2024,\n\ttitle = {Human {Leukocyte} {Antigen}-{Allelic} {Variations} {May} {Influence} the {Age} at {Cancer} {Diagnosis} in {Lynch} {Syndrome}},\n\tvolume = {14},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2075-4426},\n\turl = {https://www.mdpi.com/2075-4426/14/6/575},\n\tdoi = {10.3390/jpm14060575},\n\tabstract = {Lynch syndrome (LS) is an inherited cancer predisposition disorder associated with an elevated risk of developing various solid cancers, but mostly colorectal cancer (CRC). Despite having the same germline pathogenic variant (PV) in one of the mis-match repair genes or the EPCAM gene, Lynch syndrome variant heterozygotes (LSVH) exhibit a remarkable phenotypic variability in the risk of developing cancer. The role of human leukocyte antigen (HLA) in modifying cancer development risk prompted our hypothesis into whether HLA variations act as potential genetic modifiers influencing the age at cancer diagnosis in LSVH. To investigate this, we studied a unique cohort of 426 LSVH carrying the same germline PV in the hMLH1 gene (MLH1:c.1528C {\\textgreater} T) in South Africa. We intuitively selected 100 LSVH with the greatest diversity in age at cancer diagnosis (N = 80) and the oldest cancer unaffected LSVH (N = 20) for a high-throughput HLA genotyping of 11 HLA class I and class II loci using the shotgun next-generation sequencing (NGS) technique on the Illumina MiSeq platform. Statistical analyses employed Kaplan–Meier survival analyses with log-rank tests, and Cox proportional hazards using binned HLA data to minimize type I error. Significant associations were observed between young age at cancer diagnosis and HLA-DPB1*04:02 (mean age: 37 y (25–50); hazard ratio (HR) = 3.37; corrected p-value (q) = 0.043) as well as HLA-DPB1 binned alleles (including HLA-DPB1*09:01, HLA-DPB1*10:01, HLA-DPB1*106:01, HLA-DPB1*18:01, HLA-DPB1*20:01, HLA-DPB1*26:01, HLA-DPB1*28:01, HLA-DPB1*296:01, and HLA-DPB1*55:01) (mean age: 37 y (17–63); HR = 2.30, q = 0.045). The involvement of HLA-DPB1 alleles in the age at cancer diagnosis may highlight the potential role of HLA class II in the immune response against cancer development in LSVH. When validated in a larger cohort, these high-risk HLA-DPB1 alleles could be factored into cancer risk prediction models for personalized cancer screening in LSVH.},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Personalized Medicine},\n\tauthor = {Ndou, Lutricia and Chambuso, Ramadhani and Valley-Omar, Ziyaad and Rebello, George and Algar, Ursula and Goldberg, Paul and Boutall, Adam and Ramesar, Raj},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {575},\n}\n\n\n\n

\n

\n\n\n

\n Lynch syndrome (LS) is an inherited cancer predisposition disorder associated with an elevated risk of developing various solid cancers, but mostly colorectal cancer (CRC). Despite having the same germline pathogenic variant (PV) in one of the mis-match repair genes or the EPCAM gene, Lynch syndrome variant heterozygotes (LSVH) exhibit a remarkable phenotypic variability in the risk of developing cancer. The role of human leukocyte antigen (HLA) in modifying cancer development risk prompted our hypothesis into whether HLA variations act as potential genetic modifiers influencing the age at cancer diagnosis in LSVH. To investigate this, we studied a unique cohort of 426 LSVH carrying the same germline PV in the hMLH1 gene (MLH1:c.1528C \\textgreater T) in South Africa. We intuitively selected 100 LSVH with the greatest diversity in age at cancer diagnosis (N = 80) and the oldest cancer unaffected LSVH (N = 20) for a high-throughput HLA genotyping of 11 HLA class I and class II loci using the shotgun next-generation sequencing (NGS) technique on the Illumina MiSeq platform. Statistical analyses employed Kaplan–Meier survival analyses with log-rank tests, and Cox proportional hazards using binned HLA data to minimize type I error. Significant associations were observed between young age at cancer diagnosis and HLA-DPB1*04:02 (mean age: 37 y (25–50); hazard ratio (HR) = 3.37; corrected p-value (q) = 0.043) as well as HLA-DPB1 binned alleles (including HLA-DPB1*09:01, HLA-DPB1*10:01, HLA-DPB1*106:01, HLA-DPB1*18:01, HLA-DPB1*20:01, HLA-DPB1*26:01, HLA-DPB1*28:01, HLA-DPB1*296:01, and HLA-DPB1*55:01) (mean age: 37 y (17–63); HR = 2.30, q = 0.045). The involvement of HLA-DPB1 alleles in the age at cancer diagnosis may highlight the potential role of HLA class II in the immune response against cancer development in LSVH. When validated in a larger cohort, these high-risk HLA-DPB1 alleles could be factored into cancer risk prediction models for personalized cancer screening in LSVH.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Age and sex influence antibody profiles associated with tuberculosis progression.\n \n \n \n \n\n\n \n Davies, L. R. L.; Wang, C.; Steigler, P.; Bowman, K. A.; Fischinger, S.; Hatherill, M.; Fisher, M.; Mbandi, S. K.; Rodo, M.; Ottenhoff, T. H. M.; Dockrell, H. M.; Sutherland, J. S.; Mayanja-Kizza, H.; Boom, W. H.; Walzl, G.; Kaufmann, S. H. E.; Nemes, E.; Scriba, T. J.; Lauffenburger, D.; Alter, G.; and Fortune, S. M.\n\n\n \n\n\n\n Nature Microbiology, 9(6): 1513–1525. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Age$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{davies_age_2024,\n\ttitle = {Age and sex influence antibody profiles associated with tuberculosis progression},\n\tvolume = {9},\n\tissn = {2058-5276},\n\turl = {https://www.nature.com/articles/s41564-024-01678-x},\n\tdoi = {10.1038/s41564-024-01678-x},\n\tabstract = {Abstract \n             \n              Antibody features vary with tuberculosis (TB) disease state. Whether clinical variables, such as age or sex, influence associations between \n              Mycobacterium tuberculosis \n              -specific antibody responses and disease state is not well explored. Here we profiled \n              Mycobacterium tuberculosis \n              -specific antibody responses in 140 TB-exposed South African individuals from the Adolescent Cohort Study. We identified distinct response features in individuals progressing to active TB from non-progressing, matched controls. A multivariate antibody score differentially associated with progression (SeroScore) identified progressors up to 2 years before TB diagnosis, earlier than that achieved with the RISK6 transcriptional signature of progression. We validated these antibody response features in the Grand Challenges 6–74 cohort. Both the SeroScore and RISK6 correlated better with risk of TB progression in adolescents compared with adults, and in males compared with females. This suggests that age and sex are important, underappreciated modifiers of antibody responses associated with TB progression.},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {Nature Microbiology},\n\tauthor = {Davies, Leela R. L. and Wang, Chuangqi and Steigler, Pia and Bowman, Kathryn A. and Fischinger, Stephanie and Hatherill, Mark and Fisher, Michelle and Mbandi, Stanley Kimbung and Rodo, Miguel and Ottenhoff, Tom H. M. and Dockrell, Hazel M. and Sutherland, Jayne S. and Mayanja-Kizza, Harriet and Boom, W. Henry and Walzl, Gerhard and Kaufmann, Stefan H. E. and Nemes, Elisa and Scriba, Thomas J. and Lauffenburger, Douglas and Alter, Galit and Fortune, Sarah M.},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {1513--1525},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Novel point-of-care cytokine biomarker lateral flow test for the screening for sexually transmitted infections and bacterial vaginosis: study protocol of a multicentre multidisciplinary prospective observational clinical study to evaluate the performance and feasibility of the Genital InFlammation Test (GIFT).\n \n \n \n \n\n\n \n Ramboarina, S.; Crucitti, T.; Gill, K.; Bekker, L. G.; Harding-Esch, E. M.; Van De Wijgert, J. H H M; Huynh, B.; Fortas, C.; Harimanana, A.; Mayouya Gamana, T.; Randremanana, R. V.; Mangahasimbola, R.; Dziva Chikwari, C.; Kranzer, K.; Mackworth-Young, C. R S; Bernays, S.; Thomas, N.; Anderson, D.; Tanko, F. R.; Manhanzva, M.; Lurie, M.; Khumalo, F.; Sinanovic, E.; Honda, A.; Pidwell, T.; Francis, S. C; Masson, L.; and Passmore, J.\n\n\n \n\n\n\n BMJ Open, 14(5): e084918. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Novel$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{ramboarina_novel_2024,\n\ttitle = {Novel point-of-care cytokine biomarker lateral flow test for the screening for sexually transmitted infections and bacterial vaginosis: study protocol of a multicentre multidisciplinary prospective observational clinical study to evaluate the performance and feasibility of the {Genital} {InFlammation} {Test} ({GIFT})},\n\tvolume = {14},\n\tissn = {2044-6055, 2044-6055},\n\tshorttitle = {Novel point-of-care cytokine biomarker lateral flow test for the screening for sexually transmitted infections and bacterial vaginosis},\n\turl = {https://bmjopen.bmj.com/lookup/doi/10.1136/bmjopen-2024-084918},\n\tdoi = {10.1136/bmjopen-2024-084918},\n\tabstract = {Introduction \n              A prototype lateral flow device detecting cytokine biomarkers interleukin (IL)-1α and IL-1β has been developed as a point-of-care test—called the Genital InFlammation Test (GIFT)—for detecting genital inflammation associated with sexually transmitted infections (STIs) and/or bacterial vaginosis (BV) in women. In this paper, we describe the rationale and design for studies that will be conducted in South Africa, Zimbabwe and Madagascar to evaluate the performance of GIFT and how it could be integrated into routine care. \n             \n             \n              Methods and analysis \n               \n                We will conduct a prospective, multidisciplinary, multicentre, cross-sectional and observational clinical study comprising two distinct components: a biomedical (‘diagnostic study’) and a qualitative, modelling and economic (‘an integration into care study’) part. The diagnostic study aims to evaluate GIFT’s performance in identifying asymptomatic women with discharge-causing STIs ( \n                Chlamydia trachomatis \n                (CT), \n                Neisseria gonorrhoeae \n                (NG), \n                Trichomonas vaginalis \n                (TV) and \n                Mycoplasma genitalium \n                (MG)) and BV. Study participants will be recruited from women attending research sites and family planning services. Several vaginal swabs will be collected for the evaluation of cytokine concentrations (ELISA), STIs (nucleic acid amplification tests), BV (Nugent score) and vaginal microbiome characteristics (16S rRNA gene sequencing). The first collected vaginal swab will be used for the GIFT assay which will be performed in parallel by a healthcare worker in the clinic near the participant, and by a technician in the laboratory. The integration into care study aims to explore how GIFT could be integrated into routine care. Four activities will be conducted: user experiences and/or perceptions of the GIFT device involving qualitative focus group discussions and in-depth interviews with key stakeholders; discrete choice experiments; development of a decision tree classification algorithm; and economic evaluation of defined management algorithms. \n               \n             \n             \n              Ethics and dissemination \n              Findings will be reported to participants, collaborators and local government for the three sites, presented at national and international conferences, and disseminated in peer-reviewed publications. \n              The protocol and all study documents such as informed consent forms were reviewed and approved by the University of Cape Town Human Research Ethics Committee (HREC reference 366/2022), Medical Research Council of Zimbabwe (MRCZ/A/2966), Comité d’Ethique pour la Recherche Biomédicale de Madagascar (N° 143 MNSAP/SG/AMM/CERBM) and the London School of Hygiene and Tropical Medicine ethics committee (LSHTM reference 28046). \n               \n                Before the start, this study was submitted to the Clinicaltrials.gov public registry ( \n                NCT05723484 \n                ). \n               \n             \n             \n              Trial registration number \n               \n                NCT05723484 \n                .},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-24},\n\tjournal = {BMJ Open},\n\tauthor = {Ramboarina, Stephanie and Crucitti, Tania and Gill, Katherine and Bekker, Linda Gail and Harding-Esch, Emma Michele and Van De Wijgert, Janneke H H M and Huynh, Bich-Tram and Fortas, Camille and Harimanana, Aina and Mayouya Gamana, Théodora and Randremanana, Rindra Vatosoa and Mangahasimbola, Reziky and Dziva Chikwari, Chido and Kranzer, Katharina and Mackworth-Young, Constance R S and Bernays, Sarah and Thomas, Nicola and Anderson, David and Tanko, Fatime Ramla and Manhanzva, Monalisa and Lurie, Micaela and Khumalo, Fezile and Sinanovic, Edina and Honda, Ayako and Pidwell, Tanya and Francis, Suzanna C and Masson, Lindi and Passmore, Jo-Anne},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {e084918},\n}\n\n\n\n

\n

\n\n\n

\n Introduction A prototype lateral flow device detecting cytokine biomarkers interleukin (IL)-1α and IL-1β has been developed as a point-of-care test—called the Genital InFlammation Test (GIFT)—for detecting genital inflammation associated with sexually transmitted infections (STIs) and/or bacterial vaginosis (BV) in women. In this paper, we describe the rationale and design for studies that will be conducted in South Africa, Zimbabwe and Madagascar to evaluate the performance of GIFT and how it could be integrated into routine care. Methods and analysis We will conduct a prospective, multidisciplinary, multicentre, cross-sectional and observational clinical study comprising two distinct components: a biomedical (‘diagnostic study’) and a qualitative, modelling and economic (‘an integration into care study’) part. The diagnostic study aims to evaluate GIFT’s performance in identifying asymptomatic women with discharge-causing STIs ( Chlamydia trachomatis (CT), Neisseria gonorrhoeae (NG), Trichomonas vaginalis (TV) and Mycoplasma genitalium (MG)) and BV. Study participants will be recruited from women attending research sites and family planning services. Several vaginal swabs will be collected for the evaluation of cytokine concentrations (ELISA), STIs (nucleic acid amplification tests), BV (Nugent score) and vaginal microbiome characteristics (16S rRNA gene sequencing). The first collected vaginal swab will be used for the GIFT assay which will be performed in parallel by a healthcare worker in the clinic near the participant, and by a technician in the laboratory. The integration into care study aims to explore how GIFT could be integrated into routine care. Four activities will be conducted: user experiences and/or perceptions of the GIFT device involving qualitative focus group discussions and in-depth interviews with key stakeholders; discrete choice experiments; development of a decision tree classification algorithm; and economic evaluation of defined management algorithms. Ethics and dissemination Findings will be reported to participants, collaborators and local government for the three sites, presented at national and international conferences, and disseminated in peer-reviewed publications. The protocol and all study documents such as informed consent forms were reviewed and approved by the University of Cape Town Human Research Ethics Committee (HREC reference 366/2022), Medical Research Council of Zimbabwe (MRCZ/A/2966), Comité d’Ethique pour la Recherche Biomédicale de Madagascar (N° 143 MNSAP/SG/AMM/CERBM) and the London School of Hygiene and Tropical Medicine ethics committee (LSHTM reference 28046). Before the start, this study was submitted to the Clinicaltrials.gov public registry ( NCT05723484 ). Trial registration number NCT05723484 .\n

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\n \n\n \n \n \n \n \n \n 2,8-Disubstituted-1,5-naphthyridines as Dual Inhibitors of Plasmodium falciparum Phosphatidylinositol-4-kinase and Hemozoin Formation with In Vivo Efficacy.\n \n \n \n \n\n\n \n Dziwornu, G. A.; Seanego, D.; Fienberg, S.; Clements, M.; Ferreira, J.; Sypu, V. S.; Samanta, S.; Bhana, A. D.; Korkor, C. M.; Garnie, L. F.; Teixeira, N.; Wicht, K. J.; Taylor, D.; Olckers, R.; Njoroge, M.; Gibhard, L.; Salomane, N.; Wittlin, S.; Mahato, R.; Chakraborty, A.; Sevilleno, N.; Coyle, R.; Lee, M. C. S.; Godoy, L. C.; Pasaje, C. F.; Niles, J. C.; Reader, J.; Van Der Watt, M.; Birkholtz, L.; Bolscher, J. M.; De Bruijni, M. H. C.; Coulson, L. B.; Basarab, G. S.; Ghorpade, S. R.; and Chibale, K.\n\n\n \n\n\n\n Journal of Medicinal Chemistry, 67(13): 11401–11420. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"2,8-Disubstituted-1,5-naphthyridines$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{dziwornu_28-disubstituted-15-naphthyridines_2024,\n\ttitle = {2,8-{Disubstituted}-1,5-naphthyridines as {Dual} {Inhibitors} of \\textit{{Plasmodium} falciparum} {Phosphatidylinositol}-4-kinase and {Hemozoin} {Formation} with \\textit{{In} {Vivo}} {Efficacy}},\n\tvolume = {67},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0022-2623, 1520-4804},\n\turl = {https://pubs.acs.org/doi/10.1021/acs.jmedchem.4c01154},\n\tdoi = {10.1021/acs.jmedchem.4c01154},\n\tlanguage = {en},\n\tnumber = {13},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Medicinal Chemistry},\n\tauthor = {Dziwornu, Godwin Akpeko and Seanego, Donald and Fienberg, Stephen and Clements, Monica and Ferreira, Jasmin and Sypu, Venkata S. and Samanta, Sauvik and Bhana, Ashlyn D. and Korkor, Constance M. and Garnie, Larnelle F. and Teixeira, Nicole and Wicht, Kathryn J. and Taylor, Dale and Olckers, Ronald and Njoroge, Mathew and Gibhard, Liezl and Salomane, Nicolaas and Wittlin, Sergio and Mahato, Rohit and Chakraborty, Arnish and Sevilleno, Nicole and Coyle, Rachael and Lee, Marcus C. S. and Godoy, Luiz C. and Pasaje, Charisse Flerida and Niles, Jacquin C. and Reader, Janette and Van Der Watt, Mariette and Birkholtz, Lyn-Marié and Bolscher, Judith M. and De Bruijni, Marloes H. C. and Coulson, Lauren B. and Basarab, Gregory S. and Ghorpade, Sandeep R. and Chibale, Kelly},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {11401--11420},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Reflex Xpert MTB/XDR Testing of Residual Rifampicin-Resistant Specimens: A Clinical Laboratory-Based Diagnostic Accuracy and Feasibility Study in South Africa.\n \n \n \n \n\n\n \n Centner, C M; Munir, R; Tagliani, E; Rieß, F; Brown, P; Hayes, C; Dolby, T; Zemanay, W; Cirillo, D M; David, A; Schumacher, S G; Denkinger, C M; Ruhwald, M; Leukes, V N; Nicol, M P; Van Der Walt, I; Kisten, G; Gumede, M; Mace, A; Brink, A; Stevens, W; Scott, L; Penn-Nicholson, A; Cox, H; TB-CAPT Consortium; Leukes, V.; Penn-Nicholson, A.; Ruhwald, M.; Erkosar, B.; Schumacher, S. G; Singh, S.; Kivuma, B.; Nuru, M.; Mlenge, J.; Shija, N.; Bulime, D.; Mnzava, D.; Sabuni, P.; Temba, H.; Siru, J.; Hella, J.; Msafiri, J.; Weisser, M.; Mbaruku, M.; Sasamalo, M.; Leonard, A.; Malango, A.; Alexander, A.; Komakoma, F.; Msigala, G.; Johaness, K.; Mhalu, G.; Hamis, M.; Mlay, P.; Ndege, R.; Barasa, S.; Masoud, S.; Byakuzana, T.; Lwilla, A.; Kayombo, B.; Mangu, C.; Manyama, C.; Mbunda, T.; Siyame, E.; Sabi, I.; Mwaipopo, L.; Ntinginya, N. E.; Edom, R.; Olomi, W.; Elisio, D.; Nguenha, D.; Mambuque, E.; Cossa, J.; Cossa, M.; Gomes, N.; Manjate, P.; Munguambe, S.; Acacio, S.; Saavedra, B.; Chiconela, H.; Ribeiro, K.; Machiana, A.; Meggi, B.; Junior, C. A.; Madeira, C.; Khosa, C.; Bila, C.; Floripes, D.; Malamule, D.; Viegas, S.; Saavedra, B.; Amroune, C.; Ehrlich, J.; De La Torre Pérez, L.; Sanz, S.; Garcia-Basteiro, A.; Riess, F.; Mutuku, S.; Appalarowthu, T.; Larson, L.; Kranzer, K.; Hoelscher, M.; Heinrich, N.; Del Mar Castro Noriega, M.; Denkinger, C. M; Arif, S.; Cirillo, D. M.; Tagliani, E.; Di Marco, F.; Batignani, V.; Malhotra, A.; Dowdy, D.; Schacht, C.; Buech, J.; Stöhr, C.; Loembé, M. M.; Ondoa, P.; Ndlovu, N.; Brown, F.; Ghebrekristos, Y.; Hayes, C.; Van Der Walt, I.; Abrahams, S.; Marokane, P.; Radebe, M.; Martinson, N.; David, A.; Scott, L.; Ngwenya, L.; Da Silva, P.; Solomon, R.; Stevens, W.; Abongomera, C.; Reither, K.; Stieger, L.; Brink, A.; Centner, C. M; Cox, H.; Van Heerden, J.; Nicol, M. P; Hapeela, N.; Brown, P.; Solomon, R.; Zemanay, W.; and Dolby, T.\n\n\n \n\n\n\n Open Forum Infectious Diseases, 11(8): ofae437. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Reflex$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{centner_reflex_2024,\n\ttitle = {Reflex {Xpert} {MTB}/{XDR} {Testing} of {Residual} {Rifampicin}-{Resistant} {Specimens}: {A} {Clinical} {Laboratory}-{Based} {Diagnostic} {Accuracy} and {Feasibility} {Study} in {South} {Africa}},\n\tvolume = {11},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2328-8957},\n\tshorttitle = {Reflex {Xpert} {MTB}/{XDR} {Testing} of {Residual} {Rifampicin}-{Resistant} {Specimens}},\n\turl = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofae437/7723233},\n\tdoi = {10.1093/ofid/ofae437},\n\tabstract = {Abstract \n             \n              Background \n              The World Health Organization–approved Xpert MTB/XDR test detects Mycobacterium tuberculosis and resistance to isoniazid, fluoroquinolones, ethionamide, and injectable drugs directly in specimens. This pragmatic, laboratory-based study assessed the diagnostic accuracy and feasibility of a reflex testing approach, where Xpert MTB/XDR was performed on residual specimens previously processed for Xpert MTB/RIF Ultra. \n             \n             \n              Methods \n              Routine respiratory specimens, processed for Xpert MTB/RIF Ultra, were stored in sample reagent buffer at 2°C–8°C. If rifampicin resistant, the residual specimen was assessed for adequate volume (≥2 mL) and tested with Xpert MTB/XDR, with storage time recorded. A second specimen was used for routine and reference standard testing (culture and sequencing). \n             \n             \n              Results \n              Specimens (99\\% sputum) from 763 participants submitted to 2 large routine laboratories were included. Xpert MTB/XDR yielded valid resistance detection results in 639 (84\\%), compared with 507 (66\\%) for routine testing (difference [95\\% CI], 18\\% [13\\%–22\\%]). The median turnaround time for results was 23 hours for Xpert MTB/XDR and 15 days for routine testing. While 748 specimens (98\\%) were ≥2 mL, only 102 (13\\%) were stored for ≤4 hours. By the reference standard, 284 of 394 (72\\%) were isoniazid resistant, and 57 of 380 (15\\%) were fluroquinolone resistant. The sensitivities of Xpert MTB/XDR were 94\\% (95\\% CI, 91\\%–97\\%) for isoniazid and 91\\% (81\\%–97\\%) for fluoroquinolone resistance detection. The specificities were 98\\% (94\\%–100\\%) and 100\\% (98\\%–100\\%), respectively. \n             \n             \n              Conclusions \n              Xpert MTB/XDR performed favorably compared with the reference, and the reflex testing approach increased results availability over routine testing, while dramatically decreasing turnaround time from weeks to hours. Laboratory workflow precluded testing within the manufacturer-recommended 4-hour storage time, but longer storage did not appear detrimental.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {Open Forum Infectious Diseases},\n\tauthor = {Centner, C M and Munir, R and Tagliani, E and Rieß, F and Brown, P and Hayes, C and Dolby, T and Zemanay, W and Cirillo, D M and David, A and Schumacher, S G and Denkinger, C M and Ruhwald, M and Leukes, V N and Nicol, M P and Van Der Walt, I and Kisten, G and Gumede, M and Mace, A and Brink, A and Stevens, W and Scott, L and Penn-Nicholson, A and Cox, H and {TB-CAPT Consortium} and Leukes, Vinzeigh and Penn-Nicholson, Adam and Ruhwald, Morten and Erkosar, Berra and Schumacher, Samuel G and Singh, Sunita and Kivuma, Bernard and Nuru, Muhuminu and Mlenge, Judith and Shija, Neema and Bulime, Deogratias and Mnzava, Dorcas and Sabuni, Petro and Temba, Hosiana and Siru, Jamali and Hella, Jerry and Msafiri, Jonathan and Weisser, Maja and Mbaruku, Mohamed and Sasamalo, Mohamed and Leonard, Alice and Malango, Ambilikile and Alexander, Annastazia and Komakoma, Faith and Msigala, Gloria and Johaness, Kasmir and Mhalu, Grace and Hamis, Mwajabu and Mlay, Priscilla and Ndege, Robert and Barasa, Sera and Masoud, Swalehe and Byakuzana, Theonestina and Lwilla, Anange and Kayombo, Benedict and Mangu, Chacha and Manyama, Christina and Mbunda, Theodora and Siyame, Elimina and Sabi, Issa and Mwaipopo, Last and Ntinginya, Nyanda Elias and Edom, Raphael and Olomi, Willyhelmina and Elisio, Delio and Nguenha, Dinis and Mambuque, Edson and Cossa, Joaquim and Cossa, Marta and Gomes, Neide and Manjate, Patricia and Munguambe, Shilzia and Acacio, Sozinho and Saavedra, Belen and Chiconela, Helio and Ribeiro, Katia and Machiana, António and Meggi, Bindiya and Junior, Candido Azize and Madeira, Carla and Khosa, Celso and Bila, Claudio and Floripes, Denise and Malamule, Diosdélio and Viegas, Sofia and Saavedra, Belén and Amroune, Carole and Ehrlich, Joanna and De La Torre Pérez, Laura and Sanz, Sergi and Garcia-Basteiro, Albero and Riess, Friedrich and Mutuku, Sarah and Appalarowthu, Tejaswi and Larson, Leyla and Kranzer, Katharina and Hoelscher, Michael and Heinrich, Norbert and Del Mar Castro Noriega, Maria and Denkinger, Claudia M and Arif, Saima and Cirillo, Daniela Maria and Tagliani, Elisa and Di Marco, Federico and Batignani, Virginia and Malhotra, Akash and Dowdy, David and Schacht, Claudia and Buech, Julia and Stöhr, Caroline and Loembé, Marguerite Massinga and Ondoa, Pascale and Ndlovu, Nqobile and Brown, Fumbani and Ghebrekristos, Yonas and Hayes, Cindy and Van Der Walt, Ilse and Abrahams, Shareef and Marokane, Puleng and Radebe, Mbuti and Martinson, Neil and David, Anura and Scott, Lesley and Ngwenya, Lucky and Da Silva, Pedro and Solomon, Reyhana and Stevens, Wendy and Abongomera, Charles and Reither, Klaus and Stieger, Leon and Brink, Adrian and Centner, Chad M and Cox, Helen and Van Heerden, Judi and Nicol, Mark P and Hapeela, Nchimunya and Brown, Parveen and Solomon, Reyhana and Zemanay, Widaad and Dolby, Tania},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {ofae437},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Self-transfers, Hospital Admissions and Mortality Among Children and Adolescents Lost to Follow-up From Antiretroviral Therapy Programs in the Western Cape, South Africa Between 2004 and 2019: Linkage to Provincial Records.\n \n \n \n \n\n\n \n Nyakato, P.; Boulle, A.; Wood, R.; Eley, B.; Rabie, H.; Egger, M.; Yiannoutsos, C. T.; Davies, M.; and Cornell, M.\n\n\n \n\n\n\n Pediatric Infectious Disease Journal, 43(5): 430–436. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Self-transfers,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{nyakato_self-transfers_2024,\n\ttitle = {Self-transfers, {Hospital} {Admissions} and {Mortality} {Among} {Children} and {Adolescents} {Lost} to {Follow}-up {From} {Antiretroviral} {Therapy} {Programs} in the {Western} {Cape}, {South} {Africa} {Between} 2004 and 2019: {Linkage} to {Provincial} {Records}},\n\tvolume = {43},\n\tissn = {0891-3668},\n\tshorttitle = {Self-transfers, {Hospital} {Admissions} and {Mortality} {Among} {Children} and {Adolescents} {Lost} to {Follow}-up {From} {Antiretroviral} {Therapy} {Programs} in the {Western} {Cape}, {South} {Africa} {Between} 2004 and 2019},\n\turl = {https://journals.lww.com/10.1097/INF.0000000000004281},\n\tdoi = {10.1097/INF.0000000000004281},\n\tabstract = {Background: \n              Pediatric programs face a high rate of loss to follow-up (LTFU) among children and adolescents living with HIV (CAHIV). We assessed true outcomes and predictors of these among CAHIV who were LTFU using linkage to the Western Cape Provincial Health Data Centre at Western Cape sites of the International epidemiology Databases to Evaluate AIDS-Southern Africa collaboration. \n             \n             \n              Methods: \n              We examined factors associated with self-transfer, hospital admission and mortality using competing risks regression in a retrospective cohort of CAHIV initiating antiretroviral therapy {\\textless}15 years old between 2004 and 2019 and deemed LTFU (no recorded visit at the original facility for ≥180 days from the last visit date before database closure and not known to have officially transferred out or deceased). \n             \n             \n              Results: \n              Of the 1720 CAHIV deemed LTFU, 802 (46.6\\%) had self-transferred and were receiving care elsewhere within the Western Cape, 463 (26.9\\%) had been hospitalized and 45 (2.6\\%) CAHIV had died. The overall rates of self-transfer, hospitalization, mortality and LTFU were 9.4 [95\\% confidence interval (CI): 8.8–10.1], 5.4 (95\\% CI: 5.0–6.0), 0.5 (95\\% CI: 0.4–0.7) and 4.8 (95\\% CI: 4.4–5.3) per 100 person-years respectively. Increasing duration on antiretroviral therapy before LTFU was associated with self-transfers while male sex, older age at last visit (≥10 years vs. younger) were associated with hospital admission and immune suppression at last visit was associated with 5 times higher mortality. \n             \n             \n              Conclusions: \n              Nearly half of CAHIV classified as LTFU had self-transferred to another health facility, a quarter had been hospitalized and a small proportion had died.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-24},\n\tjournal = {Pediatric Infectious Disease Journal},\n\tauthor = {Nyakato, Patience and Boulle, Andrew and Wood, Robin and Eley, Brian and Rabie, Helena and Egger, Matthias and Yiannoutsos, Constantin T. and Davies, Mary-Ann and Cornell, Morna},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {430--436},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The International Consensus for Early TB framework (ICE-TB): Implications from a low-incidence setting.\n \n \n \n \n\n\n \n Denholm, J.; Coussens, A.; Houben, R.; Horton, K.; Wong, E.; Kendall, E.; Martinez, L.; Musvosi, M.; and Zaidi, S.\n\n\n \n\n\n\n The International Journal of Tuberculosis and Lung Disease, 28(8): 381–386. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{denholm_international_2024,\n\ttitle = {The {International} {Consensus} for {Early} {TB} framework ({ICE}-{TB}): {Implications} from a low-incidence setting},\n\tvolume = {28},\n\tissn = {1027-3719},\n\tshorttitle = {The {International} {Consensus} for {Early} {TB} framework ({ICE}-{TB})},\n\turl = {https://www.ingentaconnect.com/content/10.5588/ijtld.24.0081},\n\tdoi = {10.5588/ijtld.24.0081},\n\tabstract = {{\\textless}sec{\\textgreater}{\\textless}title{\\textgreater}BACKGROUND{\\textless}/title{\\textgreater}In recent years, there has been increasing recognition of the public health significance of the spectrum of TB disease presentation, and the existing classification systems of asymptomatic infection and symptomatic TB have been limited \n in terms of explanatory power. Accordingly, in 2022–2023, a new International Consensus framework for Early TB (ICE-TB) was developed, categorising the spectrum of TB infection and disease into five states based on the presence or absence of macroscopic pathology, host infectiousness, \n and symptoms and signs.{\\textless}/sec{\\textgreater}{\\textless}sec{\\textgreater}{\\textless}title{\\textgreater}METHODS{\\textless}/title{\\textgreater}We used the ICE-TB framework to re-analyse existing notification data for 2022 within a low-incidence setting to explore the potential utility and future challenges for its public health application.{\\textless}/sec{\\textgreater}{\\textless}sec{\\textgreater}{\\textless}title{\\textgreater}RESULTS{\\textless}/title{\\textgreater}Existing \n notification data were sufficient to allow substantial reclassification of currently recognised active disease states, but did not systematically capture \n              Mycobacterium tuberculosis \n              infection or subclinical TB. Fifty percent of existing TB notifications would be classified as ‘Clinical, \n infectious’, with the potential need to consider further subclassification.{\\textless}/sec{\\textgreater}{\\textless}sec{\\textgreater}{\\textless}title{\\textgreater}CONCLUSION{\\textless}/title{\\textgreater}Our exploration highlighted limitations in existing classification systems and diagnostic approaches and should encourage researchers and programmatic \n implementers to emphasise person-centred and programmatic needs in the development of new tools for TB management.{\\textless}/sec{\\textgreater}},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {The International Journal of Tuberculosis and Lung Disease},\n\tauthor = {Denholm, J.T. and Coussens, A. and Houben, R.M.G.J. and Horton, K.C. and Wong, E.B. and Kendall, E.A. and Martinez, L. and Musvosi, M. and Zaidi, S.M.A.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {381--386},\n}\n\n\n\n

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\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Advances in the structural basis for angiotensin-1 converting enzyme (ACE) inhibitors.\n \n \n \n \n\n\n \n Acharya, K.; Gregory, K.; and Sturrock, E.\n\n\n \n\n\n\n Bioscience Reports, 44(8): BSR20240130. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Advances$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{acharya_advances_2024,\n\ttitle = {Advances in the structural basis for angiotensin-1 converting enzyme ({ACE}) inhibitors},\n\tvolume = {44},\n\tissn = {0144-8463, 1573-4935},\n\turl = {https://portlandpress.com/bioscirep/article/44/8/BSR20240130/234726/Advances-in-the-structural-basis-for-angiotensin-1},\n\tdoi = {10.1042/BSR20240130},\n\tabstract = {Abstract \n            Human somatic angiotensin-converting enzyme (ACE) is a key zinc metallopeptidase that plays a pivotal role in the renin–angiotensin–aldosterone system (RAAS) by regulating blood pressure and electrolyte balance. Inhibition of ACE is a cornerstone in the management of hypertension, cardiovascular diseases, and renal disorders. Recent advances in structural biology techniques have provided invaluable insights into the molecular mechanisms underlying ACE inhibition, facilitating the design and development of more effective therapeutic agents. This review focuses on the latest advancements in elucidating the structural basis for ACE inhibition. High-resolution crystallographic studies of minimally glycosylated individual domains of ACE have revealed intricate molecular details of the ACE catalytic N- and C-domains, and their detailed interactions with clinically relevant and newly designed domain-specific inhibitors. In addition, the recently elucidated structure of the glycosylated form of full-length ACE by cryo-electron microscopy (cryo-EM) has shed light on the mechanism of ACE dimerization and revealed continuous conformational changes which occur prior to ligand binding. In addition to these experimental techniques, computational approaches have also played a pivotal role in elucidating the structural basis for ACE inhibition. Molecular dynamics simulations and computational docking studies have provided atomic details of inhibitor binding kinetics and energetics, facilitating the rational design of novel ACE inhibitors with improved potency and selectivity. Furthermore, computational analysis of the motions observed by cryo-EM allowed the identification of allosteric binding sites on ACE. This affords new opportunities for the development of next-generation allosteric inhibitors with enhanced pharmacological properties. Overall, the insights highlighted in this review could enable the rational design of novel ACE inhibitors with improved efficacy and safety profiles, ultimately leading to better therapeutic outcomes for patients with hypertension and cardiovascular diseases.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {Bioscience Reports},\n\tauthor = {Acharya, K. Ravi and Gregory, Kyle S. and Sturrock, Edward D.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {BSR20240130},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Human somatic angiotensin-converting enzyme (ACE) is a key zinc metallopeptidase that plays a pivotal role in the renin–angiotensin–aldosterone system (RAAS) by regulating blood pressure and electrolyte balance. Inhibition of ACE is a cornerstone in the management of hypertension, cardiovascular diseases, and renal disorders. Recent advances in structural biology techniques have provided invaluable insights into the molecular mechanisms underlying ACE inhibition, facilitating the design and development of more effective therapeutic agents. This review focuses on the latest advancements in elucidating the structural basis for ACE inhibition. High-resolution crystallographic studies of minimally glycosylated individual domains of ACE have revealed intricate molecular details of the ACE catalytic N- and C-domains, and their detailed interactions with clinically relevant and newly designed domain-specific inhibitors. In addition, the recently elucidated structure of the glycosylated form of full-length ACE by cryo-electron microscopy (cryo-EM) has shed light on the mechanism of ACE dimerization and revealed continuous conformational changes which occur prior to ligand binding. In addition to these experimental techniques, computational approaches have also played a pivotal role in elucidating the structural basis for ACE inhibition. Molecular dynamics simulations and computational docking studies have provided atomic details of inhibitor binding kinetics and energetics, facilitating the rational design of novel ACE inhibitors with improved potency and selectivity. Furthermore, computational analysis of the motions observed by cryo-EM allowed the identification of allosteric binding sites on ACE. This affords new opportunities for the development of next-generation allosteric inhibitors with enhanced pharmacological properties. Overall, the insights highlighted in this review could enable the rational design of novel ACE inhibitors with improved efficacy and safety profiles, ultimately leading to better therapeutic outcomes for patients with hypertension and cardiovascular diseases.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Synthesis,Antidiabetic and Antitubercular Evaluation of Quinoline–pyrazolopyrimidine hybrids and Quinoline‐4‐Arylamines.\n \n \n \n \n\n\n \n Cele, N.; Awolade, P.; Seboletswe, P.; Khubone, L.; Olofinsan, K.; Islam, M. S.; Jordaan, A.; Warner, D. F.; and Singh, P.\n\n\n \n\n\n\n ChemistryOpen, 13(9): e202400014. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Synthesis,Antidiabetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{cele_synthesisantidiabetic_2024,\n\ttitle = {Synthesis,{Antidiabetic} and {Antitubercular} {Evaluation} of {Quinoline}–pyrazolopyrimidine hybrids and {Quinoline}‐4‐{Arylamines}},\n\tvolume = {13},\n\tissn = {2191-1363, 2191-1363},\n\turl = {https://chemistry-europe.onlinelibrary.wiley.com/doi/10.1002/open.202400014},\n\tdoi = {10.1002/open.202400014},\n\tabstract = {Abstract \n             \n              Two libraries of quinoline‐based hybrids 1‐(7‐chloroquinolin‐4‐yl)‐1 \n              H \n              ‐pyrazolo[3,4– \n              d \n              ]pyrimidin‐4‐amine and 7‐chloro‐ \n              N \n              ‐phenylquinolin‐4‐amine were synthesized and evaluated for their α‐glucosidase inhibitory and antioxidant properties. Compounds with 4‐methylpiperidine and \n              para \n              ‐trifluoromethoxy groups, respectively, showed the most promising α‐glucosidase inhibition activity with IC \n              50 \n              =46.70 and 40.84 μM, compared to the reference inhibitor, acarbose (IC \n              50 \n              =51.73 μM). Structure‐activity relationship analysis suggested that the cyclic secondary amine pendants and \n              para \n              ‐phenyl substituents account for the variable enzyme inhibition. Antioxidant profiling further revealed that compounds with an \n              N \n              ‐methylpiperazine and \n              N \n              ‐ethylpiperazine ring, respectively, have good DPPH scavenging abilities with IC \n              50 \n              =0.18, 0.58 and 0.93 mM, as compared to ascorbic acid (IC \n              50 \n              =0.05 mM), while the best DPPH scavenger is NO \n              2 \n              ‐substituted compound (IC \n              50 \n              =0.08 mM). Also, compound with \n              N \n              ‐(2‐hydroxyethyl)piperazine moiety emerged as the best NO radical scavenger with IC \n              50 \n              =0.28 mM. Molecular docking studies showed that the present compounds are orthosteric inhibitors with their quinoline, pyrimidine, and 4‐amino units as crucial pharmacophores furnishing α‐glucosidase binding at the catalytic site. Taken together, these compounds exhibit dual potentials; \n              i. e \n              ., potent α‐glucosidase inhibitors and excellent free radical scavengers. Hence, they may serve as structural templates in the search for agents to manage Type 2 diabetes mellitus. Finally, in preliminary assays investigating the anti‐tubercular potential of these compounds, two pyrazolopyrimidine series compounds and a 7‐chloro‐ \n              N \n              ‐phenylquinolin‐4‐amine hybrid showed sub‐10 μM whole‐cell activities against \n              Mycobacterium tuberculosis \n              .},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {ChemistryOpen},\n\tauthor = {Cele, Nosipho and Awolade, Paul and Seboletswe, Pule and Khubone, Lungisani and Olofinsan, Kolawole and Islam, Md. Shahidul and Jordaan, Audrey and Warner, Digby F. and Singh, Parvesh},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {e202400014},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Chest X-ray Features of HIV-Associated Pneumocystis Pneumonia (PCP) in Adults: A Systematic Review and Meta-analysis.\n \n \n \n \n\n\n \n Wills, N. K; Adriaanse, M.; Erasmus, S.; and Wasserman, S.\n\n\n \n\n\n\n Open Forum Infectious Diseases, 11(4): ofae146. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Chest$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{wills_chest_2024,\n\ttitle = {Chest {X}-ray {Features} of {HIV}-{Associated} \\textit{{Pneumocystis}} {Pneumonia} ({PCP}) in {Adults}: {A} {Systematic} {Review} and {Meta}-analysis},\n\tvolume = {11},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2328-8957},\n\tshorttitle = {Chest {X}-ray {Features} of {HIV}-{Associated} \\textit{{Pneumocystis}} {Pneumonia} ({PCP}) in {Adults}},\n\turl = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofae146/7630708},\n\tdoi = {10.1093/ofid/ofae146},\n\tabstract = {Abstract \n             \n              Background \n              The performance of chest x-ray (CXR) features for Pneumocystis pneumonia (PCP) diagnosis has been evaluated in small studies. We conducted a systematic review and meta-analysis to describe CXR changes in adults with HIV-associated laboratory-confirmed PCP, comparing these with non-PCP respiratory disease. \n             \n             \n              Methods \n              We searched databases for studies reporting CXR changes in people \\&gt;15 years old with HIV and laboratory-confirmed PCP and those with non-PCP respiratory disease. CXR features were grouped using consensus terms. Proportions were pooled and odds ratios (ORs) generated using random-effects meta-analysis, with subgroup analyses by CD4 count, study period, radiology review method, and study region. \n             \n             \n              Results \n              Fifty-one studies (with 1821 PCP and 1052 non-PCP cases) were included. Interstitial infiltrate (59\\%; 95\\% CI, 52\\%–66\\%; 36 studies, n = 1380; I2 = 85\\%) and ground-glass opacification (48\\%; 95\\% CI, 15\\%–83\\%; 4 studies, n = 57; I2 = 86\\%) were common in PCP. Cystic lesions, central lymphadenopathy, and pneumothorax were infrequent. Pleural effusion was rare in PCP (0\\%; 95\\% CI, 0\\%–2\\%). Interstitial infiltrate (OR, 2.3; 95\\% CI, 1.4–3.9; I2 = 60\\%), interstitial–alveolar infiltrate (OR, 10.2; 95\\% CI, 3.2–32.4; I2 = 0\\%), and diffuse CXR changes (OR, 7.3; 95\\% CI, 2.7–20.2; I2 = 87\\%) were associated with PCP diagnosis. There was loss of association with alveolar infiltrate in African studies. \n             \n             \n              Conclusions \n              Diffuse CXR changes and interstitial–alveolar infiltrates indicate a higher likelihood of PCP. Pleural effusion, lymphadenopathy, and focal alveolar infiltrates suggest alternative causes. These findings could be incorporated into clinical algorithms to improve diagnosis of HIV-associated PCP.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {Open Forum Infectious Diseases},\n\tauthor = {Wills, Nicola K and Adriaanse, Marguerite and Erasmus, Shandri and Wasserman, Sean},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {ofae146},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Mtb HLA-E-tetramer-sorted CD8+ T cells have a diverse TCR repertoire.\n \n \n \n \n\n\n \n Voogd, L.; Drittij, A. M.; Dingenouts, C. K.; Franken, K. L.; Unen, V. V.; Van Meijgaarden, K. E.; Ruibal, P.; Hagedoorn, R. S.; Leitner, J. A.; Steinberger, P.; Heemskerk, M. H.; Davis, M. M.; Scriba, T. J.; Ottenhoff, T. H.; and Joosten, S. A.\n\n\n \n\n\n\n iScience, 27(3): 109233. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Mtb$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{voogd_mtb_2024,\n\ttitle = {Mtb {HLA}-{E}-tetramer-sorted {CD8}+ {T} cells have a diverse {TCR} repertoire},\n\tvolume = {27},\n\tissn = {25890042},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2589004224004541},\n\tdoi = {10.1016/j.isci.2024.109233},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {iScience},\n\tauthor = {Voogd, Linda and Drittij, Anne M.H.F. and Dingenouts, Calinda K.E. and Franken, Kees L.M.C. and Unen, Vincent Van and Van Meijgaarden, Krista E. and Ruibal, Paula and Hagedoorn, Renate S. and Leitner, Judith A. and Steinberger, Peter and Heemskerk, Mirjam H.M. and Davis, Mark M. and Scriba, Thomas J. and Ottenhoff, Tom H.M. and Joosten, Simone A.},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {109233},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n An insight into the burden of drug‐resistant tuberculosis in children.\n \n \n \n \n\n\n \n Dias, J. V.; Varandas, L.; Gonçalves, L.; and Kagina, B. M.\n\n\n \n\n\n\n Acta Paediatrica, 113(4): 781–782. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"An$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{dias_insight_2024,\n\ttitle = {An insight into the burden of drug‐resistant tuberculosis in children},\n\tvolume = {113},\n\tissn = {0803-5253, 1651-2227},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/apa.17120},\n\tdoi = {10.1111/apa.17120},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {Acta Paediatrica},\n\tauthor = {Dias, Joana Valente and Varandas, Luís and Gonçalves, Luzia and Kagina, Benjamin M.},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {781--782},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Virus-Shaped Mesoporous Silica Nanostars to Improve the Transport of Drugs across the Blood–Brain Barrier.\n \n \n \n \n\n\n \n Pinna, A.; Ragaisyte, I.; Morton, W.; Angioletti-Uberti, S.; Proust, A.; D’Antuono, R.; Luk, C. H.; Gutierrez, M. G.; Cerrone, M.; Wilkinson, K. A.; Mohammed, A. A.; McGilvery, C. M.; Suárez-Bonnet, A.; Zimmerman, M.; Gengenbacher, M.; Wilkinson, R. J.; and Porter, A. E.\n\n\n \n\n\n\n ACS Applied Materials & Interfaces, 16(29): 37623–37640. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Virus-Shaped$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{pinna_virus-shaped_2024,\n\ttitle = {Virus-{Shaped} {Mesoporous} {Silica} {Nanostars} to {Improve} the {Transport} of {Drugs} across the {Blood}–{Brain} {Barrier}},\n\tvolume = {16},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1944-8244, 1944-8252},\n\turl = {https://pubs.acs.org/doi/10.1021/acsami.4c06726},\n\tdoi = {10.1021/acsami.4c06726},\n\tlanguage = {en},\n\tnumber = {29},\n\turldate = {2025-06-24},\n\tjournal = {ACS Applied Materials \\& Interfaces},\n\tauthor = {Pinna, Alessandra and Ragaisyte, Ieva and Morton, William and Angioletti-Uberti, Stefano and Proust, Alizé and D’Antuono, Rocco and Luk, Chak Hon and Gutierrez, Maximiliano G. and Cerrone, Maddalena and Wilkinson, Katalin A. and Mohammed, Ali A. and McGilvery, Catriona M. and Suárez-Bonnet, Alejandro and Zimmerman, Matthew and Gengenbacher, Martin and Wilkinson, Robert J. and Porter, Alexandra E.},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {37623--37640},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Influence of vitamin D supplementation on growth, body composition, pubertal development and spirometry in South African schoolchildren: a randomised controlled trial (ViDiKids).\n \n \n \n \n\n\n \n Middelkoop, K.; Micklesfield, L.; Stewart, J.; Walker, N.; Jolliffe, D. A; Mendham, A. E; Coussens, A. K; Nuttall, J.; Tang, J.; Fraser, W. D; Momand, W.; Cooper, C.; Harvey, N. C; Wilkinson, R. J; Bekker, L.; and Martineau, A. R\n\n\n \n\n\n\n BMJ Paediatrics Open, 8(1): e002495. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Influence$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{middelkoop_influence_2024,\n\ttitle = {Influence of vitamin {D} supplementation on growth, body composition, pubertal development and spirometry in {South} {African} schoolchildren: a randomised controlled trial ({ViDiKids})},\n\tvolume = {8},\n\tissn = {2399-9772},\n\tshorttitle = {Influence of vitamin {D} supplementation on growth, body composition, pubertal development and spirometry in {South} {African} schoolchildren},\n\turl = {https://bmjpaedsopen.bmj.com/lookup/doi/10.1136/bmjpo-2024-002495},\n\tdoi = {10.1136/bmjpo-2024-002495},\n\tabstract = {Objective \n              To determine whether weekly oral vitamin D supplementation influences growth, body composition, pubertal development or spirometric outcomes in South African schoolchildren. \n             \n             \n              Design \n              Phase 3 double-blind randomised placebo-controlled trial. \n             \n             \n              Setting \n              Socioeconomically disadvantaged peri-urban district of Cape Town, South Africa. \n             \n             \n              Participants \n              1682 children of black African ancestry attending government primary schools and aged 6–11 years at baseline. \n             \n             \n              Interventions \n               \n                Oral vitamin D \n                3 \n                (10 000 IU/week) versus placebo for 3 years. \n               \n             \n             \n              Main outcome measures \n              Height-for-age and body mass index-for-age, measured in all participants; Tanner scores for pubertal development, spirometric lung volumes and body composition, measured in a subset of 450 children who additionally took part in a nested substudy. \n             \n             \n              Results \n               \n                Mean serum 25-hydroxyvitamin D \n                3 \n                concentration at 3-year follow-up was higher among children randomised to receive vitamin D versus placebo (104.3 vs 64.7 nmol/L, respectively; mean difference (MD) 39.7 nmol/L, 95\\% CI 37.6 to 41.9 nmol/L). No statistically significant differences in height-for-age z-score (adjusted MD (aMD) −0.08, 95\\% CI −0.19 to 0.03) or body mass index-for-age z-score (aMD −0.04, 95\\% CI −0.16 to 0.07) were seen between vitamin D versus placebo groups at follow-up. Among substudy participants, allocation to vitamin D versus placebo did not influence pubertal development scores, \\% predicted forced expiratory volume in 1 s (FEV1), \\% predicted forced vital capacity (FVC), \\% predicted FEV1/FVC, fat mass or fat-free mass. \n               \n             \n             \n              Conclusions \n               \n                Weekly oral administration of 10 000 IU vitamin D \n                3 \n                boosted vitamin D status but did not influence growth, body composition, pubertal development or spirometric outcomes in South African schoolchildren. \n               \n             \n             \n              Trial registration numbers \n               \n                ClinicalTrials.gov \n                NCT02880982 \n                , South African National Clinical Trials Register DOH-27-0916-5527.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {BMJ Paediatrics Open},\n\tauthor = {Middelkoop, Keren and Micklesfield, Lisa and Stewart, Justine and Walker, Neil and Jolliffe, David A and Mendham, Amy E and Coussens, Anna K and Nuttall, James and Tang, Jonathan and Fraser, William D and Momand, Waheedullah and Cooper, Cyrus and Harvey, Nicholas C and Wilkinson, Robert J and Bekker, Linda-Gail and Martineau, Adrian R},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {e002495},\n}\n\n\n\n

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\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Comparison of whole‐genome and immunoglobulin‐based circulating tumor DNA assays in diffuse large B‐cell lymphoma.\n \n \n \n \n\n\n \n Merryman, R. W.; Rhoades, J.; Xiong, K.; Redd, R. A.; Antel, K.; An, H. H.; McDonough, M.; Guerrero, L.; Crnjac, A.; Sridhar, S.; Blewett, T.; Cheng, J.; Dahi, P. B.; Nieto, Y.; Joyce, R. M.; Chen, Y.; Herrera, A. F.; Armand, P.; Murakami, M.; and Adalsteinsson, V. A.\n\n\n \n\n\n\n HemaSphere, 8(4): e47. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Comparison$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{merryman_comparison_2024,\n\ttitle = {Comparison of whole‐genome and immunoglobulin‐based circulating tumor {DNA} assays in diffuse large {B}‐cell lymphoma},\n\tvolume = {8},\n\tcopyright = {http://creativecommons.org/licenses/by-nc-nd/4.0/},\n\tissn = {2572-9241, 2572-9241},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/hem3.47},\n\tdoi = {10.1002/hem3.47},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {HemaSphere},\n\tauthor = {Merryman, Reid W. and Rhoades, Justin and Xiong, Kan and Redd, Robert A. and Antel, Katherine and An, Hyun Hwan and McDonough, Mikaela and Guerrero, Liliana and Crnjac, Andela and Sridhar, Sainetra and Blewett, Timothy and Cheng, Ju and Dahi, Parastoo B. and Nieto, Yago and Joyce, Robin M. and Chen, Yi‐Bin and Herrera, Alex F. and Armand, Philippe and Murakami, Mark and Adalsteinsson, Viktor A.},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {e47},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Spatial technologies to evaluate the HIV-1 reservoir and its microenvironment in the lymph node.\n \n \n \n \n\n\n \n Zaman, F.; Smith, M. L.; Balagopal, A.; Durand, C. M.; Redd, A. D.; and Tobian, A. A. R.\n\n\n \n\n\n\n mBio, 15(8): e01909–24. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Spatial$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{zaman_spatial_2024,\n\ttitle = {Spatial technologies to evaluate the {HIV}-1 reservoir and its microenvironment in the lymph node},\n\tvolume = {15},\n\tissn = {2150-7511},\n\turl = {https://journals.asm.org/doi/10.1128/mbio.01909-24},\n\tdoi = {10.1128/mbio.01909-24},\n\tabstract = {ABSTRACT \n             \n               \n              The presence of the HIV-1 reservoir, a group of immune cells that contain intact, integrated, and replication-competent proviruses, is a major challenge to cure HIV-1. HIV-1 reservoir cells are largely unaffected by the cytopathic effects of viruses, antiviral immune responses, or antiretroviral therapy (ART). The HIV-1 reservoir is seeded early during HIV-1 infection and augmented during active viral replication. CD4+ T cells are the primary target for HIV-1 infection, and recent studies suggest that memory T follicular helper cells within the lymph node, more precisely in the B cell follicle, harbor integrated provirus, which contribute to viral rebound upon ART discontinuation. The B cell follicle, more specifically the germinal center, possesses a unique environment because of its distinct property of being partly immune privileged, potentially allowing HIV-1-infected cells within the lymph nodes to be protected from CD8+ T cells. This modified immune response in the germinal center of the follicle is potentially explained by the exclusion of CD8+ T cells and the presence of T regulatory cells at the junction of the follicle and extrafollicular region. The proviral makeup of HIV-1-infected cells is similar in lymph nodes and blood, suggesting trafficking between these compartments. Little is known about the cell-to-cell interactions, microenvironment of HIV-1-infected cells in the follicle, and trafficking between the lymph node follicle and other body compartments. Applying a spatiotemporal approach that integrates genomics, transcriptomics, and proteomics to investigate the HIV-1 reservoir and its neighboring cells in the lymph node has promising potential for informing HIV-1 cure efforts.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {mBio},\n\tauthor = {Zaman, Fatima and Smith, Melissa L. and Balagopal, Ashwin and Durand, Christine M. and Redd, Andrew D. and Tobian, Aaron A. R.},\n\teditor = {Prasad, Vinayaka R.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {e01909--24},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Diagnostic accuracy of tongue swab testing on two automated tuberculosis diagnostic platforms, Cepheid Xpert MTB/RIF Ultra and Molbio Truenat MTB Ultima.\n \n \n \n \n\n\n \n Wood, R. C.; Luabeya, A. K.; Dragovich, R. B.; Olson, A. M.; Lochner, K. A.; Weigel, K. M.; Codsi, R.; Mulenga, H.; De Vos, M.; Kohli, M.; Penn-Nicholson, A.; Hatherill, M.; and Cangelosi, G. A.\n\n\n \n\n\n\n Journal of Clinical Microbiology, 62(4): e00019–24. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Diagnostic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{wood_diagnostic_2024,\n\ttitle = {Diagnostic accuracy of tongue swab testing on two automated tuberculosis diagnostic platforms, {Cepheid} {Xpert} {MTB}/{RIF} {Ultra} and {Molbio} {Truenat} {MTB} {Ultima}},\n\tvolume = {62},\n\tissn = {0095-1137, 1098-660X},\n\turl = {https://journals.asm.org/doi/10.1128/jcm.00019-24},\n\tdoi = {10.1128/jcm.00019-24},\n\tabstract = {ABSTRACT \n             \n               \n               \n                Tongue dorsum swabbing is a potential alternative to sputum collection for tuberculosis (TB) testing. Previous studies showed that Cepheid Xpert MTB/RIF Ultra (Xpert Ultra) can detect \n                Mycobacterium tuberculosis \n                DNA on tongue swabs stored in buffer, with 72\\% sensitivity and 100\\% specificity relative to a sputum microbiological reference standard (sputum MRS). The present study evaluated a more convenient sample collection protocol (dry swab storage), combined with streamlined sample processing protocols, for evaluating two commercial TB diagnostic tests: Xpert Ultra and Molbio Truenat MTB Ultima (MTB Ultima). Copan FLOQSwabs were self-collected or collected by study workers from 321 participants in Western Cape, South Africa. All participants had symptoms suggestive of TB, and 245 of them had sputum MRS-confirmed TB (by sputum MGIT culture and/or Xpert Ultra). One tongue swab per participant was tested on Xpert Ultra, and another tongue swab was tested with MTB Ultima. Xpert Ultra was 75.5\\% sensitive and 100\\% specific relative to sputum MRS, similar to previous methods that used swabs stored in buffer. MTB Ultima was 71.6\\% sensitive and 96.9\\% specific relative to sputum MRS. When sample lysates that were false-negative or invalid by MTB Ultima were frozen, thawed, and re-tested, MTB Ultima sensitivity rose to 79.1\\%. Both tests were more sensitive with swabs from participants with higher sputum Xpert Ultra semi-quantitative results. Although additional development could improve diagnostic accuracy, these results further support tongue swabs as easy-to-collect samples for TB testing. \n               \n             \n             \n              IMPORTANCE \n              Tongue dorsum swabbing is a promising alternative to sputum collection for tuberculosis (TB) testing. Our results lend further support for tongue swabs as exceptionally easy-to-collect samples for high-throughput TB testing. \n             \n          ,  \n            Tongue dorsum swabbing is a promising alternative to sputum collection for tuberculosis (TB) testing. Our results lend further support for tongue swabs as exceptionally easy-to-collect samples for high-throughput TB testing.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Clinical Microbiology},\n\tauthor = {Wood, Rachel C. and Luabeya, Angelique K. and Dragovich, Rane B. and Olson, Alaina M. and Lochner, Katherine A. and Weigel, Kris M. and Codsi, Renée and Mulenga, Humphrey and De Vos, Margaretha and Kohli, Mikashmi and Penn-Nicholson, Adam and Hatherill, Mark and Cangelosi, Gerard A.},\n\teditor = {Turenne, Christine Y.},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {e00019--24},\n}\n\n\n\n

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\n ABSTRACT Tongue dorsum swabbing is a potential alternative to sputum collection for tuberculosis (TB) testing. Previous studies showed that Cepheid Xpert MTB/RIF Ultra (Xpert Ultra) can detect Mycobacterium tuberculosis DNA on tongue swabs stored in buffer, with 72% sensitivity and 100% specificity relative to a sputum microbiological reference standard (sputum MRS). The present study evaluated a more convenient sample collection protocol (dry swab storage), combined with streamlined sample processing protocols, for evaluating two commercial TB diagnostic tests: Xpert Ultra and Molbio Truenat MTB Ultima (MTB Ultima). Copan FLOQSwabs were self-collected or collected by study workers from 321 participants in Western Cape, South Africa. All participants had symptoms suggestive of TB, and 245 of them had sputum MRS-confirmed TB (by sputum MGIT culture and/or Xpert Ultra). One tongue swab per participant was tested on Xpert Ultra, and another tongue swab was tested with MTB Ultima. Xpert Ultra was 75.5% sensitive and 100% specific relative to sputum MRS, similar to previous methods that used swabs stored in buffer. MTB Ultima was 71.6% sensitive and 96.9% specific relative to sputum MRS. When sample lysates that were false-negative or invalid by MTB Ultima were frozen, thawed, and re-tested, MTB Ultima sensitivity rose to 79.1%. Both tests were more sensitive with swabs from participants with higher sputum Xpert Ultra semi-quantitative results. Although additional development could improve diagnostic accuracy, these results further support tongue swabs as easy-to-collect samples for TB testing. IMPORTANCE Tongue dorsum swabbing is a promising alternative to sputum collection for tuberculosis (TB) testing. Our results lend further support for tongue swabs as exceptionally easy-to-collect samples for high-throughput TB testing. , Tongue dorsum swabbing is a promising alternative to sputum collection for tuberculosis (TB) testing. Our results lend further support for tongue swabs as exceptionally easy-to-collect samples for high-throughput TB testing.\n

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\n \n\n \n \n \n \n \n \n Linezolid Population Pharmacokinetic Model in Plasma and Cerebrospinal Fluid Among Patients With Tuberculosis Meningitis.\n \n \n \n \n\n\n \n Abdelgawad, N.; Wasserman, S.; Abdelwahab, M. T.; Davis, A.; Stek, C.; Wiesner, L.; Black, J.; Meintjes, G.; Wilkinson, R. J; and Denti, P.\n\n\n \n\n\n\n The Journal of Infectious Diseases, 229(4): 1200–1208. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Linezolid$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{abdelgawad_linezolid_2024,\n\ttitle = {Linezolid {Population} {Pharmacokinetic} {Model} in {Plasma} and {Cerebrospinal} {Fluid} {Among} {Patients} {With} {Tuberculosis} {Meningitis}},\n\tvolume = {229},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/229/4/1200/7280927},\n\tdoi = {10.1093/infdis/jiad413},\n\tabstract = {Abstract \n             \n              Background \n              Linezolid is evaluated in novel treatment regimens for tuberculous meningitis (TBM). Linezolid pharmacokinetics have not been characterized in this population, particularly in cerebrospinal fluid (CSF), as well as, following its co-administration with high-dose rifampicin. We aimed to characterize linezolid plasma and CSF pharmacokinetics in adults with TBM. \n             \n             \n              Methods \n              In the LASER-TBM pharmacokinetic substudy, the intervention groups received high-dose rifampicin (35 mg/kg) plus 1200 mg/day of linezolid for 28 days, which was then reduced to 600 mg/day. Plasma sampling was done on day 3 (intensive) and day 28 (sparse). A lumbar CSF sample was obtained on both visits. \n             \n             \n              Results \n              Thirty participants contributed 247 plasma and 28 CSF observations. Their median age and weight were 40 years (range, 27–56) and 58 kg (range, 30–96). Plasma pharmacokinetics was described by a 1-compartment model with first-order absorption and saturable elimination. Maximal clearance was 7.25 L/h, and the Michaelis-Menten constant was 27.2 mg/L. Rifampicin cotreatment duration did not affect linezolid pharmacokinetics. CSF-plasma partitioning correlated with CSF total protein up to 1.2 g/L, where the partition coefficient reached a maximal value of 37\\%. The plasma-CSF equilibration half-life was ∼3.5 hours. \n             \n             \n              Conclusions \n              Linezolid was readily detected in CSF despite high-dose rifampicin coadministration. These findings support continued clinical evaluation of linezolid plus high-dose rifampicin for the treatment of TBM in adults. \n              Clinical Trials Registration.  ClinicalTrials.gov (NCT03927313).},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Abdelgawad, Noha and Wasserman, Sean and Abdelwahab, Mahmoud Tareq and Davis, Angharad and Stek, Cari and Wiesner, Lubbe and Black, John and Meintjes, Graeme and Wilkinson, Robert J and Denti, Paolo},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {1200--1208},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n hERG, Plasmodium Life Cycle, and Cross Resistance Profiling of New Azabenzimidazole Analogues of Astemizole.\n \n \n \n \n\n\n \n Mambwe, D.; Coertzen, D.; Leshabane, M.; Mulubwa, M.; Njoroge, M.; Gibhard, L.; Girling, G.; Wicht, K. J.; Lee, M. C. S.; Wittlin, S.; Moreira, D. R. M.; Birkholtz, L.; and Chibale, K.\n\n\n \n\n\n\n ACS Medicinal Chemistry Letters, 15(4): 463–469. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"hERG,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{mambwe_herg_2024,\n\ttitle = {{hERG}, \\textit{{Plasmodium}} {Life} {Cycle}, and {Cross} {Resistance} {Profiling} of {New} {Azabenzimidazole} {Analogues} of {Astemizole}},\n\tvolume = {15},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1948-5875, 1948-5875},\n\turl = {https://pubs.acs.org/doi/10.1021/acsmedchemlett.3c00496},\n\tdoi = {10.1021/acsmedchemlett.3c00496},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {ACS Medicinal Chemistry Letters},\n\tauthor = {Mambwe, Dickson and Coertzen, Dina and Leshabane, Meta and Mulubwa, Mwila and Njoroge, Mathew and Gibhard, Liezl and Girling, Gareth and Wicht, Kathryn J. and Lee, Marcus C. S. and Wittlin, Sergio and Moreira, Diogo Rodrigo Magalhães and Birkholtz, Lyn-Marie and Chibale, Kelly},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {463--469},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Clinical course, management and outcomes of COVID-19 in HIV-infected renal transplant recipients: A case series.\n \n \n \n \n\n\n \n Bertels, L; Manning, K; Redd, A; Du Toit, T; Barday, Z; and Muller, E\n\n\n \n\n\n\n South African Medical Journal,e1374. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Clinical$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{bertels_clinical_2024,\n\ttitle = {Clinical course, management and outcomes of {COVID}-19 in {HIV}-infected renal transplant recipients: {A} case series},\n\tcopyright = {https://creativecommons.org/licenses/by-nc/4.0},\n\tissn = {2078-5135, 0256-9574},\n\tshorttitle = {Clinical course, management and outcomes of {COVID}-19 in {HIV}-infected renal transplant recipients},\n\turl = {https://samajournals.co.za/index.php/samj/article/view/1374},\n\tdoi = {10.7196/SAMJ.2024.v114i3b.1374},\n\tabstract = {Background. HIV‐infected kidney transplant recipients with COVID‐19 are at increased risk of acute illness and death owing to their underlying comorbidities and chronic immunosuppression. \nObjectives. To describe the incidence, clinical presentation and course of COVID‐19, vaccination status, and SARS‐CoV‐2 antibody positivity rate among HIV‐infected‐to‐HIV‐infected kidney transplant recipients in South Africa (SA). \nMethods. This retrospective study reports on rates of SARS‐CoV‐2 infection, COVID‐19 and mortality among SA HIV‐infected kidney transplant recipients who received organs from HIV‐infected donors (HIV positive to HIV positive), before and after vaccination. Patient demographics, clinical presentation, course, management and disease outcomes were analysed. Antibody serology tests were performed between May and September 2022. \nResults. Among 39 HIV‐positive‐to‐HIV‐positive transplant recipients, 11 cases of COVID‐19 were diagnosed from March 2020 to September 2022. Six patients (55\\%) required hospitalisation, of whom 3 were admitted to a high‐care unit or intensive care unit. Two patients required mechanical ventilation, and 2 received acute dialysis. One patient was declined access to intensive care. Four patients (10\\%) died of COVID‐19 pneumonia. All the COVID‐19‐positive patients had at least one comorbidity. Vaccination data were available for 24 patients, of whom 5 had refused SARS‐CoV‐2 vaccination. SARS‐CoV‐2 antibody data were available for 20 patients; 4 vaccinated patients had a negative nucleocapsid protein antibody test and a positive spike protein antibody test, suggesting vaccination‐acquired immunity. The remaining 16 patients demonstrated immunity that was probably due to COVID infection, and of these, 14 were also vaccinated. Of the 11 COVID‐19 cases, only 1 was observed after vaccination. \nConclusion. In our case series, {\\textasciitilde}10\\% of the HIV‐positive‐to‐HIV‐positive transplant recipients died of COVID‐19 pneumonia. This mortality rate appears higher than figures reported in other transplant cohorts. However, it is likely that the actual number of cases of SARS‐CoV‐2 infection was much higher, as the study only included polymerase chain reaction‐confirmed cases. It remains unclear whether HIV infection, transplant or the combination of the two drives poorer outcomes, and larger studies adjusting for important demographic and biological factors may isolate these effects.},\n\turldate = {2025-06-24},\n\tjournal = {South African Medical Journal},\n\tauthor = {Bertels, L and Manning, K and Redd, A and Du Toit, T and Barday, Z and Muller, E},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {e1374},\n}\n\n\n\n

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\n Background. HIV‐infected kidney transplant recipients with COVID‐19 are at increased risk of acute illness and death owing to their underlying comorbidities and chronic immunosuppression. Objectives. To describe the incidence, clinical presentation and course of COVID‐19, vaccination status, and SARS‐CoV‐2 antibody positivity rate among HIV‐infected‐to‐HIV‐infected kidney transplant recipients in South Africa (SA). Methods. This retrospective study reports on rates of SARS‐CoV‐2 infection, COVID‐19 and mortality among SA HIV‐infected kidney transplant recipients who received organs from HIV‐infected donors (HIV positive to HIV positive), before and after vaccination. Patient demographics, clinical presentation, course, management and disease outcomes were analysed. Antibody serology tests were performed between May and September 2022. Results. Among 39 HIV‐positive‐to‐HIV‐positive transplant recipients, 11 cases of COVID‐19 were diagnosed from March 2020 to September 2022. Six patients (55%) required hospitalisation, of whom 3 were admitted to a high‐care unit or intensive care unit. Two patients required mechanical ventilation, and 2 received acute dialysis. One patient was declined access to intensive care. Four patients (10%) died of COVID‐19 pneumonia. All the COVID‐19‐positive patients had at least one comorbidity. Vaccination data were available for 24 patients, of whom 5 had refused SARS‐CoV‐2 vaccination. SARS‐CoV‐2 antibody data were available for 20 patients; 4 vaccinated patients had a negative nucleocapsid protein antibody test and a positive spike protein antibody test, suggesting vaccination‐acquired immunity. The remaining 16 patients demonstrated immunity that was probably due to COVID infection, and of these, 14 were also vaccinated. Of the 11 COVID‐19 cases, only 1 was observed after vaccination. Conclusion. In our case series, ~10% of the HIV‐positive‐to‐HIV‐positive transplant recipients died of COVID‐19 pneumonia. This mortality rate appears higher than figures reported in other transplant cohorts. However, it is likely that the actual number of cases of SARS‐CoV‐2 infection was much higher, as the study only included polymerase chain reaction‐confirmed cases. It remains unclear whether HIV infection, transplant or the combination of the two drives poorer outcomes, and larger studies adjusting for important demographic and biological factors may isolate these effects.\n

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\n \n\n \n \n \n \n \n \n Can resistance testing improve outcomes for children and adolescents with HIV?.\n \n \n \n \n\n\n \n Levison, J. H; and Orrell, C.\n\n\n \n\n\n\n The Lancet Global Health, 12(8): e1219–e1220. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Can$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{levison_can_2024,\n\ttitle = {Can resistance testing improve outcomes for children and adolescents with {HIV}?},\n\tvolume = {12},\n\tissn = {2214109X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X24002626},\n\tdoi = {10.1016/S2214-109X(24)00262-6},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Global Health},\n\tauthor = {Levison, Julie H and Orrell, Catherine},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {e1219--e1220},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Assessing antimicrobial stewardship governance in Northeast Brazilian hospitals: a survey-based analysis.\n \n \n \n \n\n\n \n Hinrichsen, S. L.; De Lemos, M. C.; Bernardino, J. M.; Lima, J. A.; Carrazone, G.; Vilella, T.; Trova, G.; Moura, L.; De Lima-Neto, R. G.; and Brink, A. J.\n\n\n \n\n\n\n JAC-Antimicrobial Resistance, 6(4): dlae116. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Assessing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{hinrichsen_assessing_2024,\n\ttitle = {Assessing antimicrobial stewardship governance in {Northeast} {Brazilian} hospitals: a survey-based analysis},\n\tvolume = {6},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2632-1823},\n\tshorttitle = {Assessing antimicrobial stewardship governance in {Northeast} {Brazilian} hospitals},\n\turl = {https://academic.oup.com/jacamr/article/doi/10.1093/jacamr/dlae116/7727612},\n\tdoi = {10.1093/jacamr/dlae116},\n\tabstract = {Abstract \n             \n              Background \n              Effective governance of antimicrobial stewardship (AMS) and infection prevention control (IPC) in healthcare facilities is crucial for safeguarding patients against healthcare-associated infections and enhancing patient outcomes by optimizing antibiotic use and curbing the spread of antimicrobial-resistant (AMR) pathogens. \n             \n             \n              Objectives \n              To assess the current AMS governance in two public hospitals in Northeast of Brazil, specifically focusing on identifying institutional antibiotic policies and operational practices. \n             \n             \n              Methods \n              A survey was conducted by team leaders of both hospitals from 2020 to 2022 using a questionnaire adapted from the Pan American Health Organization (PAHO) recommendations for implementing AMS programmes (ASP) in Latin America and the Caribbean, alongside criteria from the National Health Surveillance Agency (ANVISA) and CDC. \n             \n             \n              Results \n              Fifty leaders, from senior management to coordinators, answered the questionnaire. Results indicate a lack of AMS process measures, specialist support, systematic antimicrobial utilization analysis and structured IPC programmes, especially in one hospital where patient records remain in paper format. \n             \n             \n              Conclusions \n              The empirical use of antimicrobials without local epidemiological or susceptibility data underscores the absence of logistical support for microbiological cultures in the region. These findings emphasize the urgent need for systematic AMS processes and multiprofessional teams to drive AMS and IPC practices, essential for patient care and safety.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {JAC-Antimicrobial Resistance},\n\tauthor = {Hinrichsen, Sylvia Lemos and De Lemos, Marcela Coelho and Bernardino, Juliana Magalhães and Lima, Juliana Andrade and Carrazone, Genaro and Vilella, Tatiana and Trova, Gabriel and Moura, Libia and De Lima-Neto, Reginaldo Gonçalves and Brink, Adrian John},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {dlae116},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n HIV-Associated Tuberculosis.\n \n \n \n \n\n\n \n Meintjes, G.; and Maartens, G.\n\n\n \n\n\n\n New England Journal of Medicine, 391(4): 343–355. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"HIV-Associated$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{hardin_hiv-associated_2024,\n\ttitle = {{HIV}-{Associated} {Tuberculosis}},\n\tvolume = {391},\n\tissn = {0028-4793, 1533-4406},\n\turl = {http://www.nejm.org/doi/10.1056/NEJMra2308181},\n\tdoi = {10.1056/NEJMra2308181},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {New England Journal of Medicine},\n\tauthor = {Meintjes, Graeme and Maartens, Gary},\n\teditor = {Hardin, C. Corey},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {343--355},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Young People’s Recommendations for Accessible, Engaging, and Relevant COVID-19 Research Communication in Australia.\n \n \n \n \n\n\n \n Douglass, C. H.; Roe, M.; Raggatt, M.; Schlotthauer, F.; Swe, Z. Y.; Main, S.; Lim, M. S. C.; and Masson, L.\n\n\n \n\n\n\n Youth & Society, 56(6): 1013–1032. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Young$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{douglass_young_2024,\n\ttitle = {Young {People}’s {Recommendations} for {Accessible}, {Engaging}, and {Relevant} {COVID}-19 {Research} {Communication} in {Australia}},\n\tvolume = {56},\n\tissn = {0044-118X, 1552-8499},\n\turl = {https://journals.sagepub.com/doi/10.1177/0044118X231211940},\n\tdoi = {10.1177/0044118X231211940},\n\tabstract = {Research is often communicated in ways that fail to reach young people. This participatory study explored young people’s recommendations for making COVID-19 research communication accessible, engaging, and relevant for young people in Australia. We held eight online Zoom workshops with nine young people (18–21 years). Participants recommended researchers share their findings on platforms young people already use, particularly social media. Young people were more likely to engage with research communicated by trusted sources, particularly medical professionals. To keep young people engaged, researchers needed to clearly communicate one main message and simplify evidence using audio-visual formats. To make research communication more relevant, young people recommended sharing findings that related to their experiences throughout the pandemic and providing young people with opportunities to shape research communication and provide feedback. Findings suggest there are opportunities to make COVID-19 research communication more accessible, engaging, and relevant for young people by incorporating their ideas.},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {Youth \\& Society},\n\tauthor = {Douglass, Caitlin H. and Roe, Merryn and Raggatt, Michelle and Schlotthauer, Felicia and Swe, Zay Yar and Main, Stephanie and Lim, Megan S. C. and Masson, Lindi},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {1013--1032},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Functional Characterisation of Surfactant Protein A as a Novel Prophylactic Means against Oncogenic HPV Infections.\n \n \n \n \n\n\n \n Carse, S.; Reid, T.; Madsen, J.; Clark, H.; Kirjakulov, A.; Bergant Marušič, M.; and Schäfer, G.\n\n\n \n\n\n\n International Journal of Molecular Sciences, 25(14): 7712. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Functional$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{carse_functional_2024,\n\ttitle = {Functional {Characterisation} of {Surfactant} {Protein} {A} as a {Novel} {Prophylactic} {Means} against {Oncogenic} {HPV} {Infections}},\n\tvolume = {25},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1422-0067},\n\turl = {https://www.mdpi.com/1422-0067/25/14/7712},\n\tdoi = {10.3390/ijms25147712},\n\tabstract = {Human papillomavirus (HPV) infection poses a significant health challenge, particularly in low- and middle-income countries (LMIC), where limited healthcare access and awareness hinder vaccine accessibility. To identify alternative HPV targeting interventions, we previously reported on surfactant protein A (SP-A) as a novel molecule capable of recognising HPV16 pseudovirions (HPV16-PsVs) and reducing infection in a murine cervicovaginal HPV challenge model. Building on these findings, our current study aimed to assess SP-A’s suitability as a broad-spectrum HPV-targeting molecule and its impact on innate immune responses. We demonstrate SP-A’s ability to agglutinate and opsonise multiple oncogenic HPV-PsVs types, enhancing their uptake and clearance by RAW264.7 murine macrophages and THP-1 human-derived immune cells. The SP-A opsonisation of HPV not only led to increased lysosomal accumulation in macrophages and HaCaT keratinocytes but also resulted in a decreased infection of HaCaT cells, which was further decreased when co-cultured with innate immune cells. An analysis of human innate immune cell cytokine profiles revealed a significant inflammatory response upon SP-A exposure, potentially contributing to the overall inhibition of HPV infection. These results highlight the multi-layered impact of SP-A on HPV, innate immune cells and keratinocytes and lay the basis for the development of alternative prophylactic interventions against diverse HPV types.},\n\tlanguage = {en},\n\tnumber = {14},\n\turldate = {2025-06-24},\n\tjournal = {International Journal of Molecular Sciences},\n\tauthor = {Carse, Sinead and Reid, Tim and Madsen, Jens and Clark, Howard and Kirjakulov, Artur and Bergant Marušič, Martina and Schäfer, Georgia},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {7712},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Phospholipase C epsilon-1 (PLCƐ1) mediates macrophage activation and protection against tuberculosis.\n \n \n \n \n\n\n \n Gupta, A.; Thirunavukkarasu, S.; Rangel-Moreno, J.; Ahmed, M.; Swanson, R. V.; Mbandi, S. K.; Smrcka, A. V.; Kaushal, D.; Scriba, T. J.; and Khader, S. A.\n\n\n \n\n\n\n Infection and Immunity, 92(4): e00495–23. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Phospholipase$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{gupta_phospholipase_2024,\n\ttitle = {Phospholipase {C} epsilon-1 ({PLCƐ1}) mediates macrophage activation and protection against tuberculosis},\n\tvolume = {92},\n\tissn = {0019-9567, 1098-5522},\n\turl = {https://journals.asm.org/doi/10.1128/iai.00495-23},\n\tdoi = {10.1128/iai.00495-23},\n\tabstract = {ABSTRACT \n             \n               \n               \n                Tuberculosis (TB) caused by \n                Mycobacterium tuberculosis \n                ( \n                Mtb \n                ) infects up to a quarter of the world’s population. Although immune responses can control \n                Mtb \n                infection, 5\\%–10\\% of infected individuals can progress to active TB disease (progressors). A myriad of host factors regulate disease progression in TB and a better understanding of immune correlates of protection and disease is pivotal for the development of new therapeutics. Comparison of human whole blood transcriptomic metadata with that of macaque TB progressors and \n                Mtb \n                -infected diversity outbred mice (DO) led to the identification of differentially regulated gene (DEG) signatures, associated with TB progression or control. The current study assessed the function of Phospholipase C epsilon ( \n                PLCƐ1 \n                ), the top downregulated gene across species in TB progressors, using a gene-specific knockout mouse model of \n                Mtb \n                infection and in vitro \n                Mtb \n                -infected bone marrow-derived macrophages. \n                PLCƐ1 \n                gene expression was downregulated in TB progressors across species. \n                PLCε1 \n                deficiency in the mouse model resulted in increased susceptibility to \n                Mtb \n                infection \n                , \n                coincident accumulation of lung myeloid cells, and reduced ability to mount antibacterial responses. However, \n                PLCε1 \n                was not required for the activation and accumulation of T cells in mice. Our results suggest an important early role for \n                PLCƐ1 \n                in shaping innate immune response to TB and may represent a putative target for host-directed therapy.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {Infection and Immunity},\n\tauthor = {Gupta, Ananya and Thirunavukkarasu, Shyamala and Rangel-Moreno, Javier and Ahmed, Mushtaq and Swanson, Rosemary V. and Mbandi, Stanley Kimbung and Smrcka, Alan V. and Kaushal, Deepak and Scriba, Thomas J. and Khader, Shabaana A.},\n\teditor = {Ehrt, Sabine},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {e00495--23},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Switch to fixed-dose doravirine (100 mg) with islatravir (0·75 mg) once daily in virologically suppressed adults with HIV-1 on antiretroviral therapy: 48-week results of a phase 3, randomised, open-label, non-inferiority trial.\n \n \n \n \n\n\n \n Molina, J.; Rizzardini, G.; Orrell, C.; Afani, A.; Calmy, A.; Oka, S.; Hinestrosa, F.; Kumar, P.; Tebas, P.; Walmsley, S.; Grandhi, A.; Klopfer, S.; Gendrano, I.; Eves, K.; Correll, T. A; Fox, M. C; and Kim, J.\n\n\n \n\n\n\n The Lancet HIV, 11(6): e369–e379. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Switch$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{molina_switch_2024,\n\ttitle = {Switch to fixed-dose doravirine (100 mg) with islatravir (0·75 mg) once daily in virologically suppressed adults with {HIV}-1 on antiretroviral therapy: 48-week results of a phase 3, randomised, open-label, non-inferiority trial},\n\tvolume = {11},\n\tissn = {23523018},\n\tshorttitle = {Switch to fixed-dose doravirine (100 mg) with islatravir (0·75 mg) once daily in virologically suppressed adults with {HIV}-1 on antiretroviral therapy},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352301824000316},\n\tdoi = {10.1016/S2352-3018(24)00031-6},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet HIV},\n\tauthor = {Molina, Jean-Michel and Rizzardini, Giuliano and Orrell, Catherine and Afani, Alejandro and Calmy, Alexandra and Oka, Shinichi and Hinestrosa, Federico and Kumar, Princy and Tebas, Pablo and Walmsley, Sharon and Grandhi, Anjana and Klopfer, Stephanie and Gendrano, Isaias and Eves, Karen and Correll, Todd A and Fox, Michelle C and Kim, Jason},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {e369--e379},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Estimating the Potential Public Health Value of BCG Revaccination.\n \n \n \n \n\n\n \n Clark, R. A; Sumner, T.; Weerasuriya, C. K; Bakker, R.; Scriba, T. J; and White, R. G\n\n\n \n\n\n\n The Journal of Infectious Diseases, 230(1): e139–e143. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Estimating$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{clark_estimating_2024,\n\ttitle = {Estimating the {Potential} {Public} {Health} {Value} of {BCG} {Revaccination}},\n\tvolume = {230},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/230/1/e139/7639736},\n\tdoi = {10.1093/infdis/jiae089},\n\tabstract = {Abstract \n            An upcoming trial may provide further evidence that adolescent/adult-targeted BCG revaccination prevents sustained Mycobacterium tuberculosis infection, but its public health value depends on its impact on overall tuberculosis morbidity and mortality, which will remain unknown. Using previously calibrated models for India and South Africa, we simulated BCG revaccination assuming 45\\% prevention-of-infection efficacy, and we evaluated scenarios varying additional prevention-of-disease efficacy between +50\\% (reducing risk) and −50\\% (increasing risk). Given the assumed prevention-of-infection efficacy and range in prevention-of-disease efficacy, BCG revaccination may have a positive health impact and be cost-effective. This may be useful when considering future evaluations and implementation of adolescent/adult BCG revaccination.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Clark, Rebecca A and Sumner, Tom and Weerasuriya, Chathika K and Bakker, Roel and Scriba, Thomas J and White, Richard G},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {e139--e143},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Mycobacterium tuberculosis transmission: the importance of precision.\n \n \n \n \n\n\n \n Dinkele, R.; Khan, P. Y; and Warner, D. F\n\n\n \n\n\n\n The Lancet Infectious Diseases, 24(7): 679–681. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Mycobacterium$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{dinkele_mycobacterium_2024,\n\ttitle = {Mycobacterium tuberculosis transmission: the importance of precision},\n\tvolume = {24},\n\tissn = {14733099},\n\tshorttitle = {Mycobacterium tuberculosis transmission},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1473309924001543},\n\tdoi = {10.1016/S1473-3099(24)00154-3},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Infectious Diseases},\n\tauthor = {Dinkele, Ryan and Khan, Palwasha Y and Warner, Digby F},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {679--681},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Influence of vitamin D supplementation on bone mineral content, bone turnover markers, and fracture risk in South African schoolchildren: multicenter double-blind randomized placebo-controlled trial (ViDiKids).\n \n \n \n \n\n\n \n Middelkoop, K.; Micklesfield, L. K; Walker, N.; Stewart, J.; Delport, C.; Jolliffe, D. A; Mendham, A. E; Coussens, A. K; Van Graan, A.; Nuttall, J.; Tang, J. C Y; Fraser, W. D; Cooper, C.; Harvey, N. C; Hooper, R. L; Wilkinson, R. J; Bekker, L.; and Martineau, A. R\n\n\n \n\n\n\n Journal of Bone and Mineral Research, 39(3): 211–221. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Influence$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{middelkoop_influence_2024,\n\ttitle = {Influence of vitamin {D} supplementation on bone mineral content, bone turnover markers, and fracture risk in {South} {African} schoolchildren: multicenter double-blind randomized placebo-controlled trial ({ViDiKids})},\n\tvolume = {39},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0884-0431, 1523-4681},\n\tshorttitle = {Influence of vitamin {D} supplementation on bone mineral content, bone turnover markers, and fracture risk in {South} {African} schoolchildren},\n\turl = {https://academic.oup.com/jbmr/article/39/3/211/7515132},\n\tdoi = {10.1093/jbmr/zjae007},\n\tabstract = {Abstract \n            Randomized controlled trials (RCTs) to determine the influence of vitamin D on BMC and fracture risk in children of Black African ancestry are lacking. We conducted a sub-study (n = 450) nested within a phase 3 RCT of weekly oral supplementation with 10 000 IU vitamin D3 vs placebo for 3 yr in HIV-uninfected Cape Town schoolchildren aged 6–11 yr. Outcomes were BMC at the whole body less head (WBLH) and LS and serum 25-hydroxyvitamin D3 (25(OH)D3), PTH, alkaline phosphatase, C-terminal telopeptide, and PINP. Incidence of fractures was a secondary outcome of the main trial (n = 1682). At baseline, mean serum 25(OH)D3 concentration was 70.0 nmol/L (SD 13.5), and 5.8\\% of participants had serum 25(OH)D3 concentrations \\&lt;50 nmol/L. Among sub-study participants, end-trial serum 25(OH)D3 concentrations were higher for participants allocated to vitamin D vs placebo (adjusted mean difference [aMD] 39.9 nmol/L, 95\\% CI, 36.1 to 43.6) and serum PTH concentrations were lower (aMD −0.55 pmol/L, 95\\% CI, −0.94 to −0.17). However, no interarm differences were seen for WBLH BMC (aMD −8.0 g, 95\\% CI, −30.7 to 14.7) or LS BMC (aMD −0.3 g, 95\\% CI, −1.3 to 0.8) or serum concentrations of bone turnover markers. Fractures were rare among participants in the main trial randomized to vitamin D vs placebo (7/755 vs 10/758 attending at least 1 follow-up; adjusted odds ratio 0.70, 95\\% CI, 0.27 to 1.85). In conclusion, a 3-yr course of weekly oral vitamin D supplementation elevated serum 25(OH)D3 concentrations and suppressed serum PTH concentrations in HIV-uninfected South African schoolchildren of Black African ancestry but did not influence BMC or serum concentrations of bone turnover markers. Fracture incidence was low, limiting power to detect an effect of vitamin D on this outcome.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Bone and Mineral Research},\n\tauthor = {Middelkoop, Keren and Micklesfield, Lisa K and Walker, Neil and Stewart, Justine and Delport, Carmen and Jolliffe, David A and Mendham, Amy E and Coussens, Anna K and Van Graan, Averalda and Nuttall, James and Tang, Jonathan C Y and Fraser, William D and Cooper, Cyrus and Harvey, Nicholas C and Hooper, Richard L and Wilkinson, Robert J and Bekker, Linda-Gail and Martineau, Adrian R},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {211--221},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Classification of early tuberculosis states to guide research for improved care and prevention: an international Delphi consensus exercise.\n \n \n \n \n\n\n \n Coussens, A. K; Zaidi, S. M A; Allwood, B. W; Dewan, P. K; Gray, G.; Kohli, M.; Kredo, T.; Marais, B. J; Marks, G. B; Martinez, L.; Ruhwald, M.; Scriba, T. J; Seddon, J. A; Tisile, P.; Warner, D. F; Wilkinson, R. J; Esmail, H.; Houben, R. M G J; Alland, D.; Behr, M. A; Beko, B. B; Burhan, E.; Churchyard, G.; Cobelens, F.; Denholm, J. T; Dinkele, R.; Ellner, J. J; Fatima, R.; Haigh, K. A; Hatherill, M.; Horton, K. C; Kendall, E. A; Khan, P. Y; MacPherson, P.; Malherbe, S. T; Mave, V.; Mendelsohn, S. C; Musvosvi, M.; Nemes, E.; Penn-Nicholson, A.; Ramamurthy, D.; Rangaka, M. X; Sahu, S.; Schwalb, A.; Shah, D. K; Sheerin, D.; Simon, D.; Steyn, A. J C; Thu Anh, N.; Walzl, G.; Weller, C. L; Williams, C. M.; Wong, E. B; Wood, R.; Xie, Y. L; and Yi, S.\n\n\n \n\n\n\n The Lancet Respiratory Medicine, 12(6): 484–498. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Classification$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{coussens_classification_2024,\n\ttitle = {Classification of early tuberculosis states to guide research for improved care and prevention: an international {Delphi} consensus exercise},\n\tvolume = {12},\n\tissn = {22132600},\n\tshorttitle = {Classification of early tuberculosis states to guide research for improved care and prevention},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2213260024000286},\n\tdoi = {10.1016/S2213-2600(24)00028-6},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Respiratory Medicine},\n\tauthor = {Coussens, Anna K and Zaidi, Syed M A and Allwood, Brian W and Dewan, Puneet K and Gray, Glenda and Kohli, Mikashmi and Kredo, Tamara and Marais, Ben J and Marks, Guy B and Martinez, Leo and Ruhwald, Morten and Scriba, Thomas J and Seddon, James A and Tisile, Phumeza and Warner, Digby F and Wilkinson, Robert J and Esmail, Hanif and Houben, Rein M G J and Alland, David and Behr, Marcel A and Beko, Busisiwe B and Burhan, Erlina and Churchyard, Gavin and Cobelens, Frank and Denholm, Justin T and Dinkele, Ryan and Ellner, Jerrold J and Fatima, Razia and Haigh, Kate A and Hatherill, Mark and Horton, Katherine C and Kendall, Emily A and Khan, Palwasha Y and MacPherson, Peter and Malherbe, Stephanus T and Mave, Vidya and Mendelsohn, Simon C and Musvosvi, Munyaradzi and Nemes, Elisa and Penn-Nicholson, Adam and Ramamurthy, Dharanidharan and Rangaka, Molebogeng X and Sahu, Suvanand and Schwalb, Alvaro and Shah, Divya K and Sheerin, Dylan and Simon, Donald and Steyn, Adrie J C and Thu Anh, Nguyen and Walzl, Gerhard and Weller, Charlotte L and Williams, Caroline Ml and Wong, Emily B and Wood, Robin and Xie, Yingda L and Yi, Siyan},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {484--498},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Kidney function in healthcare clients in Khayelitsha, South Africa: Routine laboratory testing and results reflect distinct healthcare experiences by age for healthcare clients with and without HIV.\n \n \n \n \n\n\n \n Osei-Yeboah, R.; Ngwenya, O.; and Tiffin, N.\n\n\n \n\n\n\n PLOS Global Public Health, 4(5): e0002526. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Kidney$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{osei-yeboah_kidney_2024,\n\ttitle = {Kidney function in healthcare clients in {Khayelitsha}, {South} {Africa}: {Routine} laboratory testing and results reflect distinct healthcare experiences by age for healthcare clients with and without {HIV}},\n\tvolume = {4},\n\tissn = {2767-3375},\n\tshorttitle = {Kidney function in healthcare clients in {Khayelitsha}, {South} {Africa}},\n\turl = {https://dx.plos.org/10.1371/journal.pgph.0002526},\n\tdoi = {10.1371/journal.pgph.0002526},\n\tabstract = {In South Africa, PLHIV are eligible for free ART and kidney function screening. Serum creatinine (SCr) laboratory test data from the National Health Laboratory Service are collated at the Provincial Health Data Centre and linked with other routine health data. We analysed SCr and estimated glomerular filtration rate (eGFR) results for PLHIV and HIV-negative healthcare clients aged 18–80 years accessing healthcare in Khayelitsha, South Africa and comorbidity profiles at SCr and eGFR testing. 45 640 individuals aged 18–80 years with at least one renal test accessed Khayelitsha public health facilities in 2016/2017. 22 961 (50.3\\%) were PLHIV. Median age at first SCr and eGFR test for PLHIV was 33yrs (IQR: 27,41) to 36yrs (IQR: 30,43) compared to 49yrs (IQR: 37,57) and 52yrs (IQR: 44,59) for those without HIV. PLHIV first median SCr results were 66 (IQR: 55,78) μmol/l compared to 69 (IQR: 58,82) μmol/l for HIV-negative individuals. Hypertension, diabetes, and CKD at testing were more common in HIV-negative people than PLHIV. HIV, diabetes and tuberculosis (TB) are associated with higher eGFR results; whilst hypertension, being male and older are associated with lower eGFR results. These data reflect testing practices in the Western Cape: younger people without HIV have generally worse kidney function test results; younger PLHIV have generally good test results, and older people with/without HIV have generally similar test results, reflecting regular screening for kidney function in asymptomatic PLHIV whereas young HIV-negative people are tested only when presenting with renal symptoms. Our analysis suggests we cannot infer the future healthcare requirements of younger PLHIV based on the current ageing population, due to changing ART availability for different generations of PLHIV. Instead, routine health data may be used in an agile way to assess ongoing healthcare requirements of ageing PLHIV, and to reflect implementation of treatment guidelines.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Global Public Health},\n\tauthor = {Osei-Yeboah, Richard and Ngwenya, Olina and Tiffin, Nicki},\n\teditor = {Robinson, Julia},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {e0002526},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Aerosolization of viable Mycobacterium tuberculosis bacilli by tuberculosis clinic attendees independent of sputum-Xpert Ultra status.\n \n \n \n \n\n\n \n Patterson, B.; Dinkele, R.; Gessner, S.; Koch, A.; Hoosen, Z.; January, V.; Leonard, B.; McKerry, A.; Seldon, R.; Vazi, A.; Hermans, S.; Cobelens, F.; Warner, D. F.; and Wood, R.\n\n\n \n\n\n\n Proceedings of the National Academy of Sciences, 121(12): e2314813121. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Aerosolization$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{patterson_aerosolization_2024,\n\ttitle = {Aerosolization of viable \\textit{{Mycobacterium} tuberculosis} bacilli by tuberculosis clinic attendees independent of sputum-{Xpert} {Ultra} status},\n\tvolume = {121},\n\tissn = {0027-8424, 1091-6490},\n\turl = {https://pnas.org/doi/10.1073/pnas.2314813121},\n\tdoi = {10.1073/pnas.2314813121},\n\tabstract = {Potential \n              Mycobacterium tuberculosis \n              ( \n              Mtb \n              ) transmission during different pulmonary tuberculosis (TB) disease states is poorly understood. We quantified viable aerosolized \n              Mtb \n              from TB clinic attendees following diagnosis and through six months’ follow-up thereafter. Presumptive TB patients (n=102) were classified by laboratory, radiological, and clinical features into Group A: Sputum-Xpert Ultra-positive TB (n=52), Group B: Sputum-Xpert Ultra-negative TB (n=20), or Group C: TB undiagnosed (n=30). All groups were assessed for \n              Mtb \n              bioaerosol release at baseline, and subsequently at 2 wk, 2 mo, and 6 mo. Groups A and B were notified to the national TB program and received standard anti-TB chemotherapy; \n              Mtb \n              was isolated from 92\\% and 90\\% at presentation, 87\\% and 74\\% at 2 wk, 54\\% and 44\\% at 2 mo and 32\\% and 20\\% at 6 mo, respectively. Surprisingly, similar numbers were detected in Group C not initiating TB treatment: 93\\%, 70\\%, 48\\% and 22\\% at the same timepoints. A temporal association was observed between \n              Mtb \n              bioaerosol release and TB symptoms in all three groups. Persistence of \n              Mtb \n              bioaerosol positivity was observed in {\\textasciitilde}30\\% of participants irrespective of TB chemotherapy. Captured \n              Mtb \n              bacilli were predominantly acid-fast stain-negative and poorly culturable; however, three bioaerosol samples yielded sufficient biomass following culture for whole-genome sequencing, revealing two different \n              Mtb \n              lineages. Detection of viable aerosolized \n              Mtb \n              in clinic attendees, independent of TB diagnosis, suggests that unidentified \n              Mtb \n              transmitters might contribute a significant attributable proportion of community exposure. Additional longitudinal studies with sputum culture-positive and -negative control participants are required to investigate this possibility.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {Proceedings of the National Academy of Sciences},\n\tauthor = {Patterson, Benjamin and Dinkele, Ryan and Gessner, Sophia and Koch, Anastasia and Hoosen, Zeenat and January, Vanessa and Leonard, Bryan and McKerry, Andrea and Seldon, Ronnett and Vazi, Andiswa and Hermans, Sabine and Cobelens, Frank and Warner, Digby F. and Wood, Robin},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {e2314813121},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Would you? Effects of oxytocin on moral choices in forensic psychopathic patients.\n \n \n \n \n\n\n \n Rijnders, R. J.; Van Den Hoogen, S.; Van Honk, J.; Terburg, D.; and Kempes, M. M.\n\n\n \n\n\n\n Comprehensive Psychoneuroendocrinology, 19: 100245. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Would$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{rijnders_would_2024,\n\ttitle = {Would you? {Effects} of oxytocin on moral choices in forensic psychopathic patients},\n\tvolume = {19},\n\tissn = {26664976},\n\tshorttitle = {Would you?},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666497624000213},\n\tdoi = {10.1016/j.cpnec.2024.100245},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Comprehensive Psychoneuroendocrinology},\n\tauthor = {Rijnders, Ronald J.P. and Van Den Hoogen, Sophie and Van Honk, Jack and Terburg, David and Kempes, Maaike M.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {100245},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Identification of HPV16 Lineages in South African and Mozambican Women with Normal and Abnormal Cervical Cytology.\n \n \n \n \n\n\n \n Maueia, C.; Carulei, O.; Murahwa, A. T.; Taku, O.; Manjate, A.; Mussá, T.; and Williamson, A.\n\n\n \n\n\n\n Viruses, 16(8): 1314. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Identification$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{maueia_identification_2024,\n\ttitle = {Identification of {HPV16} {Lineages} in {South} {African} and {Mozambican} {Women} with {Normal} and {Abnormal} {Cervical} {Cytology}},\n\tvolume = {16},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1999-4915},\n\turl = {https://www.mdpi.com/1999-4915/16/8/1314},\n\tdoi = {10.3390/v16081314},\n\tabstract = {Background: Human papillomavirus 16 (HPV16) is an oncogenic virus responsible for the majority of invasive cervical cancer cases worldwide. Due to genetic modifications, some variants are more oncogenic than others. We analysed the HPV16 phylogeny in HPV16-positive cervical Desoxyribonucleic Acid (DNA) samples collected from South African and Mozambican women to detect the circulating lineages. Methods: Polymerase chain reaction (PCR) amplification of the long control region (LCR) and 300 nucleotides of the E6 region was performed using HPV16-specific primers on HPV16-positive cervical samples collected in women from South Africa and Mozambique. HPV16 sequences were obtained through Next Generation Sequencing (NGS) methods. Geneious prime and MEGA 11 software were used to align the sequences to 16 HPV16 reference sequences, gathering the A, B, C, and D lineages and generating the phylogenetic tree. Single nucleotide polymorphisms (SNPs) in the LCR and E6 regions were analysed and the phylogenetic tree was generated using Geneious Prime software. Results: Fifty-eight sequences were analysed. Of these sequences, 79\\% (46/58) were from women who had abnormal cervical cytology. Fifteen SNPs in the LCR and eight in the E6 region were found to be the most common in all sequences. The phylogenetic analysis determined that 45\\% of the isolates belonged to the A1 sublineage (European variant), 34\\% belonged to the C1 sublineage (African 1 variant), 16\\% belonged to the B1 and B2 sublineage (African 2 variant), two isolates belonged to the D1–3 sublineages (Asian-American variant), and one to the North American variant. Conclusions: The African and European HPV16 variants were the most common circulating lineages in South African and Mozambican women. A high-grade squamous intraepithelial lesion (HSIL) was the most common cervical abnormality observed and linked to European and African lineages. These findings may contribute to understanding molecular HPV16 epidemiology in South Africa and Mozambique.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {Viruses},\n\tauthor = {Maueia, Cremildo and Carulei, Olivia and Murahwa, Alltalents T. and Taku, Ongeziwe and Manjate, Alice and Mussá, Tufária and Williamson, Anna-Lise},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {1314},\n}\n\n\n\n

\n

\n\n\n

\n Background: Human papillomavirus 16 (HPV16) is an oncogenic virus responsible for the majority of invasive cervical cancer cases worldwide. Due to genetic modifications, some variants are more oncogenic than others. We analysed the HPV16 phylogeny in HPV16-positive cervical Desoxyribonucleic Acid (DNA) samples collected from South African and Mozambican women to detect the circulating lineages. Methods: Polymerase chain reaction (PCR) amplification of the long control region (LCR) and 300 nucleotides of the E6 region was performed using HPV16-specific primers on HPV16-positive cervical samples collected in women from South Africa and Mozambique. HPV16 sequences were obtained through Next Generation Sequencing (NGS) methods. Geneious prime and MEGA 11 software were used to align the sequences to 16 HPV16 reference sequences, gathering the A, B, C, and D lineages and generating the phylogenetic tree. Single nucleotide polymorphisms (SNPs) in the LCR and E6 regions were analysed and the phylogenetic tree was generated using Geneious Prime software. Results: Fifty-eight sequences were analysed. Of these sequences, 79% (46/58) were from women who had abnormal cervical cytology. Fifteen SNPs in the LCR and eight in the E6 region were found to be the most common in all sequences. The phylogenetic analysis determined that 45% of the isolates belonged to the A1 sublineage (European variant), 34% belonged to the C1 sublineage (African 1 variant), 16% belonged to the B1 and B2 sublineage (African 2 variant), two isolates belonged to the D1–3 sublineages (Asian-American variant), and one to the North American variant. Conclusions: The African and European HPV16 variants were the most common circulating lineages in South African and Mozambican women. A high-grade squamous intraepithelial lesion (HSIL) was the most common cervical abnormality observed and linked to European and African lineages. These findings may contribute to understanding molecular HPV16 epidemiology in South Africa and Mozambique.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Prevalence, incidence and determinants of QuantiFERON$^{\\textrm{{TM}}}$ positivity in South African schoolchildren.\n \n \n \n \n\n\n \n Stewart, J.; Walker, N.; Jennings, K.; Delport, C.; Nuttall, J; Coussens, A.; Dyers, R; Jolliffe, D.; Tang, J.; Fraser, W.; Wilkinson, R.; Bekker, L.; Martineau, A.; and Middelkoop, K.\n\n\n \n\n\n\n IJTLD OPEN, 1(5): 206–214. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Prevalence,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{stewart_prevalence_2024,\n\ttitle = {Prevalence, incidence and determinants of {QuantiFERON}$^{\\textrm{{TM}}}$ positivity in {South} {African} schoolchildren},\n\tvolume = {1},\n\tissn = {3005-7590},\n\turl = {https://www.ingentaconnect.com/content/10.5588/ijtldopen.24.0084},\n\tdoi = {10.5588/ijtldopen.24.0084},\n\tabstract = {{\\textless}sec{\\textgreater}{\\textless}title{\\textgreater}BACKGROUND{\\textless}/title{\\textgreater}TB control requires the understanding and disruption of TB transmission. We describe prevalence, incidence and risk factors associated with childhood TB infection in Cape Town, South Africa.{\\textless}/sec{\\textgreater}{\\textless}sec{\\textgreater}{\\textless}title{\\textgreater}METHODS{\\textless}/title{\\textgreater}We \n report cross-sectional baseline and prospective incidence data from a large trial among primary school children living in high TB burden communities. Prevalent infection was defined as QuantiFERON™-TB Gold Plus (QFT-Plus) positivity as assessed at baseline. Subsequent conversion to QFT-Plus \n positivity was measured 3 years later among those QFT-Plus-negative at baseline. Multivariable logistic regression models examined factors associated with TB infection.{\\textless}/sec{\\textgreater}{\\textless}sec{\\textgreater}{\\textless}title{\\textgreater}RESULTS{\\textless}/title{\\textgreater}QuantiFERON-positivity at baseline (prevalence: 22.6\\%, 95\\% \n CI 20.9–24.4), was independently associated with increasing age (aOR 1.24 per additional year, 95\\% CI 1.15–1.34) and household exposure to TB during the participant’s lifetime (aOR 1.87, 95\\% CI 1.46–2.40). QFT-Plus conversion at year 3 (12.2\\%, 95\\% CI 10.5–14.0; \n annual infection rate: 3.95\\%) was associated with household exposure to an index TB case (aOR 2.74, 95\\% CI 1.05–7.18).{\\textless}/sec{\\textgreater}{\\textless}sec{\\textgreater}{\\textless}title{\\textgreater}CONCLUSION{\\textless}/title{\\textgreater}Rates of QFT-diagnosed TB infection remain high in this population. The strong association with household \n TB exposure reinforces the importance of contact tracing, preventative treatment and early treatment of infectious disease to reduce community transmission.{\\textless}/sec{\\textgreater}},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-24},\n\tjournal = {IJTLD OPEN},\n\tauthor = {Stewart, J. and Walker, N. and Jennings, K. and Delport, C. and Nuttall, J and Coussens, A.K. and Dyers, R and Jolliffe, D.A. and Tang, J.C.Y. and Fraser, W.D. and Wilkinson, R.J. and Bekker, L.-G. and Martineau, A.R. and Middelkoop, K.},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {206--214},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Proteomic Analysis of Human Macrophages Overexpressing Angiotensin-Converting Enzyme.\n \n \n \n \n\n\n \n Oosthuizen, D.; Ganief, T. A.; Bernstein, K. E.; and Sturrock, E. D.\n\n\n \n\n\n\n International Journal of Molecular Sciences, 25(13): 7055. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Proteomic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{oosthuizen_proteomic_2024,\n\ttitle = {Proteomic {Analysis} of {Human} {Macrophages} {Overexpressing} {Angiotensin}-{Converting} {Enzyme}},\n\tvolume = {25},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1422-0067},\n\turl = {https://www.mdpi.com/1422-0067/25/13/7055},\n\tdoi = {10.3390/ijms25137055},\n\tabstract = {Angiotensin converting enzyme (ACE) exerts strong modulation of myeloid cell function independently of its cardiovascular arm. The success of the ACE-overexpressing murine macrophage model, ACE 10/10, in treating microbial infections and cancer opens a new avenue into whether ACE overexpression in human macrophages shares these benefits. Additionally, as ACE inhibitors are a widely used antihypertensive medication, their impact on ACE expressing immune cells is of interest and currently understudied. In the present study, we utilized mass spectrometry to characterize and assess global proteomic changes in an ACE-overexpressing human THP-1 cell line. Additionally, proteomic changes and cellular uptake following treatment with an ACE C-domain selective inhibitor, lisinopril–tryptophan, were also assessed. ACE activity was significantly reduced following inhibitor treatment, despite limited uptake within the cell, and both RNA processing and immune pathways were significantly dysregulated with treatment. Also present were upregulated energy and TCA cycle proteins and dysregulated cytokine and interleukin signaling proteins with ACE overexpression. A novel, functionally enriched immune pathway that appeared both with ACE overexpression and inhibitor treatment was neutrophil degranulation. ACE overexpression within human macrophages showed similarities with ACE 10/10 murine macrophages, paving the way for mechanistic studies aimed at understanding the altered immune function.},\n\tlanguage = {en},\n\tnumber = {13},\n\turldate = {2025-06-24},\n\tjournal = {International Journal of Molecular Sciences},\n\tauthor = {Oosthuizen, Delia and Ganief, Tariq A. and Bernstein, Kenneth E. and Sturrock, Edward D.},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {7055},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n An Investigation into the In Vitro Targeted Killing of CD44-Expressing Triple-Negative Breast Cancer Cells Using Recombinant Photoimmunotherapeutics Compared to Auristatin-F-Based Antibody-Drug Conjugates.\n \n \n \n \n\n\n \n Mungra, N.; Nsole Biteghe, F. A.; Huysamen, A. M.; Hardcastle, N. S.; Bunjun, R.; Naran, K.; Lang, D.; Richter, W.; Hunter, R.; and Barth, S.\n\n\n \n\n\n\n Molecular Pharmaceutics, 21(8): 4098–4115. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"An$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{mungra_investigation_2024,\n\ttitle = {An {Investigation} into the {In} {Vitro} {Targeted} {Killing} of {CD44}-{Expressing} {Triple}-{Negative} {Breast} {Cancer} {Cells} {Using} {Recombinant} {Photoimmunotherapeutics} {Compared} to {Auristatin}-{F}-{Based} {Antibody}-{Drug} {Conjugates}},\n\tvolume = {21},\n\tcopyright = {https://doi.org/10.15223/policy-029},\n\tissn = {1543-8384, 1543-8392},\n\turl = {https://pubs.acs.org/doi/10.1021/acs.molpharmaceut.4c00449},\n\tdoi = {10.1021/acs.molpharmaceut.4c00449},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {Molecular Pharmaceutics},\n\tauthor = {Mungra, Neelakshi and Nsole Biteghe, Fleury A. and Huysamen, Allan M. and Hardcastle, Natasha S. and Bunjun, Rubina and Naran, Krupa and Lang, Dirk and Richter, Wolfgang and Hunter, Roger and Barth, Stefan},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {4098--4115},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Nitric oxide mediated kisspeptin regulation of steroidogenesis and gametogenesis in the catfish, Clarias batrachus.\n \n \n \n \n\n\n \n Singh, A.; Lal, B.; Kumar, P.; Parhar, I. S.; and Millar, R. P.\n\n\n \n\n\n\n Cell and Tissue Research, 397(2): 111–124. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Nitric$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{singh_nitric_2024,\n\ttitle = {Nitric oxide mediated kisspeptin regulation of steroidogenesis and gametogenesis in the catfish, {Clarias} batrachus},\n\tvolume = {397},\n\tissn = {0302-766X, 1432-0878},\n\turl = {https://link.springer.com/10.1007/s00441-024-03899-2},\n\tdoi = {10.1007/s00441-024-03899-2},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {Cell and Tissue Research},\n\tauthor = {Singh, Ankur and Lal, Bechan and Kumar, Pankaj and Parhar, Ishwar S. and Millar, Robert P.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {111--124},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Synthesis and In Vitro Antibacterial Evaluation of Mannich Base Nitrothiazole Derivatives.\n \n \n \n \n\n\n \n Dube, P. S.; Hart, D.; Legoabe, L. J.; Jordaan, A.; Warner, D. F.; and Beteck, R. M.\n\n\n \n\n\n\n Molbank, 2024(1): M1793. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Synthesis$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{dube_synthesis_2024,\n\ttitle = {Synthesis and {In} {Vitro} {Antibacterial} {Evaluation} of {Mannich} {Base} {Nitrothiazole} {Derivatives}},\n\tvolume = {2024},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1422-8599},\n\turl = {https://www.mdpi.com/1422-8599/2024/1/M1793},\n\tdoi = {10.3390/M1793},\n\tabstract = {Nitrothiazole derivatives have been reported to exhibit activity against aerobic, anaerobic, and microaerophilic bacteria. This activity profile makes the nitrothiazole compound class an ideal lead source against Mycobacterium tuberculosis, which flourishes in varied environments with different oxygen concentrations. In this work, we investigated six nitrothiazole derivatives for antitubercular activity. The compounds exhibited potent activity, with compounds 9 and 10 possessing an equipotent MIC90 value of 0.24 µM. The compounds were investigated for cytotoxicity against HEK293 cells and hemolysis against red blood cells, and they demonstrated no cytotoxicity nor hemolytic effects, suggesting they possess inherent antitubercular activity.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Molbank},\n\tauthor = {Dube, Phelelisiwe S. and Hart, Dylan and Legoabe, Lesetja J. and Jordaan, Audrey and Warner, Digby F. and Beteck, Richard M.},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {M1793},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Overlooked, dismissed, and downplayed: reversion of Mycobacterium tuberculosis immunoreactivity.\n \n \n \n \n\n\n \n Dale, K. D.; Schwalb, A.; Coussens, A. K.; Gibney, K. B.; Abboud, A. J.; Watts, K.; and Denholm, J. T.\n\n\n \n\n\n\n European Respiratory Review, 33(173): 240007. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Overlooked,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{dale_overlooked_2024,\n\ttitle = {Overlooked, dismissed, and downplayed: reversion of \\textit{{Mycobacterium} tuberculosis} immunoreactivity},\n\tvolume = {33},\n\tissn = {0905-9180, 1600-0617},\n\tshorttitle = {Overlooked, dismissed, and downplayed},\n\turl = {https://publications.ersnet.org/lookup/doi/10.1183/16000617.0007-2024},\n\tdoi = {10.1183/16000617.0007-2024},\n\tabstract = {Tuberculosis (TB) is caused by \n              Mycobacterium tuberculosis \n              ( \n              Mtb \n              ). Following infection, immune responses to \n              Mtb \n              antigens can be measured using the tuberculin skin test or an interferon-γ release assay. The gain of \n              Mtb \n              immunoreactivity, a change from a negative to a positive tuberculin skin test or interferon-γ release assay result, is called conversion and has long been used as a measure of \n              Mtb \n              exposure. However, the loss of immunoreactivity (reversion; a positive followed by a negative result) has often been overlooked. Instead, in clinical and epidemiological circles, \n              Mtb \n              immunoreactivity is commonly considered to persist lifelong and confer a lifetime of disease risk. We present a critical review, describing the evidence for reversion from cohort studies, ecological studies and studies of TB progression risk. We outline the inconsistent reasons why reversion has been dismissed from common understanding and present evidence demonstrating that, just as conversion predominantly indicates prior exposure to \n              Mtb \n              antigens, so its opposite, reversion, suggests the reduction or absence of exposure (endogenous or exogenous). \n              Mtb \n              immunoreactivity is dynamic in both individuals and populations and this is why it is useful for stratifying short-term TB progression risk. The neglect of reversion has shaped TB research and policy at all levels, influencing clinical management and skewing \n              Mtb \n              infection risk estimation and transmission modelling, leading to an underestimation of the contribution of re-exposure to the burden of TB, a serious oversight for an infectious disease. More than a century after it was first demonstrated, it is time to incorporate reversion into our understanding of the natural history of TB.},\n\tlanguage = {en},\n\tnumber = {173},\n\turldate = {2025-06-24},\n\tjournal = {European Respiratory Review},\n\tauthor = {Dale, Katie D. and Schwalb, Alvaro and Coussens, Anna K. and Gibney, Katherine B. and Abboud, Alison J. and Watts, Krista and Denholm, Justin T.},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {240007},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Carbapenem-resistant Enterobacterales among hospitalized patients in Cape Town, South Africa: clinical and microbiological epidemiology.\n \n \n \n \n\n\n \n Tootla, H. D.; Prentice, E.; Moodley, C.; Marais, G.; Nyakutira, N.; Reddy, K.; Bamford, C.; Niehaus, A.; Whitelaw, A.; Brink, A.; Members (collaborators) of the Cape Town Antimicrobial Stewardship Study Alliance (CT-ASSA); Page, C.; Schoeman, E.; De Klerk, E.; Lategan, K.; Pienaar, K.; Henning, L.; Du Plessis, M.; Maseko, N.; Nel, S.; Narainsamy, M.; Vermeulen, M.; Du Toit, N.; Van Heerden, T.; Sitharam, L.; Barendse, A.; Nagel, D.; Prince, J.; Vass, L.; Strauss, R.; Fakier, R.; Samuel, C.; Van Zyl, M.; Isaacs, L.; Hendricks, S.; Dodd, A.; Daniels, R.; Zemanay, W.; Van Heerden, J.; Hapeela, N.; Brown, P.; Daniels, Z.; Claassen, S.; Patel, F.; Vasuthevan, S.; Scott, E.; Ricks, E.; Curle, P.; and Wojno, J.\n\n\n \n\n\n\n JAC-Antimicrobial Resistance, 6(2): dlae051. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Carbapenem-resistant$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{tootla_carbapenem-resistant_2024,\n\ttitle = {Carbapenem-resistant {Enterobacterales} among hospitalized patients in {Cape} {Town}, {South} {Africa}: clinical and microbiological epidemiology},\n\tvolume = {6},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2632-1823},\n\tshorttitle = {Carbapenem-resistant {Enterobacterales} among hospitalized patients in {Cape} {Town}, {South} {Africa}},\n\turl = {https://academic.oup.com/jacamr/article/doi/10.1093/jacamr/dlae051/7633764},\n\tdoi = {10.1093/jacamr/dlae051},\n\tabstract = {Abstract \n             \n              Background \n              Carbapenem-resistant Enterobacterales (CRE) are a substantial problem in Cape Town. CRE epidemiology is largely unknown and mortality remains high. \n             \n             \n              Objectives \n              To describe and characterize the clinical and microbiological epidemiology of CRE within Cape Town hospitals to better inform therapy with regard to current and novel antibiotics, as well as improve antimicrobial stewardship (AMS), and infection prevention and control (IPC). \n             \n             \n              Methods \n              This prospective, multicentre study performed between 1 November 2020 and 30 November 2022, across three public and three private hospitals included hospitalized participants with CRE from clinical cultures. Participant demographics, clinical information and microbiology results were collected and analysed. \n             \n             \n              Results \n              Ninety percent of participants were from public hospitals. The age distribution ranged from 7 days to 88 years. Notable risk factors for CRE infection included recent exposure to antibiotics, medical devices and surgery. The most prevalent species was Klebsiella pneumoniae. However, a higher proportion of Serratia marcescens compared with previous reports was identified. The detected carbapenemases were blaOXA-48-like (80\\%) and blaNDM (11\\%). With the exception of amikacin (63\\%), tigecycline (65\\%), colistin (95\\%) and ceftazidime/avibactam (87\\%), susceptibility to antibiotics was low. \n             \n             \n              Conclusions \n              This study identified common risk factors for CRE infection and generated a description of carbapenemase enzymes, species distribution and antibiograms, enabling a better understanding of CRE epidemiology. This provides insights into transmission patterns and resistance determinants of CREs, beneficial to informing data-driven regional patient management, AMS and IPC strategies.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {JAC-Antimicrobial Resistance},\n\tauthor = {Tootla, Hafsah Deepa and Prentice, Elizabeth and Moodley, Clinton and Marais, Gert and Nyakutira, Nyasha and Reddy, Kessendri and Bamford, Colleen and Niehaus, Abraham and Whitelaw, Andrew and Brink, Adrian and {Members (collaborators) of the Cape Town Antimicrobial Stewardship Study Alliance (CT-ASSA)} and Page, Claudine and Schoeman, Elizabeth and De Klerk, Elizma and Lategan, Karin and Pienaar, Karlien and Henning, Liezl and Du Plessis, Mandy and Maseko, Nomfundo and Nel, Salome and Narainsamy, Melenie and Vermeulen, Michelle and Du Toit, Narissa and Van Heerden, Teresa and Sitharam, Liza and Barendse, Asa and Nagel, Dane and Prince, Jacqueline and Vass, Letitia and Strauss, Rileen and Fakier, Rushana and Samuel, Catherine and Van Zyl, Marelieze and Isaacs, Leigh-Ann and Hendricks, Shareefa and Dodd, Amy and Daniels, Reecka and Zemanay, Widaad and Van Heerden, Judi and Hapeela, Nchimunya and Brown, Parveen and Daniels, Zubayr and Claassen, Shantelle and Patel, Fadheela and Vasuthevan, Sharon and Scott, Enid and Ricks, Esmeralda and Curle, Patricia and Wojno, Justyna},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {dlae051},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Modulation of riboflavin biosynthesis and utilization in mycobacteria.\n \n \n \n \n\n\n \n Chengalroyen, M. D.; Mehaffy, C.; Lucas, M.; Bauer, N.; Raphela, M. L.; Oketade, N.; Warner, D. F.; Lewinsohn, D. A.; Lewinsohn, D. M.; Dobos, K. M.; and Mizrahi, V.\n\n\n \n\n\n\n Microbiology Spectrum, 12(8): e03207–23. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Modulation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{chengalroyen_modulation_2024,\n\ttitle = {Modulation of riboflavin biosynthesis and utilization in mycobacteria},\n\tvolume = {12},\n\tissn = {2165-0497},\n\turl = {https://journals.asm.org/doi/10.1128/spectrum.03207-23},\n\tdoi = {10.1128/spectrum.03207-23},\n\tabstract = {ABSTRACT \n             \n               \n               \n                Riboflavin (vitamin B \n                2 \n                ) is the precursor of the flavin coenzymes, FAD and FMN, which play a central role in cellular redox metabolism. While humans must obtain riboflavin from dietary sources, certain microbes, including \n                Mycobacterium tuberculosis \n                (Mtb), can biosynthesize riboflavin \n                de novo \n                . Riboflavin precursors have also been implicated in the activation of mucosal-associated invariant T (MAIT) cells which recognize metabolites derived from the riboflavin biosynthesis pathway complexed to the MHC-I-like molecule, MR1. To investigate the biosynthesis and function of riboflavin and its pathway intermediates in mycobacterial metabolism and physiology, we constructed conditional knockdowns (hypomorphs) in riboflavin biosynthesis and utilization genes in \n                Mycobacterium smegmatis \n                (Msm) and Mtb by inducible CRISPR interference. Using this comprehensive panel of hypomorphs, we analyzed the impact of gene silencing on viability, on the transcription of (other) riboflavin pathway genes, on the levels of the pathway proteins, and on riboflavin itself. Our results revealed that (i) despite lacking a canonical transporter, both Msm and Mtb assimilate exogenous riboflavin when supplied at high concentration; (ii) there is functional redundancy in lumazine synthase activity in Msm; (iii) silencing of \n                ribA2 \n                or \n                ribF \n                is profoundly bactericidal in Mtb; and (iv) in Msm, \n                ribA2 \n                silencing results in concomitant knockdown of other pathway genes coupled with RibA2 and riboflavin depletion and is also bactericidal. In addition to their use in genetic validation of potential drug targets for tuberculosis, this collection of hypomorphs provides a useful resource for future studies investigating the role of pathway intermediates in MAIT cell recognition of mycobacteria. \n               \n             \n             \n              IMPORTANCE \n               \n                The pathway for biosynthesis and utilization of riboflavin, precursor of the essential coenzymes, FMN and FAD, is of particular interest in the flavin-rich pathogen, \n                Mycobacterium tuberculosis \n                (Mtb), for two important reasons: (i) the pathway includes potential tuberculosis (TB) drug targets and (ii) intermediates from the riboflavin biosynthesis pathway provide ligands for mucosal-associated invariant T (MAIT) cells, which have been implicated in TB pathogenesis. However, the riboflavin pathway is poorly understood in mycobacteria, which lack canonical mechanisms to transport this vitamin and to regulate flavin coenzyme homeostasis. By conditionally disrupting each step of the pathway and assessing the impact on mycobacterial viability and on the levels of the pathway proteins as well as riboflavin, our work provides genetic validation of the riboflavin pathway as a target for TB drug discovery and offers a resource for further exploring the association between riboflavin biosynthesis, MAIT cell activation, and TB infection and disease. \n               \n             \n          ,  \n             \n              The pathway for biosynthesis and utilization of riboflavin, precursor of the essential coenzymes, FMN and FAD, is of particular interest in the flavin-rich pathogen, \n              Mycobacterium tuberculosis \n              (Mtb), for two important reasons: (i) the pathway includes potential tuberculosis (TB) drug targets and (ii) intermediates from the riboflavin biosynthesis pathway provide ligands for mucosal-associated invariant T (MAIT) cells, which have been implicated in TB pathogenesis. However, the riboflavin pathway is poorly understood in mycobacteria, which lack canonical mechanisms to transport this vitamin and to regulate flavin coenzyme homeostasis. By conditionally disrupting each step of the pathway and assessing the impact on mycobacterial viability and on the levels of the pathway proteins as well as riboflavin, our work provides genetic validation of the riboflavin pathway as a target for TB drug discovery and offers a resource for further exploring the association between riboflavin biosynthesis, MAIT cell activation, and TB infection and disease.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {Microbiology Spectrum},\n\tauthor = {Chengalroyen, Melissa D. and Mehaffy, Carolina and Lucas, Megan and Bauer, Niel and Raphela, Mabule L. and Oketade, Nurudeen and Warner, Digby F. and Lewinsohn, Deborah A. and Lewinsohn, David M. and Dobos, Karen M. and Mizrahi, Valerie},\n\teditor = {Lamichhane, Gyanu},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {e03207--23},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Riboflavin (vitamin B 2 ) is the precursor of the flavin coenzymes, FAD and FMN, which play a central role in cellular redox metabolism. While humans must obtain riboflavin from dietary sources, certain microbes, including Mycobacterium tuberculosis (Mtb), can biosynthesize riboflavin de novo . Riboflavin precursors have also been implicated in the activation of mucosal-associated invariant T (MAIT) cells which recognize metabolites derived from the riboflavin biosynthesis pathway complexed to the MHC-I-like molecule, MR1. To investigate the biosynthesis and function of riboflavin and its pathway intermediates in mycobacterial metabolism and physiology, we constructed conditional knockdowns (hypomorphs) in riboflavin biosynthesis and utilization genes in Mycobacterium smegmatis (Msm) and Mtb by inducible CRISPR interference. Using this comprehensive panel of hypomorphs, we analyzed the impact of gene silencing on viability, on the transcription of (other) riboflavin pathway genes, on the levels of the pathway proteins, and on riboflavin itself. Our results revealed that (i) despite lacking a canonical transporter, both Msm and Mtb assimilate exogenous riboflavin when supplied at high concentration; (ii) there is functional redundancy in lumazine synthase activity in Msm; (iii) silencing of ribA2 or ribF is profoundly bactericidal in Mtb; and (iv) in Msm, ribA2 silencing results in concomitant knockdown of other pathway genes coupled with RibA2 and riboflavin depletion and is also bactericidal. In addition to their use in genetic validation of potential drug targets for tuberculosis, this collection of hypomorphs provides a useful resource for future studies investigating the role of pathway intermediates in MAIT cell recognition of mycobacteria. IMPORTANCE The pathway for biosynthesis and utilization of riboflavin, precursor of the essential coenzymes, FMN and FAD, is of particular interest in the flavin-rich pathogen, Mycobacterium tuberculosis (Mtb), for two important reasons: (i) the pathway includes potential tuberculosis (TB) drug targets and (ii) intermediates from the riboflavin biosynthesis pathway provide ligands for mucosal-associated invariant T (MAIT) cells, which have been implicated in TB pathogenesis. However, the riboflavin pathway is poorly understood in mycobacteria, which lack canonical mechanisms to transport this vitamin and to regulate flavin coenzyme homeostasis. By conditionally disrupting each step of the pathway and assessing the impact on mycobacterial viability and on the levels of the pathway proteins as well as riboflavin, our work provides genetic validation of the riboflavin pathway as a target for TB drug discovery and offers a resource for further exploring the association between riboflavin biosynthesis, MAIT cell activation, and TB infection and disease. , The pathway for biosynthesis and utilization of riboflavin, precursor of the essential coenzymes, FMN and FAD, is of particular interest in the flavin-rich pathogen, Mycobacterium tuberculosis (Mtb), for two important reasons: (i) the pathway includes potential tuberculosis (TB) drug targets and (ii) intermediates from the riboflavin biosynthesis pathway provide ligands for mucosal-associated invariant T (MAIT) cells, which have been implicated in TB pathogenesis. However, the riboflavin pathway is poorly understood in mycobacteria, which lack canonical mechanisms to transport this vitamin and to regulate flavin coenzyme homeostasis. By conditionally disrupting each step of the pathway and assessing the impact on mycobacterial viability and on the levels of the pathway proteins as well as riboflavin, our work provides genetic validation of the riboflavin pathway as a target for TB drug discovery and offers a resource for further exploring the association between riboflavin biosynthesis, MAIT cell activation, and TB infection and disease.\n

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\n \n\n \n \n \n \n \n \n Pharmacokinetics of Single-Dose Versus Double-Dose Dolutegravir After Switching From a Failing Efavirenz-Based Regimen.\n \n \n \n \n\n\n \n Griesel, R.; Banda, C. G.; Zhao, Y.; Omar, Z.; Wiesner, L.; Meintjes, G.; Sinxadi, P.; and Maartens, G.\n\n\n \n\n\n\n JAIDS Journal of Acquired Immune Deficiency Syndromes, 96(1): 85–91. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Pharmacokinetics$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{griesel_pharmacokinetics_2024,\n\ttitle = {Pharmacokinetics of {Single}-{Dose} {Versus} {Double}-{Dose} {Dolutegravir} {After} {Switching} {From} a {Failing} {Efavirenz}-{Based} {Regimen}},\n\tvolume = {96},\n\tissn = {1525-4135},\n\turl = {https://journals.lww.com/10.1097/QAI.0000000000003402},\n\tdoi = {10.1097/QAI.0000000000003402},\n\tabstract = {Background: \n              Dolutegravir exposure is reduced after switching from efavirenz, which could select for dolutegravir resistance if switching occurs during virologic failure. \n             \n             \n              Methods: \n              We measured serial dolutegravir trough concentrations after switching from efavirenz in a clinical trial, which randomized some participants to a supplemental dolutegravir dose or placebo for the first 14 days. Changes in dolutegravir trough concentrations between days 3, 7, 14, and 28 were evaluated. The primary outcome was the geometric mean ratio of dolutegravir trough concentrations on day 7 versus day 28. \n             \n             \n              Results: \n              Twenty-four participants received double-dose dolutegravir (50 mg twice daily) and 11 standard dose for the first 14 days. Baseline characteristics were 77\\% female, median age 36 years, CD4 cell count 254 cells/mm3, and HIV-1 RNA 4.0 log10 copies/mL. The geometric mean ratio (90\\% CI) of dolutegravir trough concentrations on day 7 versus day 28 was 0.637 (0.485 to 0.837) in the standard-dose group and 1.654 (1.404 to 1.948) in the double-dose group. There was a prolonged induction effect at day 28 in participants with efavirenz slow metaboliser genotypes. One participant in the double-dose group had a dolutegravir trough concentration below the protein-binding adjusted concentration needed to inhibit 90\\% of HIV-1 (PA-IC90) at day 3. \n             \n             \n              Conclusions: \n              No participants on standard-dose dolutegravir had dolutegravir trough concentrations below the PA-IC90. Slow efavirenz metaboliser genotypes had higher baseline efavirenz concentrations and more pronounced and longer period of induction postswitch. These findings suggest that a 14-day lead-in supplemental dolutegravir dose may not be necessary when switching from a failing efavirenz-based first-line regimen.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},\n\tauthor = {Griesel, Rulan and Banda, Clifford G. and Zhao, Ying and Omar, Zaayid and Wiesner, Lubbe and Meintjes, Graeme and Sinxadi, Phumla and Maartens, Gary},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {85--91},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Detection of Mycobacterium tuberculosis from tongue swabs using sonication and sequence-specific hybridization capture.\n \n \n \n \n\n\n \n Yan, A. J.; Olson, A. M.; Weigel, K. M.; Luabeya, A. K.; Heiniger, E.; Hatherill, M.; Cangelosi, G. A.; and Yager, P.\n\n\n \n\n\n\n PLOS ONE, 19(8): e0308235. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Detection$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{yan_detection_2024,\n\ttitle = {Detection of {Mycobacterium} tuberculosis from tongue swabs using sonication and sequence-specific hybridization capture},\n\tvolume = {19},\n\tissn = {1932-6203},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0308235},\n\tdoi = {10.1371/journal.pone.0308235},\n\tabstract = {Tongue swabs hold promise as a non-invasive sample for diagnosing tuberculosis (TB). However, their utility as replacements for sputum has been limited by their varied diagnostic performance in PCR assays compared to sputum. The use of silica-based DNA extraction methods may limit sensitivity due to incomplete lysis of \n              Mycobacterium tuberculosis \n              (MTB) cells and co-extraction of non-target nucleic acid, which may inhibit PCR. Specificity may also be compromised because these methods are labor-intensive and prone to cross-contamination. To address these limitations, we developed a sample preparation method that combines sonication for MTB lysis and a sequence-specific MTB DNA capture method using hybridization probes immobilized on magnetic beads. In spiked tongue swabs, our hybridization capture method demonstrated a 100-fold increase in MTB DNA yield over silica-based Qiagen DNA extraction and ethanol precipitation. In a study conducted on clinical samples from South Africa, our protocol had 74\\% (70/94) sensitivity and 98\\% (41/42) specificity for detecting active pulmonary TB with sputum Xpert MTB/RIF Ultra as the reference standard. While hybridization capture did not show improved sensitivity over Qiagen DNA extraction and ethanol precipitation, it demonstrated better specificity than previously reported methods and was easier to perform. With integration into point-of-care platforms, these strategies have the potential to help enable rapid non-sputum-based TB diagnosis across key underserved patient populations.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Yan, Alexander J. and Olson, Alaina M. and Weigel, Kris M. and Luabeya, Angelique K. and Heiniger, Erin and Hatherill, Mark and Cangelosi, Gerard A. and Yager, Paul},\n\teditor = {Vashist, Atul},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {e0308235},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Identifying quantitative sncRNAs signature using global sequencing as a potential biomarker for tuberculosis diagnosis and their role in regulating host response.\n \n \n \n \n\n\n \n Kaul, S.; Nair, V.; Gcanga, L.; Lakshmanan, V.; Kalamuddin, M.; Anang, V.; Rathore, S.; Dhawan, S.; Alam, T.; Khanna, V.; Lohiya, S.; Ali, S.; Mannan, S.; Rade, K.; Parihar, S. P.; Khanna, A.; Malhotra, P.; Brombacher, F.; Dasaradhi, P. V.; Guler, R.; and Mohmmed, A.\n\n\n \n\n\n\n International Journal of Biological Macromolecules, 271: 132714. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Identifying$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kaul_identifying_2024,\n\ttitle = {Identifying quantitative {sncRNAs} signature using global sequencing as a potential biomarker for tuberculosis diagnosis and their role in regulating host response},\n\tvolume = {271},\n\tissn = {01418130},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0141813024035190},\n\tdoi = {10.1016/j.ijbiomac.2024.132714},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {International Journal of Biological Macromolecules},\n\tauthor = {Kaul, Sheetal and Nair, Vivek and Gcanga, Lorna and Lakshmanan, Vairavan and Kalamuddin, M. and Anang, Vandana and Rathore, Sumit and Dhawan, Shikha and Alam, Tanvir and Khanna, Vishal and Lohiya, Sheelu and Ali, Shakir and Mannan, Shamim and Rade, Kirankumar and Parihar, Suraj P. and Khanna, Ashwani and Malhotra, Pawan and Brombacher, Frank and Dasaradhi, Palakodeti Vn and Guler, Reto and Mohmmed, Asif},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {132714},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Effects of individual drug and combination antiretroviral therapy on trophoblast proliferation.\n \n \n \n \n\n\n \n Nzuza, S.; Hadebe, S. I.; Katz, A. A.; and Matjila, M.\n\n\n \n\n\n\n European Journal of Obstetrics & Gynecology and Reproductive Biology, 298: 66–73. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Effects$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{nzuza_effects_2024,\n\ttitle = {Effects of individual drug and combination antiretroviral therapy on trophoblast proliferation},\n\tvolume = {298},\n\tissn = {03012115},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0301211524002100},\n\tdoi = {10.1016/j.ejogrb.2024.04.035},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {European Journal of Obstetrics \\& Gynecology and Reproductive Biology},\n\tauthor = {Nzuza, Sanelisiwe and Hadebe, Silindile I. and Katz, Arieh A. and Matjila, Mushi},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {66--73},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Correcting mortality estimates among children and youth on antiretroviral therapy in southern Africa: A comparative analysis between a multi‐country tracing study and linkage to a health information exchange.\n \n \n \n \n\n\n \n Nyakato, P.; Schomaker, M.; Boulle, A.; Euvrard, J.; Wood, R.; Eley, B.; Prozesky, H.; Christ, B.; Anderegg, N.; Ayakaka, I.; Rafael, I.; Kunzekwenyika, C.; Moore, C. B.; Van Lettow, M.; Chimbetete, C.; Mbewe, S.; Ballif, M.; Egger, M.; Yiannoutsos, C. T.; Cornell, M.; and Davies, M.\n\n\n \n\n\n\n Tropical Medicine & International Health, 29(8): 739–751. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Correcting$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{nyakato_correcting_2024,\n\ttitle = {Correcting mortality estimates among children and youth on antiretroviral therapy in southern {Africa}: {A} comparative analysis between a multi‐country tracing study and linkage to a health information exchange},\n\tvolume = {29},\n\tissn = {1360-2276, 1365-3156},\n\tshorttitle = {Correcting mortality estimates among children and youth on antiretroviral therapy in southern {Africa}},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/tmi.14030},\n\tdoi = {10.1111/tmi.14030},\n\tabstract = {Abstract \n             \n              Objectives \n              The objective of this study is to assess the outcomes of children, adolescents and young adults with HIV reported as lost to follow‐up, correct mortality estimates for children, adolescents and young adults with HIV for unascertained outcomes in those loss to follow‐up (LTFU) based on tracing and linkage data separately using data from the International epidemiology Databases to Evaluate AIDS in Southern Africa. \n             \n             \n              Methods \n              We included data from two different populations of children, adolescents and young adults with HIV; (1) clinical data from children, adolescents and young adults with HIV aged ≤24 years from Lesotho, Malawi, Mozambique, Zambia and Zimbabwe; (2) clinical data from children, adolescents and young adults with HIV aged ≤14 years from the Western Cape (WC) in South Africa. Outcomes of patients lost to follow‐up were available from (1) a tracing study and (2) linkage to a health information exchange. For both populations, we compared six methods for correcting mortality estimates for all children, adolescents and young adults with HIV. \n             \n             \n              Results \n              We found substantial variations of mortality estimates among children, adolescents and young adults with HIV reported as lost to follow‐up versus those retained in care. Ascertained mortality was higher among lost and traceable children, adolescents and young adults with HIV and lower among lost and linkable than those retained in care (mortality: 13.4\\% [traced] vs. 12.6\\% [retained‐other Southern Africa countries]; 3.4\\% [linked] vs. 9.4\\% [retained‐WC]). A high proportion of lost to follow‐up children, adolescents and young adults with HIV had self‐transferred (21.0\\% and 47.0\\%) in the traced and linked samples, respectively. The uncorrected method of non‐informative censoring yielded the lowest mortality estimates among all methods for both tracing (6.0\\%) and linkage (4.0\\%) approaches at 2 years from ART start. Among corrected methods using ascertained data, multiple imputation, incorporating ascertained data (MI(asc.)) and inverse probability weighting with logistic weights were most robust for the tracing approach. In contrast, for the linkage approach, MI(asc.) was the most robust. \n             \n             \n              Conclusions \n              Our findings emphasise that lost to follow‐up is non‐ignorable and both tracing and linkage improved outcome ascertainment: tracing identified substantial mortality in those reported as lost to follow‐up, whereas linkage did not identify out‐of‐facility deaths, but showed that a large proportion of those reported as lost to follow‐up were self‐transfers.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {Tropical Medicine \\& International Health},\n\tauthor = {Nyakato, Patience and Schomaker, Michael and Boulle, Andrew and Euvrard, Jonathan and Wood, Robin and Eley, Brian and Prozesky, Hans and Christ, Benedikt and Anderegg, Nanina and Ayakaka, Irene and Rafael, Idiovino and Kunzekwenyika, Cordelia and Moore, Carolyn B. and Van Lettow, Monique and Chimbetete, Cleophas and Mbewe, Safari and Ballif, Marie and Egger, Matthias and Yiannoutsos, Constantin T. and Cornell, Morna and Davies, Mary‐Ann},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {739--751},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Objectives The objective of this study is to assess the outcomes of children, adolescents and young adults with HIV reported as lost to follow‐up, correct mortality estimates for children, adolescents and young adults with HIV for unascertained outcomes in those loss to follow‐up (LTFU) based on tracing and linkage data separately using data from the International epidemiology Databases to Evaluate AIDS in Southern Africa. Methods We included data from two different populations of children, adolescents and young adults with HIV; (1) clinical data from children, adolescents and young adults with HIV aged ≤24 years from Lesotho, Malawi, Mozambique, Zambia and Zimbabwe; (2) clinical data from children, adolescents and young adults with HIV aged ≤14 years from the Western Cape (WC) in South Africa. Outcomes of patients lost to follow‐up were available from (1) a tracing study and (2) linkage to a health information exchange. For both populations, we compared six methods for correcting mortality estimates for all children, adolescents and young adults with HIV. Results We found substantial variations of mortality estimates among children, adolescents and young adults with HIV reported as lost to follow‐up versus those retained in care. Ascertained mortality was higher among lost and traceable children, adolescents and young adults with HIV and lower among lost and linkable than those retained in care (mortality: 13.4% [traced] vs. 12.6% [retained‐other Southern Africa countries]; 3.4% [linked] vs. 9.4% [retained‐WC]). A high proportion of lost to follow‐up children, adolescents and young adults with HIV had self‐transferred (21.0% and 47.0%) in the traced and linked samples, respectively. The uncorrected method of non‐informative censoring yielded the lowest mortality estimates among all methods for both tracing (6.0%) and linkage (4.0%) approaches at 2 years from ART start. Among corrected methods using ascertained data, multiple imputation, incorporating ascertained data (MI(asc.)) and inverse probability weighting with logistic weights were most robust for the tracing approach. In contrast, for the linkage approach, MI(asc.) was the most robust. Conclusions Our findings emphasise that lost to follow‐up is non‐ignorable and both tracing and linkage improved outcome ascertainment: tracing identified substantial mortality in those reported as lost to follow‐up, whereas linkage did not identify out‐of‐facility deaths, but showed that a large proportion of those reported as lost to follow‐up were self‐transfers.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Safety and immunogenicity of booster vaccination and fractional dosing with Ad26.COV2.S or BNT162b2 in Ad26.COV2.S-vaccinated participants.\n \n \n \n \n\n\n \n Riou, C.; Bhiman, J. N.; Ganga, Y.; Sawry, S.; Ayres, F.; Baguma, R.; Balla, S. R.; Benede, N.; Bernstein, M.; Besethi, A. S.; Cele, S.; Crowther, C.; Dhar, M.; Geyer, S.; Gill, K.; Grifoni, A.; Hermanus, T.; Kaldine, H.; Keeton, R. S.; Kgagudi, P.; Khan, K.; Lazarus, E.; Le Roux, J.; Lustig, G.; Madzivhandila, M.; Magugu, S. F. J.; Makhado, Z.; Manamela, N. P.; Mkhize, Q.; Mosala, P.; Motlou, T. P.; Mutavhatsindi, H.; Mzindle, N. B.; Nana, A.; Nesamari, R.; Ngomti, A.; Nkayi, A. A.; Nkosi, T. P.; Omondi, M. A.; Panchia, R.; Patel, F.; Sette, A.; Singh, U.; Van Graan, S.; Venter, E. M.; Walters, A.; Moyo-Gwete, T.; Richardson, S. I.; Garrett, N.; Rees, H.; Bekker, L.; Gray, G.; Burgers, W. A.; Sigal, A.; Moore, P. L.; and Fairlie, L.\n\n\n \n\n\n\n PLOS Global Public Health, 4(4): e0002703. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Safety$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{riou_safety_2024,\n\ttitle = {Safety and immunogenicity of booster vaccination and fractional dosing with {Ad26}.{COV2}.{S} or {BNT162b2} in {Ad26}.{COV2}.{S}-vaccinated participants},\n\tvolume = {4},\n\tissn = {2767-3375},\n\turl = {https://dx.plos.org/10.1371/journal.pgph.0002703},\n\tdoi = {10.1371/journal.pgph.0002703},\n\tabstract = {We report the safety and immunogenicity of fractional and full dose Ad26.COV2.S and BNT162b2 in an open label phase 2 trial of participants previously vaccinated with a single dose of Ad26.COV2.S, with 91.4\\% showing evidence of previous SARS-CoV-2 infection. A total of 286 adults (with or without HIV) were enrolled {\\textgreater}4 months after an Ad26.COV2.S prime and randomized 1:1:1:1 to receive either a full or half-dose booster of Ad26.COV2.S or BNT162b2 vaccine. B cell responses (binding, neutralization and antibody dependent cellular cytotoxicity-ADCC), and spike-specific T-cell responses were evaluated at baseline, 2, 12 and 24 weeks post-boost. Antibody and T-cell immunity targeting the Ad26 vector was also evaluated. No vaccine-associated serious adverse events were recorded. The full- and half-dose BNT162b2 boosted anti-SARS-CoV-2 binding antibody levels (3.9- and 4.5-fold, respectively) and neutralizing antibody levels (4.4- and 10-fold). Binding and neutralizing antibodies following half-dose Ad26.COV2.S were not significantly boosted. Full-dose Ad26.COV2.S did not boost binding antibodies but slightly enhanced neutralizing antibodies (2.1-fold). ADCC was marginally increased only after a full-dose BNT162b2. T-cell responses followed a similar pattern to neutralizing antibodies. Six months post-boost, antibody and T-cell responses had waned to baseline levels. While we detected strong anti-vector immunity, there was no correlation between anti-vector immunity in Ad26.COV2.S recipients and spike-specific neutralizing antibody or T-cell responses post-Ad26.COV2.S boosting. Overall, in the context of hybrid immunity, boosting with heterologous full- or half-dose BNT162b2 mRNA vaccine demonstrated superior immunogenicity 2 weeks post-vaccination compared to homologous Ad26.COV2.S, though rapid waning occurred by 12 weeks post-boost. \n             \n              Trial Registration: \n              The study has been registered to the South African National Clinical Trial Registry (SANCTR): \n              DOH-27-012022-7841 \n              . The approval letter from SANCTR has been provided in the up-loaded documents.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Global Public Health},\n\tauthor = {Riou, Catherine and Bhiman, Jinal N. and Ganga, Yashica and Sawry, Shobna and Ayres, Frances and Baguma, Richard and Balla, Sashkia R. and Benede, Ntombi and Bernstein, Mallory and Besethi, Asiphe S. and Cele, Sandile and Crowther, Carol and Dhar, Mrinmayee and Geyer, Sohair and Gill, Katherine and Grifoni, Alba and Hermanus, Tandile and Kaldine, Haajira and Keeton, Roanne S. and Kgagudi, Prudence and Khan, Khadija and Lazarus, Erica and Le Roux, Jean and Lustig, Gila and Madzivhandila, Mashudu and Magugu, Siyabulela F. J. and Makhado, Zanele and Manamela, Nelia P. and Mkhize, Qiniso and Mosala, Paballo and Motlou, Thopisang P. and Mutavhatsindi, Hygon and Mzindle, Nonkululeko B. and Nana, Anusha and Nesamari, Rofhiwa and Ngomti, Amkele and Nkayi, Anathi A. and Nkosi, Thandeka P. and Omondi, Millicent A. and Panchia, Ravindre and Patel, Faeezah and Sette, Alessandro and Singh, Upasna and Van Graan, Strauss and Venter, Elizabeth M. and Walters, Avril and Moyo-Gwete, Thandeka and Richardson, Simone I. and Garrett, Nigel and Rees, Helen and Bekker, Linda-Gail and Gray, Glenda and Burgers, Wendy A. and Sigal, Alex and Moore, Penny L. and Fairlie, Lee},\n\teditor = {Dinga, Jerome Nyhalah},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {e0002703},\n}\n\n\n\n

\n

\n\n\n

\n We report the safety and immunogenicity of fractional and full dose Ad26.COV2.S and BNT162b2 in an open label phase 2 trial of participants previously vaccinated with a single dose of Ad26.COV2.S, with 91.4% showing evidence of previous SARS-CoV-2 infection. A total of 286 adults (with or without HIV) were enrolled \\textgreater4 months after an Ad26.COV2.S prime and randomized 1:1:1:1 to receive either a full or half-dose booster of Ad26.COV2.S or BNT162b2 vaccine. B cell responses (binding, neutralization and antibody dependent cellular cytotoxicity-ADCC), and spike-specific T-cell responses were evaluated at baseline, 2, 12 and 24 weeks post-boost. Antibody and T-cell immunity targeting the Ad26 vector was also evaluated. No vaccine-associated serious adverse events were recorded. The full- and half-dose BNT162b2 boosted anti-SARS-CoV-2 binding antibody levels (3.9- and 4.5-fold, respectively) and neutralizing antibody levels (4.4- and 10-fold). Binding and neutralizing antibodies following half-dose Ad26.COV2.S were not significantly boosted. Full-dose Ad26.COV2.S did not boost binding antibodies but slightly enhanced neutralizing antibodies (2.1-fold). ADCC was marginally increased only after a full-dose BNT162b2. T-cell responses followed a similar pattern to neutralizing antibodies. Six months post-boost, antibody and T-cell responses had waned to baseline levels. While we detected strong anti-vector immunity, there was no correlation between anti-vector immunity in Ad26.COV2.S recipients and spike-specific neutralizing antibody or T-cell responses post-Ad26.COV2.S boosting. Overall, in the context of hybrid immunity, boosting with heterologous full- or half-dose BNT162b2 mRNA vaccine demonstrated superior immunogenicity 2 weeks post-vaccination compared to homologous Ad26.COV2.S, though rapid waning occurred by 12 weeks post-boost. Trial Registration: The study has been registered to the South African National Clinical Trial Registry (SANCTR): DOH-27-012022-7841 . The approval letter from SANCTR has been provided in the up-loaded documents.\n

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\n \n\n \n \n \n \n \n \n Genetic Factors Contributing to the Pathogenesis of Essential Hypertension in Two African Populations.\n \n \n \n \n\n\n \n Kalideen, K.; Rayner, B.; and Ramesar, R.\n\n\n \n\n\n\n Journal of Personalized Medicine, 14(3): 323. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{kalideen_genetic_2024,\n\ttitle = {Genetic {Factors} {Contributing} to the {Pathogenesis} of {Essential} {Hypertension} in {Two} {African} {Populations}},\n\tvolume = {14},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2075-4426},\n\turl = {https://www.mdpi.com/2075-4426/14/3/323},\n\tdoi = {10.3390/jpm14030323},\n\tabstract = {The African continent has the highest prevalence of hypertension globally, with South Africa reporting the highest prevalence in Southern Africa. While the influence of genetic variability in the pathogenesis of hypertension is well described internationally, limited reports are available for African populations. This study aimed to assess the association of genetic variants and essential hypertension in a cohort of two ethnic South African population groups. Two hundred and seventy-seven hypertensive and one hundred and seventy-six normotensive individuals were genotyped for 78 variants. Genotyping was performed using the Illumina GoldenGate Assay and allele-specific polymerase chain reaction. The association of variants was assessed using the Fisher Exact test under the additive and allelic genetic models, while multivariate logistic regression was used to predict the development of hypertension. Five variants (CYP11B2 rs179998, AGT rs5051 and rs699, AGTR1 rs5186, and ACE rs4646994) were significantly associated with essential hypertension in the cohort under study. Furthermore, AGTR1 rs5186 and AGT rs699 were identified as risk factors for the development of hypertension in both ethnic groups. In two ethnic South African populations, an association was observed between renin–angiotensin–aldosterone system (RAAS)-related genes and the development of hypertension.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Personalized Medicine},\n\tauthor = {Kalideen, Kusha and Rayner, Brian and Ramesar, Raj},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {323},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The injectable contraceptives depot medroxyprogesterone acetate and norethisterone enanthate substantially and differentially decrease testosterone and sex hormone binding globulin levels: A secondary study from the WHICH randomized clinical trial.\n \n \n \n \n\n\n \n Avenant, C.; Singata-Madliki, M.; Bick, A. J.; Africander, D.; Balakrishna, Y.; Storbeck, K.; Moliki, J. M.; Dlamini, S.; Skosana, S.; Smit, J.; Beksinska, M.; Beesham, I.; Seocharan, I.; Batting, J.; Hofmeyr, G. J.; and Hapgood, J. P.\n\n\n \n\n\n\n PLOS ONE, 19(8): e0307736. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{avenant_injectable_2024,\n\ttitle = {The injectable contraceptives depot medroxyprogesterone acetate and norethisterone enanthate substantially and differentially decrease testosterone and sex hormone binding globulin levels: {A} secondary study from the {WHICH} randomized clinical trial},\n\tvolume = {19},\n\tissn = {1932-6203},\n\tshorttitle = {The injectable contraceptives depot medroxyprogesterone acetate and norethisterone enanthate substantially and differentially decrease testosterone and sex hormone binding globulin levels},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0307736},\n\tdoi = {10.1371/journal.pone.0307736},\n\tabstract = {HIV acquisition risk with norethisterone (NET) enanthate (NET-EN) is reportedly less than for depo-medroxyprogesterone acetate intramuscular (DMPA-IM). We investigated the effects of these progestin-only injectable contraceptives on serum testosterone and sex hormone binding globulin (SHBG) levels, since these may play a role in sexual behavior and HIV acquisition. The open-label WHICH clinical trial, conducted at two sites in South Africa from 2018–2019, randomized HIV-negative women aged 18–40 years to 150 mg DMPA-IM 12-weekly (n = 262) or 200 mg NET-EN 8-weekly (n = 259). We measured testosterone by UHPLC-MS/MS and SHBG by immunoassay in matched pairs of serum samples collected at baseline (D0) and at peak serum progestin levels at 25 weeks post initiation (25W) (n = 214–218 pairs). Both contraceptives substantially decreased, from D0 to 25W, the total testosterone [DMPA-IM D0 0.560, 25W 0.423 nmol/L, -24.3\\% (p {\\textless} 0.0001); NET-EN D0 0.551, 25W 0.253 nmol/L, -54.1\\%, (p {\\textless} 0.0001)], SHBG [DMPA-IM D0 45.0, 25W 32.7 nmol/L, -29.8\\% (p {\\textless} 0.0001); NET-EN D0 50.2, 25W 17.6 nmol/L, -65.1\\% (p {\\textless} 0.0001)], and calculated free testosterone levels [DMPA-IM D0 6.87, 25W 5.38 pmol/L, -17.2\\% (p = 0.0371); NET-EN D0 6.00, 25W 3.70, -40.0\\% (p {\\textless} 0.0001)]. After adjusting for change from D0, the total testosterone, SHBG and calculated free testosterone levels were significantly higher for DMPA-IM than NET-EN (64.9\\%, p {\\textless} 0.0001; 101.2\\%, p {\\textless} 0.0001; and 38.0\\%, p = 0.0120, respectively). The substantial and differential decrease in testosterone and SHBG levels does not explain our previous finding of no detected decrease in risky sexual behavior or sexual function for DMPA-IM or NET-EN users from D0 to 25W. Medroxyprogesterone (MPA) and NET are androgenic and are both present in molar excess over testosterone and SHBG concentrations at 25W. Any within or between contraceptive group androgenic effects on behavior in the brain are likely dominated by the androgenic activities of MPA and NET and not by the decreased endogenous testosterone levels. The clinical trial was registered with the Pan African Clinical Trials Registry (PACTR 202009758229976).},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Avenant, Chanel and Singata-Madliki, Mandisa and Bick, Alexis J. and Africander, Donita and Balakrishna, Yusentha and Storbeck, Karl-Heinz and Moliki, Johnson M. and Dlamini, Sigcinile and Skosana, Salndave and Smit, Jenni and Beksinska, Mags and Beesham, Ivana and Seocharan, Ishen and Batting, Joanne and Hofmeyr, George J. and Hapgood, Janet P.},\n\teditor = {Ridzon, Renee},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {e0307736},\n}\n\n\n\n

\n

\n\n\n

\n HIV acquisition risk with norethisterone (NET) enanthate (NET-EN) is reportedly less than for depo-medroxyprogesterone acetate intramuscular (DMPA-IM). We investigated the effects of these progestin-only injectable contraceptives on serum testosterone and sex hormone binding globulin (SHBG) levels, since these may play a role in sexual behavior and HIV acquisition. The open-label WHICH clinical trial, conducted at two sites in South Africa from 2018–2019, randomized HIV-negative women aged 18–40 years to 150 mg DMPA-IM 12-weekly (n = 262) or 200 mg NET-EN 8-weekly (n = 259). We measured testosterone by UHPLC-MS/MS and SHBG by immunoassay in matched pairs of serum samples collected at baseline (D0) and at peak serum progestin levels at 25 weeks post initiation (25W) (n = 214–218 pairs). Both contraceptives substantially decreased, from D0 to 25W, the total testosterone [DMPA-IM D0 0.560, 25W 0.423 nmol/L, -24.3% (p \\textless 0.0001); NET-EN D0 0.551, 25W 0.253 nmol/L, -54.1%, (p \\textless 0.0001)], SHBG [DMPA-IM D0 45.0, 25W 32.7 nmol/L, -29.8% (p \\textless 0.0001); NET-EN D0 50.2, 25W 17.6 nmol/L, -65.1% (p \\textless 0.0001)], and calculated free testosterone levels [DMPA-IM D0 6.87, 25W 5.38 pmol/L, -17.2% (p = 0.0371); NET-EN D0 6.00, 25W 3.70, -40.0% (p \\textless 0.0001)]. After adjusting for change from D0, the total testosterone, SHBG and calculated free testosterone levels were significantly higher for DMPA-IM than NET-EN (64.9%, p \\textless 0.0001; 101.2%, p \\textless 0.0001; and 38.0%, p = 0.0120, respectively). The substantial and differential decrease in testosterone and SHBG levels does not explain our previous finding of no detected decrease in risky sexual behavior or sexual function for DMPA-IM or NET-EN users from D0 to 25W. Medroxyprogesterone (MPA) and NET are androgenic and are both present in molar excess over testosterone and SHBG concentrations at 25W. Any within or between contraceptive group androgenic effects on behavior in the brain are likely dominated by the androgenic activities of MPA and NET and not by the decreased endogenous testosterone levels. The clinical trial was registered with the Pan African Clinical Trials Registry (PACTR 202009758229976).\n

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\n \n\n \n \n \n \n \n \n Discovery of antiplasmodial pyridine carboxamides and thiocarboxamides.\n \n \n \n \n\n\n \n Redway, A.; Spry, C.; Brown, A.; Wiedemann, U.; Fathoni, I.; Garnie, L. F.; Qiu, D.; Egan, T. J.; Lehane, A. M.; Jackson, Y.; Saliba, K. J.; and Downer-Riley, N.\n\n\n \n\n\n\n International Journal for Parasitology: Drugs and Drug Resistance, 25: 100536. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Discovery$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{redway_discovery_2024,\n\ttitle = {Discovery of antiplasmodial pyridine carboxamides and thiocarboxamides},\n\tvolume = {25},\n\tissn = {22113207},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2211320724000174},\n\tdoi = {10.1016/j.ijpddr.2024.100536},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {International Journal for Parasitology: Drugs and Drug Resistance},\n\tauthor = {Redway, Alexa and Spry, Christina and Brown, Ainka and Wiedemann, Ursula and Fathoni, Imam and Garnie, Larnelle F. and Qiu, Deyun and Egan, Timothy J. and Lehane, Adele M. and Jackson, Yvette and Saliba, Kevin J. and Downer-Riley, Nadale},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {100536},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Diagnostic yield as an important metric for the evaluation of novel tuberculosis tests: rationale and guidance for future research.\n \n \n \n \n\n\n \n Broger, T.; Marx, F. M; Theron, G.; Marais, B. J; Nicol, M. P; Kerkhoff, A. D; Nathavitharana, R.; Huerga, H.; Gupta-Wright, A.; Kohli, M.; Nichols, B. E; Muyoyeta, M.; Meintjes, G.; Ruhwald, M.; Peeling, R. W; Pai, N. P.; Pollock, N. R; Pai, M.; Cattamanchi, A.; Dowdy, D. W; Dewan, P.; and Denkinger, C. M\n\n\n \n\n\n\n The Lancet Global Health, 12(7): e1184–e1191. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Diagnostic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{broger_diagnostic_2024,\n\ttitle = {Diagnostic yield as an important metric for the evaluation of novel tuberculosis tests: rationale and guidance for future research},\n\tvolume = {12},\n\tissn = {2214109X},\n\tshorttitle = {Diagnostic yield as an important metric for the evaluation of novel tuberculosis tests},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X24001487},\n\tdoi = {10.1016/S2214-109X(24)00148-7},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Global Health},\n\tauthor = {Broger, Tobias and Marx, Florian M and Theron, Grant and Marais, Ben J and Nicol, Mark P and Kerkhoff, Andrew D and Nathavitharana, Ruvandhi and Huerga, Helena and Gupta-Wright, Ankur and Kohli, Mikashmi and Nichols, Brooke E and Muyoyeta, Monde and Meintjes, Graeme and Ruhwald, Morten and Peeling, Rosanna W and Pai, Nitika Pant and Pollock, Nira R and Pai, Madhukar and Cattamanchi, Adithya and Dowdy, David W and Dewan, Puneet and Denkinger, Claudia M},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {e1184--e1191},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Tuberculosis treatment-shortening.\n \n \n \n \n\n\n \n Singh, V.\n\n\n \n\n\n\n Drug Discovery Today, 29(5): 103955. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Tuberculosis$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{singh_tuberculosis_2024,\n\ttitle = {Tuberculosis treatment-shortening},\n\tvolume = {29},\n\tissn = {13596446},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1359644624000801},\n\tdoi = {10.1016/j.drudis.2024.103955},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-24},\n\tjournal = {Drug Discovery Today},\n\tauthor = {Singh, Vinayak},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {103955},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A systematic efficacy analysis of tuberculosis treatment with \\textlessspan style=\"font-variant:small-caps;\"\\textgreaterBPaL\\textless/span\\textgreater ‐containing regimens using a multiscale modeling approach.\n \n \n \n \n\n\n \n Budak, M.; Via, L. E.; Weiner, D. M.; Barry, C. E.; Nanda, P.; Michael, G.; Mdluli, K.; and Kirschner, D.\n\n\n \n\n\n\n CPT: Pharmacometrics & Systems Pharmacology, 13(4): 673–685. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{budak_systematic_2024,\n\ttitle = {A systematic efficacy analysis of tuberculosis treatment with {\\textless}span style="font-variant:small-caps;"{\\textgreater}{BPaL}{\\textless}/span{\\textgreater} ‐containing regimens using a multiscale modeling approach},\n\tvolume = {13},\n\tissn = {2163-8306, 2163-8306},\n\tshorttitle = {A systematic efficacy analysis of tuberculosis treatment with {\\textless}span style="font-variant},\n\turl = {https://ascpt.onlinelibrary.wiley.com/doi/10.1002/psp4.13117},\n\tdoi = {10.1002/psp4.13117},\n\tabstract = {Abstract \n            Tuberculosis (TB) is a life‐threatening infectious disease. The standard treatment is up to 90\\% effective; however, it requires the administration of four antibiotics (isoniazid, rifampicin, pyrazinamide, and ethambutol [HRZE]) over long time periods. This harsh treatment process causes adherence issues for patients because of the long treatment times and a myriad of adverse effects. Therefore, the World Health Organization has focused goals of shortening standard treatment regimens for TB in their End TB Strategy efforts, which aim to reduce TB‐related deaths by 95\\% by 2035. For this purpose, many novel and promising combination antibiotics are being explored that have recently been discovered, such as the bedaquiline, pretomanid, and linezolid (BPaL) regimen. As a result, testing the number of possible combinations with all possible novel regimens is beyond the limit of experimental resources. In this study, we present a unique framework that uses a primate granuloma modeling approach to screen many combination regimens that are currently under clinical and experimental exploration and assesses their efficacies to inform future studies. We tested well‐studied regimens such as HRZE and BPaL to evaluate the validity and accuracy of our framework. We also simulated additional promising combination regimens that have not been sufficiently studied clinically or experimentally, and we provide a pipeline for regimen ranking based on their efficacies in granulomas. Furthermore, we showed a correlation between simulation rankings and new marmoset data rankings, providing evidence for the credibility of our framework. This framework can be adapted to any TB regimen and can rank any number of single or combination regimens.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {CPT: Pharmacometrics \\& Systems Pharmacology},\n\tauthor = {Budak, Maral and Via, Laura E. and Weiner, Danielle M. and Barry, Clifton E. and Nanda, Pariksheet and Michael, Gabrielle and Mdluli, Khisimuzi and Kirschner, Denise},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {673--685},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n We choose: Adolescent girls and young women’s choice for an HIV prevention product in a cross-over randomized clinical trial conducted in South Africa, Uganda, and Zimbabwe.\n \n \n \n \n\n\n \n Atujuna, M.; Williams, K.; Roberts, S. T.; Young, A.; Browne, E. N.; Mangxilana, N. T.; Tenza, S.; Shapley-Quinn, M. K.; Tauya, T.; Ngure, K.; and Van Der Straten, A.\n\n\n \n\n\n\n PLOS ONE, 19(8): e0308577. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"We$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{atujuna_we_2024,\n\ttitle = {We choose: {Adolescent} girls and young women’s choice for an {HIV} prevention product in a cross-over randomized clinical trial conducted in {South} {Africa}, {Uganda}, and {Zimbabwe}},\n\tvolume = {19},\n\tissn = {1932-6203},\n\tshorttitle = {We choose},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0308577},\n\tdoi = {10.1371/journal.pone.0308577},\n\tabstract = {With new pre-exposure prophylaxis (PrEP) modalities for HIV prevention becoming available, understanding how adolescent girls and young women (AGYW) navigate through PrEP options is essential, including factors underlying their choice. Through 16 focus group discussions (FGDs) and 52 in-depth interviews (IDIs) from REACH, an open-label crossover study in which AGYW were allocated 1:1 (between 06 February 2019 and 18 March 2020) to receive oral PrEP for six months and the dapivirine ring for six months, in a randomized sequence, followed by a 6-month period where either product (or neither) could be chosen, we explored decision-making process and product choice, using a mixed inductive-deductive analytical approach. Key themes included the desire to remain HIV-negative and weighing product attributes through experiential learning. Product triability appeared important in informing product choice as individual circumstances changed or assuaging side effects with a given product. Approved biomedical prevention innovations may also benefit from hands-on experience to help with adoption and use during real-world implementation. Furthermore, support from trusted providers will remain critical as AGYW contemplate navigating through PrEP options and choice.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Atujuna, Millicent and Williams, Kristin and Roberts, Sarah T. and Young, Alinda and Browne, Erica N. and Mangxilana, Nomvuyo T. and Tenza, Siyanda and Shapley-Quinn, Mary Kate and Tauya, Thelma and Ngure, Kenneth and Van Der Straten, Ariane},\n\teditor = {Pulido Tarquino, Ivan Alejandro},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {e0308577},\n}\n\n\n\n

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\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Outcomes of childhood TB in countries with a universal BCG vaccination policy.\n \n \n \n \n\n\n \n Dias, J.; Varandas, L.; Gonçalves, L.; and Kagina, B.\n\n\n \n\n\n\n The International Journal of Tuberculosis and Lung Disease, 28(6): 273–277. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Outcomes$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{dias_outcomes_2024,\n\ttitle = {Outcomes of childhood {TB} in countries with a universal {BCG} vaccination policy},\n\tvolume = {28},\n\tissn = {1027-3719},\n\turl = {https://www.ingentaconnect.com/content/10.5588/ijtld.23.0321},\n\tdoi = {10.5588/ijtld.23.0321},\n\tabstract = {{\\textless}sec id="st1"{\\textgreater}{\\textless}title{\\textgreater}BACKGROUND{\\textless}/title{\\textgreater}TB remains an important cause of childhood morbidity and mortality. Underdiagnosis, underreporting and limited data on the outcomes of childhood TB have led to an underestimation of its impact.{\\textless}/sec{\\textgreater}{\\textless}sec id="st2"{\\textgreater}{\\textless}title{\\textgreater}METHODS{\\textless}/title{\\textgreater}This \n was a systematic review to characterise childhood TB outcomes. Studies reporting relevant epidemiological data on children between 0 and 14 years of age, with a particular focus on treatment outcomes, from countries with universal bacilli Calmette-Guérin (BCG) vaccination and conducted \n between 2000 and 2020 were selected. Random effects meta-analysis was performed in R software.{\\textless}/sec{\\textgreater}{\\textless}sec id="st3"{\\textgreater}{\\textless}title{\\textgreater}RESULTS{\\textless}/title{\\textgreater}We identified 1,806 references and included 35 articles. Among children with TB, the overall proportion of unfavourable outcomes \n was 19.5\\% (95\\% CI 14.4–25.8) and pooled case-fatality ratio was 6.1\\% (95\\% CI 4.3–8.4). The proportion of deaths observed among children between 0 and 4 years old was 6.6\\% (95\\% CI 4.9–8.7) and 4.6\\% (95\\% CI 3.1–6.9) in older children. TB and HIV co-infected children presented \n a case-fatality ratio of 15.1\\% (95\\% CI 7.9–27.0).{\\textless}/sec{\\textgreater}{\\textless}sec id="st4"{\\textgreater}{\\textless}title{\\textgreater}CONCLUSIONS{\\textless}/title{\\textgreater}Despite the efforts made in the last decades, treatment outcomes in childhood TB are still worrisome. Efforts to fill existing gaps and design health policies \n targeting vulnerable populations, such as children, should be intensified to tackle the global TB burden.{\\textless}/sec{\\textgreater}},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {The International Journal of Tuberculosis and Lung Disease},\n\tauthor = {Dias, J.V. and Varandas, L. and Gonçalves, L. and Kagina, B.},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {273--277},\n}\n\n\n\n

\n

\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Major Genetic Drivers of Statin Treatment Response in African Populations and Pharmacogenetics of Dyslipidemia Through a One Health Lens.\n \n \n \n \n\n\n \n Lusiki, Z.; Blom, D.; Soko, N. D.; Malema, S.; Jones, E.; Rayner, B.; Blackburn, J.; Sinxadi, P.; Dandara, M. T.; and Dandara, C.\n\n\n \n\n\n\n OMICS: A Journal of Integrative Biology, 28(6): 261–279. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Major$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{lusiki_major_2024,\n\ttitle = {Major {Genetic} {Drivers} of {Statin} {Treatment} {Response} in {African} {Populations} and {Pharmacogenetics} of {Dyslipidemia} {Through} a {One} {Health} {Lens}},\n\tvolume = {28},\n\tcopyright = {https://www.liebertpub.com/nv/resources-tools/text-and-data-mining-policy/121/},\n\tissn = {1557-8100},\n\turl = {https://www.liebertpub.com/doi/10.1089/omi.2023.0122},\n\tdoi = {10.1089/omi.2023.0122},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {OMICS: A Journal of Integrative Biology},\n\tauthor = {Lusiki, Zizo and Blom, Dirk and Soko, Nyarai D. and Malema, Smangele and Jones, Erika and Rayner, Brian and Blackburn, Jonathan and Sinxadi, Phumla and Dandara, Michelle T. and Dandara, Collet},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {261--279},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Global trends in carbapenem- and difficult-to-treat-resistance among World Health Organization priority bacterial pathogens: ATLAS surveillance program 2018–2022.\n \n \n \n \n\n\n \n Wise, M. G.; Karlowsky, J. A.; Mohamed, N.; Hermsen, E. D.; Kamat, S.; Townsend, A.; Brink, A.; Soriano, A.; Paterson, D. L.; Moore, L. S.; and Sahm, D. F.\n\n\n \n\n\n\n Journal of Global Antimicrobial Resistance, 37: 168–175. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Global$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{wise_global_2024,\n\ttitle = {Global trends in carbapenem- and difficult-to-treat-resistance among {World} {Health} {Organization} priority bacterial pathogens: {ATLAS} surveillance program 2018–2022},\n\tvolume = {37},\n\tissn = {22137165},\n\tshorttitle = {Global trends in carbapenem- and difficult-to-treat-resistance among {World} {Health} {Organization} priority bacterial pathogens},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2213716524000729},\n\tdoi = {10.1016/j.jgar.2024.03.020},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Global Antimicrobial Resistance},\n\tauthor = {Wise, Mark G. and Karlowsky, James A. and Mohamed, Naglaa and Hermsen, Elizabeth D. and Kamat, Shweta and Townsend, Andy and Brink, Adrian and Soriano, Alex and Paterson, David L. and Moore, Luke S.P. and Sahm, Daniel F.},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {168--175},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Ongoing Implementation and Prospective Validation of Artificial Intelligence/Machine Learning Tools at an African Drug Discovery Center.\n \n \n \n \n\n\n \n Hlozek, J.; Chibale, K.; and Woodland, J. G.\n\n\n \n\n\n\n ACS Medicinal Chemistry Letters, 15(7): 989–993. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Ongoing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{hlozek_ongoing_2024,\n\ttitle = {Ongoing {Implementation} and {Prospective} {Validation} of {Artificial} {Intelligence}/{Machine} {Learning} {Tools} at an {African} {Drug} {Discovery} {Center}},\n\tvolume = {15},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1948-5875, 1948-5875},\n\turl = {https://pubs.acs.org/doi/10.1021/acsmedchemlett.4c00243},\n\tdoi = {10.1021/acsmedchemlett.4c00243},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {ACS Medicinal Chemistry Letters},\n\tauthor = {Hlozek, Jason and Chibale, Kelly and Woodland, John G.},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {989--993},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Integrated plasma proteomics identifies tuberculosis-specific diagnostic biomarkers.\n \n \n \n \n\n\n \n Schiff, H. F.; Walker, N. F.; Ugarte-Gil, C.; Tebruegge, M.; Manousopoulou, A.; Garbis, S. D.; Mansour, S.; Wong, P. H.; Rockett, G.; Piazza, P.; Niranjan, M.; Vallejo, A. F.; Woelk, C. H.; Wilkinson, R. J.; Tezera, L. B.; Garay-Baquero, D.; and Elkington, P.\n\n\n \n\n\n\n JCI Insight. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Integrated$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{schiff_integrated_2024,\n\ttitle = {Integrated plasma proteomics identifies tuberculosis-specific diagnostic biomarkers},\n\tcopyright = {http://creativecommons.org/licenses/by/4.0/},\n\tissn = {2379-3708},\n\turl = {http://insight.jci.org/articles/view/173273},\n\tdoi = {10.1172/jci.insight.173273},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {JCI Insight},\n\tauthor = {Schiff, Hannah F. and Walker, Naomi F. and Ugarte-Gil, Cesar and Tebruegge, Marc and Manousopoulou, Antigoni and Garbis, Spiros D. and Mansour, Salah and Wong, Pak Ho and Rockett, Gabrielle and Piazza, Paolo and Niranjan, Mahesan and Vallejo, Andres F. and Woelk, Christopher H. and Wilkinson, Robert J. and Tezera, Liku B. and Garay-Baquero, Diana and Elkington, Paul},\n\tmonth = mar,\n\tyear = {2024},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n A Nanopore Sequencing-based Pharmacogenomic Panel to Personalize Tuberculosis Drug Dosing.\n \n \n \n \n\n\n \n Verma, R.; Da Silva, K. E.; Rockwood, N.; Wasmann, R. E.; Yende, N.; Song, T.; Kim, E.; Denti, P.; Wilkinson, R. J.; and Andrews, J. R.\n\n\n \n\n\n\n American Journal of Respiratory and Critical Care Medicine, 209(12): 1486–1496. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{verma_nanopore_2024,\n\ttitle = {A {Nanopore} {Sequencing}-based {Pharmacogenomic} {Panel} to {Personalize} {Tuberculosis} {Drug} {Dosing}},\n\tvolume = {209},\n\tissn = {1073-449X, 1535-4970},\n\turl = {https://www.atsjournals.org/doi/10.1164/rccm.202309-1583OC},\n\tdoi = {10.1164/rccm.202309-1583OC},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {American Journal of Respiratory and Critical Care Medicine},\n\tauthor = {Verma, Renu and Da Silva, Kesia Esther and Rockwood, Neesha and Wasmann, Roeland E. and Yende, Nombuso and Song, Taeksun and Kim, Eugene and Denti, Paolo and Wilkinson, Robert J. and Andrews, Jason R.},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {1486--1496},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Reduced anti-viral IgG repertoire in HIV-exposed but uninfected infants compared to HIV-unexposed infants.\n \n \n \n \n\n\n \n Gachogo, R.; Happel, A.; Alinde, B.; Gray, C. M.; Jaspan, H.; and Dzanibe, S.\n\n\n \n\n\n\n iScience, 27(7): 110282. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Reduced$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{gachogo_reduced_2024,\n\ttitle = {Reduced anti-viral {IgG} repertoire in {HIV}-exposed but uninfected infants compared to {HIV}-unexposed infants},\n\tvolume = {27},\n\tissn = {25890042},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2589004224015074},\n\tdoi = {10.1016/j.isci.2024.110282},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {iScience},\n\tauthor = {Gachogo, Rachael and Happel, Anna-Ursula and Alinde, Berenice and Gray, Clive M. and Jaspan, Heather and Dzanibe, Sonwabile},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {110282},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Revealed masks: Facial mimicry after oxytocin administration in forensic psychopathic patients.\n \n \n \n \n\n\n \n Rijnders, R. J.; Van Boxtel, A.; De Wied, M.; Van Honk, J.; Kempes, M. M.; and Bos, P. A.\n\n\n \n\n\n\n Journal of Psychiatric Research, 176: 422–429. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Revealed$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{rijnders_revealed_2024,\n\ttitle = {Revealed masks: {Facial} mimicry after oxytocin administration in forensic psychopathic patients},\n\tvolume = {176},\n\tissn = {00223956},\n\tshorttitle = {Revealed masks},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0022395624003595},\n\tdoi = {10.1016/j.jpsychires.2024.06.032},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Psychiatric Research},\n\tauthor = {Rijnders, Ronald J.P. and Van Boxtel, Anton and De Wied, Minet and Van Honk, Jack and Kempes, Maaike M. and Bos, Peter A.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {422--429},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Rifabutin central nervous system concentrations in a rabbit model of tuberculous meningitis.\n \n \n \n \n\n\n \n Wasserman, S.; Antilus-Sainte, R.; Abdelgawad, N.; Odjourian, N. M.; Cristaldo, M.; Dougher, M.; Kaya, F.; Zimmerman, M.; Denti, P.; and Gengenbacher, M.\n\n\n \n\n\n\n Antimicrobial Agents and Chemotherapy, 68(8): e00783–24. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Rifabutin$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{wasserman_rifabutin_2024,\n\ttitle = {Rifabutin central nervous system concentrations in a rabbit model of tuberculous meningitis},\n\tvolume = {68},\n\tissn = {0066-4804, 1098-6596},\n\turl = {https://journals.asm.org/doi/10.1128/aac.00783-24},\n\tdoi = {10.1128/aac.00783-24},\n\tabstract = {ABSTRACT \n             \n               \n              Tuberculous meningitis (TBM) has a high mortality, possibly due to suboptimal therapy. Drug exposure data of antituberculosis agents in the central nervous system (CNS) are required to develop more effective regimens. Rifabutin is a rifamycin equivalently potent to rifampin in human pulmonary tuberculosis. Here, we show that human-equivalent doses of rifabutin achieved potentially therapeutic exposure in relevant CNS tissues in a rabbit model of TBM, supporting further evaluation in clinical trials.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {Antimicrobial Agents and Chemotherapy},\n\tauthor = {Wasserman, Sean and Antilus-Sainte, Rosleine and Abdelgawad, Noha and Odjourian, Narineh M. and Cristaldo, Melissa and Dougher, Maureen and Kaya, Firat and Zimmerman, Matthew and Denti, Paolo and Gengenbacher, Martin},\n\teditor = {Silverman, Jared A.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {e00783--24},\n}\n\n\n\n

\n

\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Temporary increase in circulating replication-competent latent HIV-infected resting CD4+ T cells after switch to an integrase inhibitor based antiretroviral regimen.\n \n \n \n \n\n\n \n Ferreira, R.; Reynolds, S. J.; Capoferri, A. A.; Baker, O. R.; Brown, E. E.; Klock, E.; Miller, J.; Lai, J.; Saraf, S.; Kirby, C.; Lynch, B.; Hackman, J.; Gowanlock, S. N.; Tomusange, S.; Jamiru, S.; Anok, A.; Kityamuweesi, T.; Buule, P.; Bruno, D.; Martens, C.; Rose, R.; Lamers, S. L.; Galiwango, R. M.; Poon, A. F.; Quinn, T. C.; Prodger, J. L.; and Redd, A. D.\n\n\n \n\n\n\n eBioMedicine, 102: 105040. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Temporary$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{ferreira_temporary_2024,\n\ttitle = {Temporary increase in circulating replication-competent latent {HIV}-infected resting {CD4}+ {T} cells after switch to an integrase inhibitor based antiretroviral regimen},\n\tvolume = {102},\n\tissn = {23523964},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352396424000756},\n\tdoi = {10.1016/j.ebiom.2024.105040},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {eBioMedicine},\n\tauthor = {Ferreira, Roux-Cil and Reynolds, Steven J. and Capoferri, Adam A. and Baker, Owen R. and Brown, Erin E. and Klock, Ethan and Miller, Jernelle and Lai, Jun and Saraf, Sharada and Kirby, Charles and Lynch, Briana and Hackman, Jada and Gowanlock, Sarah N. and Tomusange, Stephen and Jamiru, Samiri and Anok, Aggrey and Kityamuweesi, Taddeo and Buule, Paul and Bruno, Daniel and Martens, Craig and Rose, Rebecca and Lamers, Susanna L. and Galiwango, Ronald M. and Poon, Art F.Y. and Quinn, Thomas C. and Prodger, Jessica L. and Redd, Andrew D.},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {105040},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Changes in access to viral load testing, incidence rates of viral load suppression and rebound following the introduction of the ‘universal test and treat’ guidelines in Cameroon: A retrospective follow-up analysis.\n \n \n \n \n\n\n \n Bekolo, C. E.; Ndeso, S. A.; Moifo, L. L.; Mangala, N.; Ateudjieu, J.; Kouanfack, C.; Dzudie, A.; Thienemann, F.; Tendongfor, N.; Nsagha, D. S.; and Choukem, S. P.\n\n\n \n\n\n\n PLOS Global Public Health, 4(4): e0003042. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Changes$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{bekolo_changes_2024,\n\ttitle = {Changes in access to viral load testing, incidence rates of viral load suppression and rebound following the introduction of the ‘universal test and treat’ guidelines in {Cameroon}: {A} retrospective follow-up analysis},\n\tvolume = {4},\n\tissn = {2767-3375},\n\tshorttitle = {Changes in access to viral load testing, incidence rates of viral load suppression and rebound following the introduction of the ‘universal test and treat’ guidelines in {Cameroon}},\n\turl = {https://dx.plos.org/10.1371/journal.pgph.0003042},\n\tdoi = {10.1371/journal.pgph.0003042},\n\tabstract = {Cameroon adopted and started implementing in 2016, the ‘universal test and treat’ (UTT) guidelines to fast-track progress towards the 95-95-95 ambitious targets to end the HIV epidemic. Achieving the third 95 (viral load suppression) is the most desirable target in HIV care. We aimed to evaluate the effectiveness of this novel approach on access to viral load testing (VLT), viral suppression (VLS), and viral load rebound (VLR). A retrospective cohort study was conducted at The Nkongsamba Regional Hospital to compare VLT outcomes between the pre-UTT (2002 to 2015) and the post-UTT (2016 to 2020) periods. We used a data extraction form to collect routine data on adult patients living with HIV. We measured uptake levels of the first and serial VLT and compared the incidence rates of VLS (VL{\\textless}1000 copies/ml) and viral load rebound (VLR) before and after introducing the UTT approach using Kaplan Meier plots and log-rank tests. Cox regression was used to screen for factors independently associated with VLS and VLR events between the guideline periods. Access to initial VLT increased significantly from 6.11\\% to 25.56\\% at 6 months and from 12.00\\% to 73.75\\% at 12 months before and after introducing the UTT guidelines respectively. After a total observation time at risk of 17001.63 person-months, the UTT group achieved an incidence rate of 90.36 VLS per 1000 person-months, four-fold higher than the 21.71 VLS per 1000 person-months observed in the pre-UTT group (p{\\textless}0.0001). After adjusting for confounding, the VLS rate was about 6-fold higher in the UTT group than in the pre-UTT group (adjusted Hazard Rate (aHR) = 5.81 (95\\% confidence interval (95\\%CI): 4.43–7.60). The incidence of VLR increased from 12.60 (95\\%CI: 9.50–16.72) to 19.11 (95\\%CI: 14.22–25.67) per 1000 person-months before and after the introduction of UTT guidelines respectively. After adjusting, VLR was more than twice as high in the UTT group than in the pre-UTT group (aHR = 2.32, 95\\%CI: 1.30–4.13). Increased access to initial VLT and higher rates of VLS have been observed but there are concerns that the suppressed viral load may not be durable since the introduction of the UTT policy in this setting.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Global Public Health},\n\tauthor = {Bekolo, C. E. and Ndeso, S. A. and Moifo, L. L. and Mangala, N. and Ateudjieu, J. and Kouanfack, C. and Dzudie, A. and Thienemann, F. and Tendongfor, N. and Nsagha, D. S. and Choukem, S. P.},\n\teditor = {Fatokun, Omotayo},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {e0003042},\n}\n\n\n\n

\n

\n\n\n

\n Cameroon adopted and started implementing in 2016, the ‘universal test and treat’ (UTT) guidelines to fast-track progress towards the 95-95-95 ambitious targets to end the HIV epidemic. Achieving the third 95 (viral load suppression) is the most desirable target in HIV care. We aimed to evaluate the effectiveness of this novel approach on access to viral load testing (VLT), viral suppression (VLS), and viral load rebound (VLR). A retrospective cohort study was conducted at The Nkongsamba Regional Hospital to compare VLT outcomes between the pre-UTT (2002 to 2015) and the post-UTT (2016 to 2020) periods. We used a data extraction form to collect routine data on adult patients living with HIV. We measured uptake levels of the first and serial VLT and compared the incidence rates of VLS (VL\\textless1000 copies/ml) and viral load rebound (VLR) before and after introducing the UTT approach using Kaplan Meier plots and log-rank tests. Cox regression was used to screen for factors independently associated with VLS and VLR events between the guideline periods. Access to initial VLT increased significantly from 6.11% to 25.56% at 6 months and from 12.00% to 73.75% at 12 months before and after introducing the UTT guidelines respectively. After a total observation time at risk of 17001.63 person-months, the UTT group achieved an incidence rate of 90.36 VLS per 1000 person-months, four-fold higher than the 21.71 VLS per 1000 person-months observed in the pre-UTT group (p\\textless0.0001). After adjusting for confounding, the VLS rate was about 6-fold higher in the UTT group than in the pre-UTT group (adjusted Hazard Rate (aHR) = 5.81 (95% confidence interval (95%CI): 4.43–7.60). The incidence of VLR increased from 12.60 (95%CI: 9.50–16.72) to 19.11 (95%CI: 14.22–25.67) per 1000 person-months before and after the introduction of UTT guidelines respectively. After adjusting, VLR was more than twice as high in the UTT group than in the pre-UTT group (aHR = 2.32, 95%CI: 1.30–4.13). Increased access to initial VLT and higher rates of VLS have been observed but there are concerns that the suppressed viral load may not be durable since the introduction of the UTT policy in this setting.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Prostate Cancer Diagnosis Rates among Insured Men with and without HIV in South Africa: A Cohort Study.\n \n \n \n \n\n\n \n Ruffieux, Y.; Fernández Villalobos, N. V.; Didden, C.; Haas, A. D.; Chinogurei, C.; Cornell, M.; Egger, M.; Maartens, G.; Folb, N.; and Rohner, E.\n\n\n \n\n\n\n Cancer Epidemiology, Biomarkers & Prevention, 33(8): 1057–1064. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Prostate$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{ruffieux_prostate_2024,\n\ttitle = {Prostate {Cancer} {Diagnosis} {Rates} among {Insured} {Men} with and without {HIV} in {South} {Africa}: {A} {Cohort} {Study}},\n\tvolume = {33},\n\tissn = {1055-9965, 1538-7755},\n\tshorttitle = {Prostate {Cancer} {Diagnosis} {Rates} among {Insured} {Men} with and without {HIV} in {South} {Africa}},\n\turl = {https://aacrjournals.org/cebp/article/33/8/1057/746521/Prostate-Cancer-Diagnosis-Rates-among-Insured-Men},\n\tdoi = {10.1158/1055-9965.EPI-24-0137},\n\tabstract = {Abstract \n             \n              Background: \n              Several studies have found lower prostate cancer diagnosis rates among men with human immunodeficiency virus (HIV; MWH) than men without HIV but reasons for this finding remain unclear. \n             \n             \n              Methods: \n              We used claims data from a South African private medical insurance scheme (July 2017– July 2020) to assess prostate cancer diagnosis rates among men aged ≥ 18 years with and without HIV. Using flexible parametric survival models, we estimated hazard ratios (HR) for the association between HIV and incident prostate cancer diagnoses. We accounted for potential confounding by age, population group, and sexually transmitted infections (confounder-adjusted model) and additionally for potential mediation by prostatitis diagnoses, prostate-specific antigen testing, and prostate biopsies (fully adjusted model). \n             \n             \n              Results: \n              We included 288,194 men, of whom 20,074 (7\\%) were living with HIV. Prostate cancer was diagnosed in 1,614 men without HIV (median age at diagnosis: 67 years) and in 82 MWH (median age at diagnosis: 60 years). In the unadjusted analysis, prostate cancer diagnosis rates were 35\\% lower among MWH than men without HIV [HR, 0.65; 95\\% confidence interval (CI), 0.52–0.82]. However, this association was no longer evident in the confounder-adjusted model (HR, 1.03; 95\\% CI, 0.82–1.30) or in the fully adjusted model (HR, 1.14; 95\\% CI, 0.91–1.44). \n             \n             \n              Conclusions: \n              When accounting for potential confounders and mediators, our analysis found no evidence of lower prostate cancer diagnosis rates among MWH than men without HIV in South Africa. \n             \n             \n              Impact: \n              Our results do not support the hypothesis that HIV decreases the risk of prostate cancer.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {Cancer Epidemiology, Biomarkers \\& Prevention},\n\tauthor = {Ruffieux, Yann and Fernández Villalobos, Nathalie V. and Didden, Christiane and Haas, Andreas D. and Chinogurei, Chido and Cornell, Morna and Egger, Matthias and Maartens, Gary and Folb, Naomi and Rohner, Eliane},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {1057--1064},\n}\n\n\n\n

\n

\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Structural Biology in Drug Discovery and Development: Call for Papers.\n \n \n \n \n\n\n \n Heppner, D. E.; Bigi-Botterill, S. V.; Riley, A. P.; Chibale, K.; and Lindsley, C. W.\n\n\n \n\n\n\n Journal of Medicinal Chemistry, 67(15): 12461–12462. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Structural$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{heppner_structural_2024,\n\ttitle = {Structural {Biology} in {Drug} {Discovery} and {Development}: {Call} for {Papers}},\n\tvolume = {67},\n\tcopyright = {https://doi.org/10.15223/policy-001},\n\tissn = {0022-2623, 1520-4804},\n\tshorttitle = {Structural {Biology} in {Drug} {Discovery} and {Development}},\n\turl = {https://pubs.acs.org/doi/10.1021/acs.jmedchem.4c01492},\n\tdoi = {10.1021/acs.jmedchem.4c01492},\n\tlanguage = {en},\n\tnumber = {15},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Medicinal Chemistry},\n\tauthor = {Heppner, David E. and Bigi-Botterill, Simone V. and Riley, Andrew P. and Chibale, Kelly and Lindsley, Craig W.},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {12461--12462},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Building momentum through networks: Bioimaging across the Americas.\n \n \n \n \n\n\n \n De Niz, M.; Escobedo García, R.; Terán Ramirez, C.; Pakowski, Y.; Abonza, Y.; Bialy, N.; Orr, V. L.; Olivera, A.; Abonza, V.; Alleva, K.; Allodi, S.; Almeida, M. F.; Becerril Cuevas, A. R.; Bonnet, F.; Burgos Solorio, A.; Chew, T.; Chiabrando, G.; Cimini, B.; Cleret‐Buhot, A.; Contreras Jiménez, G.; Daza, L.; De Sá, V.; De Val, N.; Delgado‐Álvarez, D. L.; Eliceiri, K.; Fiolka, R.; Grecco, H.; Hanein, D.; Hernández Herrera, P.; Hockberger, P.; Hernandez, H. O.; Hernandez Guadarrama, Y.; Itano, M.; Jacobs, C. A.; Jiménez‐García, L. F.; Jiménez Sabinina, V.; Kamaid, A.; Keppler, A.; Kumar, A.; Lacoste, J.; Lovy, A.; Luby‐Phelps, K.; Mahadevan‐Jansen, A.; Malacrida, L.; Mehta, S. B.; Miller, C.; Miranda, K.; Moore, J. A.; North, A.; O'Toole, P.; Olivares Urbano, M.; Pietrasanta, L. I.; Portugal, R. V.; Rossi, A. H.; Sanchez Contreras, J.; Strambio‐De‐Castilla, C.; Soldevila, G.; Vale, B.; Vazquez, D.; Wood, C.; Brown, C. M.; and Guerrero, A.\n\n\n \n\n\n\n Journal of Microscopy, 294(3): 420–439. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Building$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{de_niz_building_2024,\n\ttitle = {Building momentum through networks: {Bioimaging} across the {Americas}},\n\tvolume = {294},\n\tissn = {0022-2720, 1365-2818},\n\tshorttitle = {Building momentum through networks},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/jmi.13318},\n\tdoi = {10.1111/jmi.13318},\n\tabstract = {Abstract \n            In September 2023, the two largest bioimaging networks in the Americas, Latin America Bioimaging (LABI) and BioImaging North America (BINA), came together during a 1‐week meeting in Mexico. This meeting provided opportunities for participants to interact closely with decision‐makers from imaging core facilities across the Americas. The meeting was held in a hybrid format and attended in‐person by imaging scientists from across the Americas, including Canada, the United States, Mexico, Colombia, Peru, Argentina, Chile, Brazil and Uruguay. The aims of the meeting were to discuss progress achieved over the past year, to foster networking and collaborative efforts among members of both communities, to bring together key members of the international imaging community to promote the exchange of experience and expertise, to engage with industry partners, and to establish future directions within each individual network, as well as common goals. This meeting report summarises the discussions exchanged, the achievements shared, and the goals set during the LABIxBINA2023: Bioimaging across the Americas meeting.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Microscopy},\n\tauthor = {De Niz, Mariana and Escobedo García, Rodrigo and Terán Ramirez, Celina and Pakowski, Ysa and Abonza, Yuriney and Bialy, Nikki and Orr, Vanessa L. and Olivera, Andres and Abonza, Victor and Alleva, Karina and Allodi, Silvana and Almeida, Michael F. and Becerril Cuevas, Alexis Ricardo and Bonnet, Frederic and Burgos Solorio, Armando and Chew, Teng‐Leong and Chiabrando, Gustavo and Cimini, Beth and Cleret‐Buhot, Aurélie and Contreras Jiménez, Gastón and Daza, Laura and De Sá, Vanessa and De Val, Natalia and Delgado‐Álvarez, Diego L. and Eliceiri, Kevin and Fiolka, Reto and Grecco, Hernan and Hanein, Dorit and Hernández Herrera, Paúl and Hockberger, Phil and Hernandez, Haydee O. and Hernandez Guadarrama, Yael and Itano, Michelle and Jacobs, Caron A. and Jiménez‐García, Luis F. and Jiménez Sabinina, Vilma and Kamaid, Andres and Keppler, Antje and Kumar, Abhishek and Lacoste, Judith and Lovy, Alenka and Luby‐Phelps, Kate and Mahadevan‐Jansen, Anita and Malacrida, Leonel and Mehta, Shalin B. and Miller, Caroline and Miranda, Kildare and Moore, Joshua A. and North, Alison and O'Toole, Peter and Olivares Urbano, Mariana and Pietrasanta, Lía I. and Portugal, Rodrigo V. and Rossi, Andrés H. and Sanchez Contreras, Jonathan and Strambio‐De‐Castilla, Caterina and Soldevila, Gloria and Vale, Bruno and Vazquez, Diana and Wood, Chris and Brown, Claire M. and Guerrero, Adan},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {420--439},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Characterization of antimalarial activity of artemisinin-based hybrid drugs.\n \n \n \n \n\n\n \n Quadros, H. C.; Herrmann, L.; Manaranche, J.; Paloque, L.; Borges-Silva, M. C.; Dziwornu, G. A.; D'Alessandro, S.; Chibale, K.; Basilico, N.; Benoit-Vical, F.; Tsogoeva, S. B.; and Moreira, D. R. M.\n\n\n \n\n\n\n Antimicrobial Agents and Chemotherapy, 68(7): e00143–24. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Characterization$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{quadros_characterization_2024,\n\ttitle = {Characterization of antimalarial activity of artemisinin-based hybrid drugs},\n\tvolume = {68},\n\tissn = {0066-4804, 1098-6596},\n\turl = {https://journals.asm.org/doi/10.1128/aac.00143-24},\n\tdoi = {10.1128/aac.00143-24},\n\tabstract = {ABSTRACT \n             \n               \n               \n                In response to the spread of artemisinin (ART) resistance, ART-based hybrid drugs were developed, and their activity profile was characterized against drug-sensitive and drug-resistant \n                Plasmodium falciparum \n                parasites. Two hybrids were found to display parasite growth reduction, stage-specificity, speed of activity, additivity of activity in drug combinations, and stability in hepatic microsomes of similar levels to those displayed by dihydroartemisinin (DHA). Conversely, the rate of chemical homolysis of the peroxide bonds is slower in hybrids than in DHA. From a mechanistic perspective, heme plays a central role in the chemical homolysis of peroxide, inhibiting heme detoxification and disrupting parasite heme redox homeostasis. The hybrid exhibiting slow homolysis of peroxide bonds was more potent in reducing the viability of ART-resistant parasites in a ring-stage survival assay than the hybrid exhibiting fast homolysis. However, both hybrids showed limited activity against ART-induced quiescent parasites in the quiescent-stage survival assay. Our findings are consistent with previous results showing that slow homolysis of peroxide-containing drugs may retain activity against proliferating ART-resistant parasites. However, our data suggest that this property does not overcome the limited activity of peroxides in killing non-proliferating parasites in a quiescent state.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2025-06-24},\n\tjournal = {Antimicrobial Agents and Chemotherapy},\n\tauthor = {Quadros, Helenita Costa and Herrmann, Lars and Manaranche, Jeanne and Paloque, Lucie and Borges-Silva, Mariana C. and Dziwornu, Godwin Akpeko and D'Alessandro, Sarah and Chibale, Kelly and Basilico, Nicoletta and Benoit-Vical, Françoise and Tsogoeva, Svetlana B. and Moreira, Diogo Rodrigo M.},\n\teditor = {Odom John, Audrey},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {e00143--24},\n}\n\n\n\n

\n

\n\n\n\n\n\n

\n \n\n \n \n \n \n \n \n Region-wide assessment of National Immunization Technical Advisory Groups (NITAGs) using the NITAG Maturity Assessment Tool (NMAT) – Experience from the Eastern Mediterranean Region of the World Health Organization, 2023.\n \n \n \n \n\n\n \n Sume, G. E.; Hasan, Q.; Shefer, A.; Henaff, L.; Cavallaro, K. F.; Tencza, C. B.; Hadler, S. C.; Sidy, N.; Sardar, P.; Kagina, B. M.; and Hutin, Y.\n\n\n \n\n\n\n Vaccine, 42(9): 2239–2245. April 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Region-wide$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{sume_region-wide_2024,\n\ttitle = {Region-wide assessment of {National} {Immunization} {Technical} {Advisory} {Groups} ({NITAGs}) using the {NITAG} {Maturity} {Assessment} {Tool} ({NMAT}) – {Experience} from the {Eastern} {Mediterranean} {Region} of the {World} {Health} {Organization}, 2023},\n\tvolume = {42},\n\tissn = {0264410X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0264410X24002172},\n\tdoi = {10.1016/j.vaccine.2024.02.058},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {Vaccine},\n\tauthor = {Sume, Gerald Etapelong and Hasan, Quamrul and Shefer, Abigail and Henaff, Louise and Cavallaro, Kathleen F. and Tencza, Catherine B. and Hadler, Stephen C. and Sidy, Ndiaye and Sardar, Parwiz and Kagina, Benjamin M. and Hutin, Yvan},\n\tmonth = apr,\n\tyear = {2024},\n\tpages = {2239--2245},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Precision ophthalmology: a call for Africa not to be left in the dark.\n \n \n \n \n\n\n \n Roberts, L.\n\n\n \n\n\n\n Gene Therapy, 31(5-6): 199–201. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Precision$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{roberts_precision_2024,\n\ttitle = {Precision ophthalmology: a call for {Africa} not to be left in the dark},\n\tvolume = {31},\n\tissn = {0969-7128, 1476-5462},\n\tshorttitle = {Precision ophthalmology},\n\turl = {https://www.nature.com/articles/s41434-024-00448-y},\n\tdoi = {10.1038/s41434-024-00448-y},\n\tlanguage = {en},\n\tnumber = {5-6},\n\turldate = {2025-06-24},\n\tjournal = {Gene Therapy},\n\tauthor = {Roberts, Lisa},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {199--201},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Carbapenem-resistant Klebsiella pneumoniae among hospitalized patients in Cape Town, South Africa: molecular epidemiology and characterization.\n \n \n \n \n\n\n \n Marais, G.; Moodley, C.; Claassen-Weitz, S.; Patel, F.; Prentice, E.; Tootla, H.; Nyakutira, N.; Lennard, K.; Reddy, K.; Bamford, C.; Niehaus, A.; Whitelaw, A.; Brink, A.; Cape Town Antimicrobial Stewardship Study Alliance; Page, C.; Schoeman, E.; De Klerk, E.; Lategan, K.; Pienaar, K.; Henning, L.; Du Plessis, M.; Maseko, N.; Nel, S.; Narainsamy, M.; Vermeulen, M.; Du Toit, N.; Van Heerden, T.; Sitharam, L.; Barendse, A.; Nagel, D.; Prince, J.; Vass, L.; Strauss, R.; Fakier, R.; Samuel, C.; Van Zyl, M.; Isaacs, L.; Hendricks, S.; Dodd, A.; Daniels, R.; Zemanay, W.; Van Heerden, J.; Hapeela, N.; Brown, P.; Daniels, Z.; Vasuthevan, S.; Scott, E.; Ricks, E.; Curle, P.; and Wojno, J.\n\n\n \n\n\n\n JAC-Antimicrobial Resistance, 6(2): dlae050. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Carbapenem-resistant$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{marais_carbapenem-resistant_2024,\n\ttitle = {Carbapenem-resistant \\textit{{Klebsiella} pneumoniae} among hospitalized patients in {Cape} {Town}, {South} {Africa}: molecular epidemiology and characterization},\n\tvolume = {6},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2632-1823},\n\tshorttitle = {Carbapenem-resistant \\textit{{Klebsiella} pneumoniae} among hospitalized patients in {Cape} {Town}, {South} {Africa}},\n\turl = {https://academic.oup.com/jacamr/article/doi/10.1093/jacamr/dlae050/7634687},\n\tdoi = {10.1093/jacamr/dlae050},\n\tabstract = {Abstract \n             \n              Background \n              The molecular epidemiology of carbapenem-resistant Enterobacterales in Cape Town remains largely unknown. \n             \n             \n              Objectives \n              This study aimed to describe the molecular epidemiology, resistome, virulome and mobilome of carbapenem-resistant Klebsiella pneumoniae (CRKP) within Cape Town to guide therapy, antimicrobial stewardship and infection prevention and control practices. \n             \n             \n              Methods \n              Eighty-five CRKP isolates from hospitalized patients underwent WGS as part of a prospective, multicentre, cross-sectional study, conducted between 1 November 2020 and 30 November 2022, across public-sector and private-sector hospitals in Cape Town, South Africa. \n             \n             \n              Results \n              MLST revealed three novel types, ST6785, ST6786 and ST6787, while the most common were ST219, ST307, ST17, ST13 and ST2497. Different predominant clones were noted in each hospital. The most common carbapenemase gene was blaOXA-48-like, detected in 71\\% of isolates, with blaNDM detected in 5\\%. Notably, co-detection of two carbapenemase genes (blaOXA-48-like and blaNDM) occurred in 13\\% of isolates. The yersiniabactin siderophore was detected in 73\\% of isolates, and was most commonly associated with the ICEKp5 mobile element. All carbapenemases were located on plasmids. The genes blaOXA-181 and blaOXA-232 colocalized with a ColKP3 replicon type on assembled contigs in 83\\% and 100\\% of cases, respectively. \n             \n             \n              Conclusions \n              CRKP epidemiology in Cape Town reflects institutionally dominant, rather than regional, clones. The most prevalent carbapenemase gene was blaOXA-48-like, in keeping with CRKP epidemiology in South Africa in general. Emerging clones harbouring both blaOXA-48-like and blaNDM, such as ST17, ST2497 and the novel ST6787, are a concern due to the limited availability of appropriate antimicrobial agents in South Africa.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2025-06-24},\n\tjournal = {JAC-Antimicrobial Resistance},\n\tauthor = {Marais, Gert and Moodley, Clinton and Claassen-Weitz, Shantelle and Patel, Fadheela and Prentice, Elizabeth and Tootla, Hafsah and Nyakutira, Nyasha and Lennard, Katie and Reddy, Kessendri and Bamford, Colleen and Niehaus, Abraham and Whitelaw, Andrew and Brink, Adrian and {Cape Town Antimicrobial Stewardship Study Alliance} and Page, Claudine and Schoeman, Elizabeth and De Klerk, Elizma and Lategan, Karin and Pienaar, Karlien and Henning, Liezl and Du Plessis, Mandy and Maseko, Nomfundo and Nel, Salome and Narainsamy, Melenie and Vermeulen, Michelle and Du Toit, Narissa and Van Heerden, Teresa and Sitharam, Liza and Barendse, Asa and Nagel, Dane and Prince, Jacqueline and Vass, Letitia and Strauss, Rileen and Fakier, Rushana and Samuel, Catherine and Van Zyl, Marelieze and Isaacs, Leigh-Ann and Hendricks, Shareefa and Dodd, Amy and Daniels, Reecka and Zemanay, Widaad and Van Heerden, Judi and Hapeela, Nchimunya and Brown, Parveen and Daniels, Zubayr and Vasuthevan, Sharon and Scott, Enid and Ricks, Esmeralda and Curle, Patricia and Wojno, Justyna},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {dlae050},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Forging a Future Free from Neglected Tropical Diseases.\n \n \n \n \n\n\n \n Da Silva Emery, F.; and Chibale, K.\n\n\n \n\n\n\n ACS Medicinal Chemistry Letters, 15(3): 314–315. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Forging$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{da_silva_emery_forging_2024,\n\ttitle = {Forging a {Future} {Free} from {Neglected} {Tropical} {Diseases}},\n\tvolume = {15},\n\tcopyright = {https://doi.org/10.15223/policy-001},\n\tissn = {1948-5875, 1948-5875},\n\turl = {https://pubs.acs.org/doi/10.1021/acsmedchemlett.4c00060},\n\tdoi = {10.1021/acsmedchemlett.4c00060},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {ACS Medicinal Chemistry Letters},\n\tauthor = {Da Silva Emery, Flavio and Chibale, Kelly},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {314--315},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Effects of injectable contraception with depot medroxyprogesterone acetate or norethisterone enanthate on estradiol levels and menstrual, psychological and behavioral measures relevant to HIV risk: The WHICH randomized trial.\n \n \n \n \n\n\n \n Singata-Madliki, M.; Smit, J.; Beksinska, M.; Balakrishna, Y.; Avenant, C.; Beesham, I.; Seocharan, I.; Batting, J.; Hapgood, J. P.; and Hofmeyr, G. J.\n\n\n \n\n\n\n PLOS ONE, 19(3): e0295764. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Effects$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{singata-madliki_effects_2024,\n\ttitle = {Effects of injectable contraception with depot medroxyprogesterone acetate or norethisterone enanthate on estradiol levels and menstrual, psychological and behavioral measures relevant to {HIV} risk: {The} {WHICH} randomized trial},\n\tvolume = {19},\n\tissn = {1932-6203},\n\tshorttitle = {Effects of injectable contraception with depot medroxyprogesterone acetate or norethisterone enanthate on estradiol levels and menstrual, psychological and behavioral measures relevant to {HIV} risk},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0295764},\n\tdoi = {10.1371/journal.pone.0295764},\n\tabstract = {Background \n              Observational data suggest lower HIV risk with norethisterone enanthate (NET-EN) than with depo-medroxyprogesterone acetate intramuscular (DMPA-IM) injectable contraceptives. If confirmed, a switch between these similar injectable methods would be programmatically feasible and could impact the trajectory of the HIV epidemic. We aimed in this paper to investigate the effects of DMPA-IM and NET-EN on estradiol levels, measures of depression and sexual activity and menstrual effects, relevant to HIV risk; and to ascertain whether these measures are associated with estradiol levels. \n             \n             \n              Methods \n              This open-label trial conducted at two sites in South Africa from 5 November 2018 to 30 November 2019, randomized HIV-negative women aged 18–40 to DMPA-IM 150 mg intramuscular 12-weekly (n = 262) or NET-EN 200 mg intramuscular 8-weekly (n = 259). Data were collected on hormonal, behavioral and menstrual effects at baseline and at 25 weeks (25W). \n             \n             \n              Results \n              At 25W, median 17β estradiol levels were substantially lower than at baseline (p{\\textless}0.001) for both methods: 76.5 pmol/L (interquartile range (IQR) 54.1 to 104.2) in the DMPA-IM group (n = 222), and 69.8 pmol/L (IQR: 55.1 to 89.3) in the NET-EN group (n = 225), with no statistical difference between the two methods (p = 0.450). Compared with DMPA-IM, NET-EN users reported significantly less amenorrhoea, fewer sexual acts, fewer users reporting at least one act of unprotected sex, more condom use with steady partner, more days with urge for sexual intercourse, more days feeling partner does not love her, and more days feeling sad for no reason. We did not find a clear association between estradiol levels and sexual behavior, depression and menstrual effects. Behavioral outcomes suggest less sexual exposure with NET-EN than DMPA-IM. The strength of this evidence is high due to the randomized study design and the consistency of results across the outcomes measured. \n             \n             \n              Conclusions \n              Estradiol levels were reduced to postmenopausal levels by both methods. Secondary outcomes suggesting less sexual exposure with NET-EN are consistent with reported observational evidence of less HIV risk with NET-EN. A randomized trial powered for HIV acquisition is feasible and needed to answer this important question. \n             \n             \n              Trial registration \n               \n                PACTR 202009758229976 \n                .},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Singata-Madliki, Mandisa and Smit, Jenni and Beksinska, Mags and Balakrishna, Yusentha and Avenant, Chanel and Beesham, Ivana and Seocharan, Ishen and Batting, Joanne and Hapgood, Janet P. and Hofmeyr, G. Justus},\n\teditor = {Landenmark, Hanna},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {e0295764},\n}\n\n\n\n

\n

\n\n\n

\n Background Observational data suggest lower HIV risk with norethisterone enanthate (NET-EN) than with depo-medroxyprogesterone acetate intramuscular (DMPA-IM) injectable contraceptives. If confirmed, a switch between these similar injectable methods would be programmatically feasible and could impact the trajectory of the HIV epidemic. We aimed in this paper to investigate the effects of DMPA-IM and NET-EN on estradiol levels, measures of depression and sexual activity and menstrual effects, relevant to HIV risk; and to ascertain whether these measures are associated with estradiol levels. Methods This open-label trial conducted at two sites in South Africa from 5 November 2018 to 30 November 2019, randomized HIV-negative women aged 18–40 to DMPA-IM 150 mg intramuscular 12-weekly (n = 262) or NET-EN 200 mg intramuscular 8-weekly (n = 259). Data were collected on hormonal, behavioral and menstrual effects at baseline and at 25 weeks (25W). Results At 25W, median 17β estradiol levels were substantially lower than at baseline (p\\textless0.001) for both methods: 76.5 pmol/L (interquartile range (IQR) 54.1 to 104.2) in the DMPA-IM group (n = 222), and 69.8 pmol/L (IQR: 55.1 to 89.3) in the NET-EN group (n = 225), with no statistical difference between the two methods (p = 0.450). Compared with DMPA-IM, NET-EN users reported significantly less amenorrhoea, fewer sexual acts, fewer users reporting at least one act of unprotected sex, more condom use with steady partner, more days with urge for sexual intercourse, more days feeling partner does not love her, and more days feeling sad for no reason. We did not find a clear association between estradiol levels and sexual behavior, depression and menstrual effects. Behavioral outcomes suggest less sexual exposure with NET-EN than DMPA-IM. The strength of this evidence is high due to the randomized study design and the consistency of results across the outcomes measured. Conclusions Estradiol levels were reduced to postmenopausal levels by both methods. Secondary outcomes suggesting less sexual exposure with NET-EN are consistent with reported observational evidence of less HIV risk with NET-EN. A randomized trial powered for HIV acquisition is feasible and needed to answer this important question. Trial registration PACTR 202009758229976 .\n

\n\n\n

\n \n\n \n \n \n \n \n \n Recent advances in the treatment of tuberculosis.\n \n \n \n \n\n\n \n Motta, I.; Boeree, M.; Chesov, D.; Dheda, K.; Günther, G.; Horsburgh, C. R.; Kherabi, Y.; Lange, C.; Lienhardt, C.; McIlleron, H. M.; Paton, N. I.; Stagg, H. R.; Thwaites, G.; Udwadia, Z.; Van Crevel, R.; Velásquez, G. E.; Wilkinson, R. J.; Guglielmetti, L.; Motta, I.; Kherabi, Y.; Van Crevel, R.; and Guglielmetti, L.\n\n\n \n\n\n\n Clinical Microbiology and Infection, 30(9): 1107–1114. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Recent$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{motta_recent_2024,\n\ttitle = {Recent advances in the treatment of tuberculosis},\n\tvolume = {30},\n\tissn = {1198743X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1198743X23003397},\n\tdoi = {10.1016/j.cmi.2023.07.013},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {Clinical Microbiology and Infection},\n\tauthor = {Motta, Ilaria and Boeree, Martin and Chesov, Dumitru and Dheda, Keertan and Günther, Gunar and Horsburgh, Charles Robert and Kherabi, Yousra and Lange, Christoph and Lienhardt, Christian and McIlleron, Helen M. and Paton, Nicholas I. and Stagg, Helen R. and Thwaites, Guy and Udwadia, Zarir and Van Crevel, Reinout and Velásquez, Gustavo E. and Wilkinson, Robert J. and Guglielmetti, Lorenzo and Motta, Ilaria and Kherabi, Yousra and Van Crevel, Reinout and Guglielmetti, Lorenzo},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {1107--1114},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Restoring function to inactivating G protein‐coupled receptor variants in the hypothalamic–pituitary–gonadal axis$^{\\textrm{1}}$.\n \n \n \n \n\n\n \n Radomsky, T.; Anderson, R. C.; Millar, R. P.; and Newton, C. L.\n\n\n \n\n\n\n Journal of Neuroendocrinology, 36(9): e13418. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Restoring$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{radomsky_restoring_2024,\n\ttitle = {Restoring function to inactivating {G} protein‐coupled receptor variants in the hypothalamic–pituitary–gonadal axis$^{\\textrm{1}}$},\n\tvolume = {36},\n\tissn = {0953-8194, 1365-2826},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/jne.13418},\n\tdoi = {10.1111/jne.13418},\n\tabstract = {Abstract \n            G protein‐coupled receptors (GPCRs) are central to the functioning of the hypothalamic–pituitary–gonadal axis (HPG axis) and include the rhodopsin‐like GPCR family members, neurokinin 3 receptor, kappa‐opioid receptor, kisspeptin 1 receptor, gonadotropin‐releasing hormone receptor, and the gonadotropin receptors, luteinizing hormone/choriogonadotropin receptor and follicle‐stimulating hormone receptor. Unsurprisingly, inactivating variants of these receptors have been implicated in a spectrum of reproductive phenotypes, including failure to undergo puberty, and infertility. Clinical induction of puberty in patients harbouring such variants is possible, but restoration of fertility is not always a realisable outcome, particularly for those patients suffering from primary hypogonadism. Thus, novel pharmaceuticals and/or a fundamental change in approach to treating these patients are required. The increasing wealth of data describing the effects of coding‐region genetic variants on GPCR function has highlighted that the majority appear to be dysfunctional as a result of misfolding of the encoded receptor protein, which, in turn, results in impaired receptor trafficking through the secretory pathway to the cell surface. As such, these intracellularly retained receptors may be amenable to ‘rescue’ using a pharmacological chaperone (PC)‐based approach. PCs are small, cell permeant molecules hypothesised to interact with misfolded intracellularly retained proteins, stabilising their folding and promoting their trafficking through the secretory pathway. In support of the use of this approach as a viable therapeutic option, it has been observed that many rescued variant GPCRs retain at least a degree of functionality when ‘rescued’ to the cell surface. In this review, we examine the GPCR PC research landscape, focussing on the rescue of inactivating variant GPCRs with important roles in the HPG axis, and describe what is known regarding the mechanisms by which PCs restore trafficking and function. We also discuss some of the merits and obstacles associated with taking this approach forward into a clinical setting.},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Neuroendocrinology},\n\tauthor = {Radomsky, Tarryn and Anderson, Ross C. and Millar, Robert P. and Newton, Claire L.},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {e13418},\n}\n\n\n\n

\n

\n\n\n

\n Abstract G protein‐coupled receptors (GPCRs) are central to the functioning of the hypothalamic–pituitary–gonadal axis (HPG axis) and include the rhodopsin‐like GPCR family members, neurokinin 3 receptor, kappa‐opioid receptor, kisspeptin 1 receptor, gonadotropin‐releasing hormone receptor, and the gonadotropin receptors, luteinizing hormone/choriogonadotropin receptor and follicle‐stimulating hormone receptor. Unsurprisingly, inactivating variants of these receptors have been implicated in a spectrum of reproductive phenotypes, including failure to undergo puberty, and infertility. Clinical induction of puberty in patients harbouring such variants is possible, but restoration of fertility is not always a realisable outcome, particularly for those patients suffering from primary hypogonadism. Thus, novel pharmaceuticals and/or a fundamental change in approach to treating these patients are required. The increasing wealth of data describing the effects of coding‐region genetic variants on GPCR function has highlighted that the majority appear to be dysfunctional as a result of misfolding of the encoded receptor protein, which, in turn, results in impaired receptor trafficking through the secretory pathway to the cell surface. As such, these intracellularly retained receptors may be amenable to ‘rescue’ using a pharmacological chaperone (PC)‐based approach. PCs are small, cell permeant molecules hypothesised to interact with misfolded intracellularly retained proteins, stabilising their folding and promoting their trafficking through the secretory pathway. In support of the use of this approach as a viable therapeutic option, it has been observed that many rescued variant GPCRs retain at least a degree of functionality when ‘rescued’ to the cell surface. In this review, we examine the GPCR PC research landscape, focussing on the rescue of inactivating variant GPCRs with important roles in the HPG axis, and describe what is known regarding the mechanisms by which PCs restore trafficking and function. We also discuss some of the merits and obstacles associated with taking this approach forward into a clinical setting.\n

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\n \n\n \n \n \n \n \n \n Author Correction: Antimalarial drug discovery: progress and approaches.\n \n \n \n \n\n\n \n Siqueira-Neto, J. L.; Wicht, K. J.; Chibale, K.; Burrows, J. N.; Fidock, D. A.; and Winzeler, E. A.\n\n\n \n\n\n\n Nature Reviews Drug Discovery, 23(11): 880–880. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Author$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{siqueira-neto_author_2024,\n\ttitle = {Author {Correction}: {Antimalarial} drug discovery: progress and approaches},\n\tvolume = {23},\n\tissn = {1474-1776, 1474-1784},\n\tshorttitle = {Author {Correction}},\n\turl = {https://www.nature.com/articles/s41573-024-01045-9},\n\tdoi = {10.1038/s41573-024-01045-9},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2025-06-24},\n\tjournal = {Nature Reviews Drug Discovery},\n\tauthor = {Siqueira-Neto, Jair L. and Wicht, Kathryn J. and Chibale, Kelly and Burrows, Jeremy N. and Fidock, David A. and Winzeler, Elizabeth A.},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {880--880},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Dose-fractionation studies of a Plasmodium phosphatidylinositol 4-kinase inhibitor in a humanized mouse model of malaria.\n \n \n \n \n\n\n \n Gibhard, L.; Njoroge, M.; Mulubwa, M.; Lawrence, N.; Smith, D.; Duffy, J.; Le Manach, C.; Brunschwig, C.; Taylor, D.; Van Der Westhuyzen, R.; Street, L. J.; Basarab, G. S.; and Chibale, K.\n\n\n \n\n\n\n Antimicrobial Agents and Chemotherapy, 68(10): e00842–24. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Dose-fractionation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{gibhard_dose-fractionation_2024,\n\ttitle = {Dose-fractionation studies of a \\textit{{Plasmodium}} phosphatidylinositol 4-kinase inhibitor in a humanized mouse model of malaria},\n\tvolume = {68},\n\tissn = {0066-4804, 1098-6596},\n\turl = {https://journals.asm.org/doi/10.1128/aac.00842-24},\n\tdoi = {10.1128/aac.00842-24},\n\tabstract = {ABSTRACT \n             \n               \n               \n                UCT594 is a 2-aminopyrazine carboxylic acid \n                Plasmodium \n                phosphatidylinositol 4-kinase inhibitor with potent asexual blood-stage activity, the potential for interrupting transmission, as well as liver-stage activities. Herein, we investigated pharmacokinetic/pharmacodynamic (PK/PD) relationships relative to blood-stage activity toward predicting the human dose. Dose-fractionation studies were conducted in the \n                Plasmodium falciparum \n                NSG mouse model to determine the PK/PD indices of UCT594, using the \n                in vivo \n                minimum parasiticidal concentration as a threshold. UCT594 demonstrated concentration-dependent killing in the \n                P. falciparum \n                -infected NSG mouse model. Using this data and the preclinical pharmacokinetic data led to a low predicted human dose of {\\textless}50 mg. This makes UCT594 an attractive potential antimalarial drug.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {Antimicrobial Agents and Chemotherapy},\n\tauthor = {Gibhard, Liezl and Njoroge, Mathew and Mulubwa, Mwila and Lawrence, Nina and Smith, Dennis and Duffy, James and Le Manach, Claire and Brunschwig, Christel and Taylor, Dale and Van Der Westhuyzen, Renier and Street, Leslie J. and Basarab, Gregory S. and Chibale, Kelly},\n\teditor = {Odom John, Audrey},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {e00842--24},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Fatty acid metabolism in neutrophils promotes lung damage and bacterial replication during tuberculosis.\n \n \n \n \n\n\n \n Sankar, P.; Ramos, R. B.; Corro, J.; Mishra, L. K.; Nafiz, T. N.; Bhargavi, G.; Saqib, M.; Poswayo, S. K. L.; Parihar, S. P.; Cai, Y.; Subbian, S.; Ojha, A. K.; and Mishra, B. B.\n\n\n \n\n\n\n PLOS Pathogens, 20(10): e1012188. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Fatty$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{sankar_fatty_2024,\n\ttitle = {Fatty acid metabolism in neutrophils promotes lung damage and bacterial replication during tuberculosis},\n\tvolume = {20},\n\tissn = {1553-7374},\n\turl = {https://dx.plos.org/10.1371/journal.ppat.1012188},\n\tdoi = {10.1371/journal.ppat.1012188},\n\tabstract = {Mycobacterium tuberculosis \n              (Mtb) infection induces a marked influx of neutrophils into the lungs, which intensifies the severity of tuberculosis (TB). The metabolic state of neutrophils significantly influences their functional response during inflammation and interaction with bacterial pathogens. However, the effect of Mtb infection on neutrophil metabolism and its consequent role in TB pathogenesis remain unclear. In this study, we examined the contribution of glycolysis and fatty acid metabolism on neutrophil responses to Mtb HN878 infection using \n              ex-vivo \n              assays and murine infection models. We discover that blocking glycolysis aggravates TB pathology, whereas inhibiting fatty acid oxidation (FAO) yields protective outcomes, including reduced weight loss, immunopathology, and bacterial burden in lung. Intriguingly, FAO inhibition preferentially disrupts the recruitment of a pathogen-permissive immature neutrophil population (Ly6G \n              lo/dim \n              ), known to accumulate during TB. Targeting carnitine palmitoyl transferase 1a (Cpt1a)-a crucial enzyme in mitochondrial β-oxidation-either through chemical or genetic methods impairs neutrophils’ ability to migrate to infection sites while also enhancing their antimicrobial function. Our findings illuminate the critical influence of neutrophil immunometabolism in TB pathogenesis, suggesting that manipulating fatty acid metabolism presents a novel avenue for host-directed TB therapies by modulating neutrophil functions.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Pathogens},\n\tauthor = {Sankar, Poornima and Ramos, Ramon Bossardi and Corro, Jamie and Mishra, Lokesh K. and Nafiz, Tanvir Noor and Bhargavi, Gunapati and Saqib, Mohd and Poswayo, Sibongiseni K. L. and Parihar, Suraj P. and Cai, Yi and Subbian, Selvakumar and Ojha, Anil K. and Mishra, Bibhuti B.},\n\teditor = {Boshoff, Helena Ingrid},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {e1012188},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Rethinking Tuberculosis Morbidity Quantification: A Systematic Review and Critical Appraisal of TB Disability Weights in Cost-Effectiveness Analyses.\n \n \n \n \n\n\n \n Tomeny, E. M.; Hampton, T.; Tran, P. B.; Rosu, L.; Phiri, M. D.; Haigh, K. A.; Nidoi, J.; Wingfield, T.; and Worrall, E.\n\n\n \n\n\n\n PharmacoEconomics, 42(11): 1209–1236. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Rethinking$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{tomeny_rethinking_2024,\n\ttitle = {Rethinking {Tuberculosis} {Morbidity} {Quantification}: {A} {Systematic} {Review} and {Critical} {Appraisal} of {TB} {Disability} {Weights} in {Cost}-{Effectiveness} {Analyses}},\n\tvolume = {42},\n\tissn = {1170-7690, 1179-2027},\n\tshorttitle = {Rethinking {Tuberculosis} {Morbidity} {Quantification}},\n\turl = {https://link.springer.com/10.1007/s40273-024-01410-x},\n\tdoi = {10.1007/s40273-024-01410-x},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2025-06-24},\n\tjournal = {PharmacoEconomics},\n\tauthor = {Tomeny, Ewan M. and Hampton, Thomas and Tran, Phuong Bich and Rosu, Laura and Phiri, Mphatso D. and Haigh, Kathryn A. and Nidoi, Jasper and Wingfield, Tom and Worrall, Eve},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {1209--1236},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Differential requirement of formyl peptide receptor 1 in macrophages and neutrophils in the host defense against Mycobacterium tuberculosis Infection.\n \n \n \n \n\n\n \n Nafiz, T. N.; Sankar, P.; Mishra, L. K.; Rousseau, R. P.; Saqib, M.; Subbian, S.; Parihar, S. P.; and Mishra, B. B.\n\n\n \n\n\n\n Scientific Reports, 14(1): 23595. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Differential$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{nafiz_differential_2024,\n\ttitle = {Differential requirement of formyl peptide receptor 1 in macrophages and neutrophils in the host defense against {Mycobacterium} tuberculosis {Infection}},\n\tvolume = {14},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-024-71180-1},\n\tdoi = {10.1038/s41598-024-71180-1},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Scientific Reports},\n\tauthor = {Nafiz, Tanvir Noor and Sankar, Poornima and Mishra, Lokesh K. and Rousseau, Robert P. and Saqib, Mohd and Subbian, Selvakumar and Parihar, Suraj P. and Mishra, Bibhuti B.},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {23595},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Causal Inference for Continuous Multiple Time Point Interventions.\n \n \n \n \n\n\n \n Schomaker, M.; McIlleron, H.; Denti, P.; and Díaz, I.\n\n\n \n\n\n\n Statistics in Medicine, 43(28): 5380–5400. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Causal$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{schomaker_causal_2024,\n\ttitle = {Causal {Inference} for {Continuous} {Multiple} {Time} {Point} {Interventions}},\n\tvolume = {43},\n\tissn = {0277-6715, 1097-0258},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/sim.10246},\n\tdoi = {10.1002/sim.10246},\n\tabstract = {ABSTRACT \n            There are limited options to estimate the treatment effects of variables which are continuous and measured at multiple time points, particularly if the true dose–response curve should be estimated as closely as possible. However, these situations may be of relevance: in pharmacology, one may be interested in how outcomes of people living with—and treated for—HIV, such as viral failure, would vary for time‐varying interventions such as different drug concentration trajectories. A challenge for doing causal inference with continuous interventions is that the positivity assumption is typically violated. To address positivity violations, we develop projection functions, which reweigh and redefine the estimand of interest based on functions of the conditional support for the respective interventions. With these functions, we obtain the desired dose–response curve in areas of enough support, and otherwise a meaningful estimand that does not require the positivity assumption. We develop ‐computation type plug‐in estimators for this case. Those are contrasted with g‐computation estimators which are applied to continuous interventions without specifically addressing positivity violations, which we propose to be presented with diagnostics. The ideas are illustrated with longitudinal data from HIV positive children treated with an efavirenz‐based regimen as part of the CHAPAS‐3 trial, which enrolled children  years in Zambia/Uganda. Simulations show in which situations a standard g‐computation approach is appropriate, and in which it leads to bias and how the proposed weighted estimation approach then recovers the alternative estimand of interest.},\n\tlanguage = {en},\n\tnumber = {28},\n\turldate = {2025-06-24},\n\tjournal = {Statistics in Medicine},\n\tauthor = {Schomaker, Michael and McIlleron, Helen and Denti, Paolo and Díaz, Iván},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {5380--5400},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Physiologically based pharmacokinetic modeling of drug–drug interactions between ritonavir‐boosted atazanavir and rifampicin in pregnancy.\n \n \n \n \n\n\n \n Atoyebi, S.; Montanha, M. C.; Nakijoba, R.; Orrell, C.; Mugerwa, H.; Siccardi, M.; Denti, P.; and Waitt, C.\n\n\n \n\n\n\n CPT: Pharmacometrics & Systems Pharmacology, 13(11): 1967–1977. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Physiologically$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{atoyebi_physiologically_2024,\n\ttitle = {Physiologically based pharmacokinetic modeling of drug–drug interactions between ritonavir‐boosted atazanavir and rifampicin in pregnancy},\n\tvolume = {13},\n\tissn = {2163-8306, 2163-8306},\n\turl = {https://ascpt.onlinelibrary.wiley.com/doi/10.1002/psp4.13268},\n\tdoi = {10.1002/psp4.13268},\n\tabstract = {Abstract \n             \n              Ritonavir‐boosted atazanavir (ATV/r) and rifampicin are mainstays of second‐line antiretroviral and multiple anti‐TB regimens, respectively. Rifampicin induces CYP3A4, a major enzyme involved in atazanavir metabolism, causing a drug–drug interaction (DDI) which might be exaggerated in pregnancy. Having demonstrated that increasing the dose of ATV/r from once daily (OD) to twice daily (BD) in non‐pregnant adults can safely overcome this DDI, we developed a pregnancy physiologically based pharmacokinetic (PBPK) model to explore the impact of pregnancy. Predicted pharmacokinetic parameters were validated with separate clinical datasets of ATV/r alone (NCT03923231) and rifampicin alone in pregnant women. The pregnancy model was considered validated when the absolute average fold error (AAFE) for \n              C \n              trough \n              and AUC \n              0‐24 \n              of both drugs were {\\textless}2 when comparing predicted vs. observed data. Thereafter, predicted atazanavir \n              C \n              trough \n              was compared against its protein‐adjusted IC \n              90 \n              (14 ng/mL) when simulating the co‐administration of ATV/r 300/100 mg OD and rifampicin 600 mg OD. Pregnancy was predicted to increase the rifampicin DDI effect on atazanavir. For the dosing regimens of ATV/r 300/100 mg OD, ATV/r 300/200 mg OD, and ATV/r 300/100 mg BD (all with rifampicin 600 mg OD), predicted atazanavir \n              C \n              trough \n              was above 14 ng/mL in 29\\%, 71\\%, and 100\\%; and 32\\%, 73\\% and 100\\% of the population in second and third trimesters, respectively. Thus, PBPK modeling suggests ATV/r 300/100 mg BD could maintain antiviral efficacy when co‐administered with rifampicin 600 mg OD in pregnancy. Clinical studies are warranted to confirm safety and efficacy in pregnancy.},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2025-06-24},\n\tjournal = {CPT: Pharmacometrics \\& Systems Pharmacology},\n\tauthor = {Atoyebi, Shakir and Montanha, Maiara Camotti and Nakijoba, Ritah and Orrell, Catherine and Mugerwa, Henry and Siccardi, Marco and Denti, Paolo and Waitt, Catriona},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {1967--1977},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n All-optical reporting of inhibitory receptor driving force in the nervous system.\n \n \n \n \n\n\n \n Selfe, J. S.; Steyn, T. J. S.; Shorer, E. F.; Burman, R. J.; Düsterwald, K. M.; Kraitzick, A. Z.; Abdelfattah, A. S.; Schreiter, E. R.; Newey, S. E.; Akerman, C. J.; and Raimondo, J. V.\n\n\n \n\n\n\n Nature Communications, 15(1): 8913. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"All-optical$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{selfe_all-optical_2024,\n\ttitle = {All-optical reporting of inhibitory receptor driving force in the nervous system},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-53074-y},\n\tdoi = {10.1038/s41467-024-53074-y},\n\tabstract = {Abstract \n             \n              Ionic driving forces provide the net electromotive force for ion movement across receptors, channels, and transporters, and are a fundamental property of all cells. In the nervous system, fast synaptic inhibition is mediated by chloride permeable GABA \n              A \n              and glycine receptors, and single-cell intracellular recordings have been the only method for estimating driving forces across these receptors (DF \n              GABAA \n              ). Here we present a tool for quantifying inhibitory receptor driving force named ORCHID: all-Optical Reporting of CHloride Ion Driving force. We demonstrate ORCHID’s ability to provide accurate, high-throughput measurements of resting and dynamic DF \n              GABAA \n              from genetically targeted cell types over multiple timescales. ORCHID confirms theoretical predictions about the biophysical mechanisms that establish DF \n              GABAA \n              , reveals differences in DF \n              GABAA \n              between neurons and astrocytes, and affords the first in vivo measurements of intact DF \n              GABAA \n              . This work extends our understanding of inhibitory synaptic transmission and demonstrates the potential for all-optical methods to assess ionic driving forces.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Selfe, Joshua S. and Steyn, Teresa J. S. and Shorer, Eran F. and Burman, Richard J. and Düsterwald, Kira M. and Kraitzick, Ariel Z. and Abdelfattah, Ahmed S. and Schreiter, Eric R. and Newey, Sarah E. and Akerman, Colin J. and Raimondo, Joseph V.},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {8913},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A temporal cortex cell atlas highlights gene expression dynamics during human brain maturation.\n \n \n \n \n\n\n \n Steyn, C.; Mishi, R.; Fillmore, S.; Verhoog, M. B.; More, J.; Rohlwink, U. K.; Melvill, R.; Butler, J.; Enslin, J. M. N.; Jacobs, M.; Sauka-Spengler, T.; Greco, M.; Quiñones, S.; Dulla, C. G.; Raimondo, J. V.; Figaji, A.; and Hockman, D.\n\n\n \n\n\n\n Nature Genetics, 56(12): 2718–2730. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{steyn_temporal_2024,\n\ttitle = {A temporal cortex cell atlas highlights gene expression dynamics during human brain maturation},\n\tvolume = {56},\n\tissn = {1061-4036, 1546-1718},\n\turl = {https://www.nature.com/articles/s41588-024-01990-6},\n\tdoi = {10.1038/s41588-024-01990-6},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {Nature Genetics},\n\tauthor = {Steyn, Christina and Mishi, Ruvimbo and Fillmore, Stephanie and Verhoog, Matthijs B. and More, Jessica and Rohlwink, Ursula K. and Melvill, Roger and Butler, James and Enslin, Johannes M. N. and Jacobs, Muazzam and Sauka-Spengler, Tatjana and Greco, Maria and Quiñones, Sadi and Dulla, Chris G. and Raimondo, Joseph V. and Figaji, Anthony and Hockman, Dorit},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {2718--2730},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Bedaquiline: what might the future hold?.\n \n \n \n \n\n\n \n Shaw, E. S; Stoker, N. G; Potter, J. L; Claassen, H.; Leslie, A.; Tweed, C. D; Chiang, C.; Conradie, F.; Esmail, H.; Lange, C.; Pinto, L.; Rucsineanu, O.; Sloan, D. J; Theron, G.; Tisile, P.; Voo, T. C.; Warren, R. M; Lebina, L.; and Lipman, M.\n\n\n \n\n\n\n The Lancet Microbe, 5(12): 100909. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Bedaquiline:$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{shaw_bedaquiline_2024,\n\ttitle = {Bedaquiline: what might the future hold?},\n\tvolume = {5},\n\tissn = {26665247},\n\tshorttitle = {Bedaquiline},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524724001496},\n\tdoi = {10.1016/S2666-5247(24)00149-6},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Shaw, Emily S and Stoker, Neil G and Potter, Jessica L and Claassen, Helgard and Leslie, Alasdair and Tweed, Conor D and Chiang, Chen-Yuan and Conradie, Francesca and Esmail, Hanif and Lange, Christoph and Pinto, Lancelot and Rucsineanu, Oxana and Sloan, Derek J and Theron, Grant and Tisile, Phumeza and Voo, Teck Chuan and Warren, Robin M and Lebina, Limakatso and Lipman, Marc},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {100909},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Urine-Xpert Ultra for the diagnosis of tuberculosis in people living with HIV: a prospective, multicentre, diagnostic accuracy study.\n \n \n \n \n\n\n \n Sossen, B.; Székely, R.; Mukoka, M.; Muyoyeta, M.; Nakabugo, E.; Hella, J.; Van Nguyen, H.; Ubolyam, S.; Erkosar, B.; Vermeulen, M.; Centner, C. M; Nyangu, S.; Sanjase, N.; Sasamalo, M.; Dinh, H. T.; Ngo, T. A.; Manosuthi, W.; Jirajariyavej, S.; Nguyen, N. V.; Avihingsanon, A.; Kerkhoff, A. D; Denkinger, C. M; Reither, K.; Nakiyingi, L.; MacPherson, P.; Meintjes, G.; Ruhwald, M.; Sossen, B.; Székely, R.; Mukoka, M.; Muyoyeta, M.; Nakabugo, E.; Hella, J.; Van Nguyen, H.; Nguyen, V. A. T.; Ubolyam, S.; Erkosar, B.; Vermeulen, M.; Centner, C. M; Nyangu, S.; Sanjase, N.; Cavallini, A.; Macé, A.; Shuma, B.; Sasamalo, M.; Dinh, H. T.; Ngo, T. A.; Manosuthi, W.; Jirajariyavej, S.; Armstrong, D. T; Carmona, S.; Broger, T.; Khlaiphuengsin, A.; Mahanontharit, A.; Pham, T. T. T.; Nguyen, H. T.; Van Pham, Q.; Nguyen, N. V.; Avihingsanon, A.; Kerkhoff, A. D; Denkinger, C. M; Reither, K.; Nakiyingi, L.; MacPherson, P. P.; Meintjes, P. G.; and Ruhwald, M.\n\n\n \n\n\n\n The Lancet Global Health, 12(12): e2024–2034. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Urine-Xpert$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{sossen_urine-xpert_2024,\n\ttitle = {Urine-{Xpert} {Ultra} for the diagnosis of tuberculosis in people living with {HIV}: a prospective, multicentre, diagnostic accuracy study},\n\tvolume = {12},\n\tissn = {2214109X},\n\tshorttitle = {Urine-{Xpert} {Ultra} for the diagnosis of tuberculosis in people living with {HIV}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X24003577},\n\tdoi = {10.1016/S2214-109X(24)00357-7},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Global Health},\n\tauthor = {Sossen, Bianca and Székely, Rita and Mukoka, Madalo and Muyoyeta, Monde and Nakabugo, Elizabeth and Hella, Jerry and Van Nguyen, Hung and Ubolyam, Sasiwimol and Erkosar, Berra and Vermeulen, Marcia and Centner, Chad M and Nyangu, Sarah and Sanjase, Nsala and Sasamalo, Mohamed and Dinh, Huong Thi and Ngo, The Anh and Manosuthi, Weerawat and Jirajariyavej, Supunnee and Nguyen, Nhung Viet and Avihingsanon, Anchalee and Kerkhoff, Andrew D and Denkinger, Claudia M and Reither, Klaus and Nakiyingi, Lydia and MacPherson, Peter and Meintjes, Graeme and Ruhwald, Morten and Sossen, Bianca and Székely, Rita and Mukoka, Madalo and Muyoyeta, Monde and Nakabugo, Elizabeth and Hella, Jerry and Van Nguyen, Hung and Nguyen, Van Anh Thi and Ubolyam, Sasiwimol and Erkosar, Berra and Vermeulen, Marcia and Centner, Chad M and Nyangu, Sarah and Sanjase, Nsala and Cavallini, Andrea and Macé, Aurélien and Shuma, Brian and Sasamalo, Mohamed and Dinh, Huong Thi and Ngo, The Anh and Manosuthi, Weerawat and Jirajariyavej, Supunnee and Armstrong, Derek T and Carmona, Sergio and Broger, Tobias and Khlaiphuengsin, Apichaya and Mahanontharit, Aphicha and Pham, Trang Thi Thu and Nguyen, Hieu Thi and Van Pham, Quang and Nguyen, Nhung Viet and Avihingsanon, Anchalee and Kerkhoff, Andrew D and Denkinger, Claudia M and Reither, Klaus and Nakiyingi, Lydia and MacPherson, Prof Peter and Meintjes, Prof Graeme and Ruhwald, Morten},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {e2024--2034},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The relationship between selected sexually transmitted pathogens, HPV and HIV infection status in women presenting with gynaecological symptoms in Maputo City, Mozambique.\n \n \n \n \n\n\n \n Maueia, C.; Murahwa, A.; Manjate, A.; Sacarlal, J.; Kenga, D.; Unemo, M.; Andersson, S.; Mussá, T.; and Williamson, A.\n\n\n \n\n\n\n PLOS ONE, 19(9): e0307781. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{maueia_relationship_2024,\n\ttitle = {The relationship between selected sexually transmitted pathogens, {HPV} and {HIV} infection status in women presenting with gynaecological symptoms in {Maputo} {City}, {Mozambique}},\n\tvolume = {19},\n\tissn = {1932-6203},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0307781},\n\tdoi = {10.1371/journal.pone.0307781},\n\tabstract = {Sexually transmitted infections (STIs) have a profound impact on sexual and reproductive health worldwide. Syphilis, gonorrhea, chlamydia, and trichomoniasis are four currently curable STIs. However, most STI cases are asymptomatic and not detected without laboratory diagnostics. Hepatitis B virus, herpes simplex virus, human immunodeficiency virus (HIV), and human papillomavirus (HPV) are four viral and incurable infections, but they can be mitigated by treatment. We investigated the prevalence of selected sexually transmitted pathogens and their relationship with HPV and HIV infection in women from Maputo, the capital of Mozambique. A cross-sectional study was conducted on 233 non-pregnant women seeking health care relating to gynecological symptoms in Mavalane Health facilities in Maputo, between the 1 \n               \n                st \n               \n              of February 2018 and the 30 \n               \n                th \n               \n              of July 2019. Cervical brush samples were collected and DNA was extracted. Selected STIs including HPV were detected using multiplex STD and HPV Direct Flow Chip Kits through a manual Hybrispot platform (Vitro, Master Diagnostica, Sevilla, Spain). HIV testing was performed using rapid tests: Determine HIV 1/2 test (Alere Abbott Laboratories, Tokyo, Japan) for screening, and UniGold HIV (Trinity Biotech, Ireland) for confirmation. All women (n = 233) were negative for \n              Haemophilus ducreyi \n              and Herpes Simplex Virus-1 (HSV-1). Among the 233 women, a high prevalence of STIs was found (89\\%), 63\\% of the women were positive for HPV and 24\\% were HIV positive. \n              Treponema pallidum \n              (TP), \n              Trichomonas vaginalis \n              (TV), Herpes Simplex Virus-2 (HSV-2), and \n              Chlamydia trachomatis \n              (CT) were detected in 17\\%, 14\\%, 8\\%, and 8\\% of the women, respectively. As a common phenomenon, vaginal discharge (90\\%) was the lower genital tract symptom reported by the majority of the women. Co-infection with any STI and HPV was detected in 56\\% (130/233) while 45\\% (59/130) of the co-infections were with high-risk HPV (hrHPV) genotypes. Among the HPV-positive participants, infection by TP was the most prevalent (27\\%). In total, 28\\% (66/233) of the participants were positive for any hrHPV genotypes. Co-infection with any STI and HIV was found in 15\\% (34/233) of the study participants. There was a significant association between HPV infection and TP (p = 0.039) and HSV-2 (p = 0.005). TV, TP, and CT-S1-CT-S2 positivity were significantly more prevalent in HIV-positive participants. Pathobionts Ureaplasma urealyticum/parvum and Mycoplasma hominis were detected in 84.0\\% (195/233) and 45\\% (105/233), respectively. This present study describes a high prevalence of STIs. Co-infection between HPV and STIs was found in the majority of the study subjects. The high prevalence of HPV emphasizes the need for HPV vaccination to prevent cervical cancer in this population. Management of STIs is also important in women presenting with gynecological symptoms.},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Maueia, Cremildo and Murahwa, Alltalents and Manjate, Alice and Sacarlal, Jahit and Kenga, Darlene and Unemo, Magnus and Andersson, Sören and Mussá, Tufária and Williamson, Anna-Lise},\n\teditor = {Zenebe, Mengistu Hailemariam},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {e0307781},\n}\n\n\n\n

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\n Sexually transmitted infections (STIs) have a profound impact on sexual and reproductive health worldwide. Syphilis, gonorrhea, chlamydia, and trichomoniasis are four currently curable STIs. However, most STI cases are asymptomatic and not detected without laboratory diagnostics. Hepatitis B virus, herpes simplex virus, human immunodeficiency virus (HIV), and human papillomavirus (HPV) are four viral and incurable infections, but they can be mitigated by treatment. We investigated the prevalence of selected sexually transmitted pathogens and their relationship with HPV and HIV infection in women from Maputo, the capital of Mozambique. A cross-sectional study was conducted on 233 non-pregnant women seeking health care relating to gynecological symptoms in Mavalane Health facilities in Maputo, between the 1 st of February 2018 and the 30 th of July 2019. Cervical brush samples were collected and DNA was extracted. Selected STIs including HPV were detected using multiplex STD and HPV Direct Flow Chip Kits through a manual Hybrispot platform (Vitro, Master Diagnostica, Sevilla, Spain). HIV testing was performed using rapid tests: Determine HIV 1/2 test (Alere Abbott Laboratories, Tokyo, Japan) for screening, and UniGold HIV (Trinity Biotech, Ireland) for confirmation. All women (n = 233) were negative for Haemophilus ducreyi and Herpes Simplex Virus-1 (HSV-1). Among the 233 women, a high prevalence of STIs was found (89%), 63% of the women were positive for HPV and 24% were HIV positive. Treponema pallidum (TP), Trichomonas vaginalis (TV), Herpes Simplex Virus-2 (HSV-2), and Chlamydia trachomatis (CT) were detected in 17%, 14%, 8%, and 8% of the women, respectively. As a common phenomenon, vaginal discharge (90%) was the lower genital tract symptom reported by the majority of the women. Co-infection with any STI and HPV was detected in 56% (130/233) while 45% (59/130) of the co-infections were with high-risk HPV (hrHPV) genotypes. Among the HPV-positive participants, infection by TP was the most prevalent (27%). In total, 28% (66/233) of the participants were positive for any hrHPV genotypes. Co-infection with any STI and HIV was found in 15% (34/233) of the study participants. There was a significant association between HPV infection and TP (p = 0.039) and HSV-2 (p = 0.005). TV, TP, and CT-S1-CT-S2 positivity were significantly more prevalent in HIV-positive participants. Pathobionts Ureaplasma urealyticum/parvum and Mycoplasma hominis were detected in 84.0% (195/233) and 45% (105/233), respectively. This present study describes a high prevalence of STIs. Co-infection between HPV and STIs was found in the majority of the study subjects. The high prevalence of HPV emphasizes the need for HPV vaccination to prevent cervical cancer in this population. Management of STIs is also important in women presenting with gynecological symptoms.\n

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\n \n\n \n \n \n \n \n \n Targeted deep sequencing of mycobacteria species from extrapulmonary sites not identified by routine line probe assays: A retrospective laboratory analysis of stored clinical cultures.\n \n \n \n \n\n\n \n Opperman, C.; Steyn, J.; Matthews, M. C.; Singh, S.; Ghebrekristos, Y.; Kerr, T. J.; Miller, M.; Esmail, A.; Cox, H.; Warren, R.; Ghielmetti, G.; and Goosen, W.\n\n\n \n\n\n\n IJID Regions, 13: 100464. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Targeted$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{opperman_targeted_2024,\n\ttitle = {Targeted deep sequencing of mycobacteria species from extrapulmonary sites not identified by routine line probe assays: {A} retrospective laboratory analysis of stored clinical cultures},\n\tvolume = {13},\n\tissn = {27727076},\n\tshorttitle = {Targeted deep sequencing of mycobacteria species from extrapulmonary sites not identified by routine line probe assays},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2772707624001358},\n\tdoi = {10.1016/j.ijregi.2024.100464},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {IJID Regions},\n\tauthor = {Opperman, Christoffel and Steyn, Janré and Matthews, Megan Ceris and Singh, Sarishna and Ghebrekristos, Yonas and Kerr, Tanya Jane and Miller, Michele and Esmail, Aliasgar and Cox, Helen and Warren, Robin and Ghielmetti, Giovanni and Goosen, Wynand},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {100464},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Persistent Mycobacterium tuberculosis bioaerosol release in a tuberculosis-endemic setting.\n \n \n \n \n\n\n \n Dinkele, R.; Gessner, S.; Patterson, B.; McKerry, A.; Hoosen, Z.; Vazi, A.; Seldon, R.; Koch, A.; Warner, D. F.; and Wood, R.\n\n\n \n\n\n\n iScience, 27(9): 110731. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Persistent$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{dinkele_persistent_2024,\n\ttitle = {Persistent {Mycobacterium} tuberculosis bioaerosol release in a tuberculosis-endemic setting},\n\tvolume = {27},\n\tissn = {25890042},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2589004224019564},\n\tdoi = {10.1016/j.isci.2024.110731},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {iScience},\n\tauthor = {Dinkele, Ryan and Gessner, Sophia and Patterson, Benjamin and McKerry, Andrea and Hoosen, Zeenat and Vazi, Andiswa and Seldon, Ronnett and Koch, Anastasia and Warner, Digby F. and Wood, Robin},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {110731},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Exploring Health-Related Quality of Life (HRQOL) among patients with HIV-associated TB in Khayelitsha, South Africa.\n \n \n \n \n\n\n \n Hickman, J.; Swartz, A.; Sicwebu, N.; Stek, C.; Masimini, N.; and Nöstlinger, C.\n\n\n \n\n\n\n PLOS ONE, 19(11): e0275554. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Exploring$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{hickman_exploring_2024,\n\ttitle = {Exploring {Health}-{Related} {Quality} of {Life} ({HRQOL}) among patients with {HIV}-associated {TB} in {Khayelitsha}, {South} {Africa}},\n\tvolume = {19},\n\tissn = {1932-6203},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0275554},\n\tdoi = {10.1371/journal.pone.0275554},\n\tabstract = {Background \n              Health-related quality of life (HRQOL) is an important and frequently used patient-reported outcome in health research. However, little qualitative research exists in this field in South Africa. This study was set in Khayelitsha, one of the largest informal settlements in South Africa, where the burden of HIV and tuberculosis (TB) co-infection are amongst the highest in the world and significantly affect HRQOL. \n             \n             \n              Objective \n              To explore the experience of HRQOL among patients living with HIV-associated TB. \n             \n             \n              Methods \n              We conducted sixteen interviews with male (n = 10) and female (n = 6) adult participants (ages 24–56; median age 35) to explore their HRQOL living with HIV-associated TB, related treatment and how this impacted on life domains they considered relevant for HRQOL. We used thematic analysis to analyse data, using both an inductive and deductive analysis using an interpretive phenomenological approach (IPA). \n             \n             \n              Results \n              Experiences of HRQOL were identified along the predominantly emerging themes of physical, social, and mental aspects of HRQOL. Identified sub-themes included well-being, loss of strength, and self-care for the physical domain; usual activities and stigma for the social domain; concerns and coping for the mental domain. The findings illustrate that HRQOL domains are interconnected through social experience. The social experience of HRQOL was identified as the common denominator connecting all domains, around which HRQOL revolved for these participants. \n             \n             \n              Conclusion \n              HRQOL is experienced socially. The interpersonal connections patients have with significant others present as key to high HRQOL among patients living with HIV-associated TB. This study adds to the existing literature of HRQOL and examines HRQOL using IPA which may help to inform future interventions to improve HRQOL among HIV/TB patients.},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Hickman, John-Henry and Swartz, Alison and Sicwebu, Namhla and Stek, Cari and Masimini, Nobom and Nöstlinger, Christiana},\n\teditor = {Morgan, Julia},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {e0275554},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Post-tuberculosis treatment paradoxical reactions.\n \n \n \n \n\n\n \n Hermans, S. M.; Akkerman, O. W.; Meintjes, G.; and Grobusch, M. P.\n\n\n \n\n\n\n Infection, 52(5): 2083–2095. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Post-tuberculosis$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{hermans_post-tuberculosis_2024,\n\ttitle = {Post-tuberculosis treatment paradoxical reactions},\n\tvolume = {52},\n\tissn = {0300-8126, 1439-0973},\n\turl = {https://link.springer.com/10.1007/s15010-024-02310-0},\n\tdoi = {10.1007/s15010-024-02310-0},\n\tabstract = {Abstract \n            Paradoxical reactions (PR) to tuberculosis (TB) treatment are common during treatment, but have also been described after treatment. A presentation with recurrent signs or symptoms of TB after cure or completion of prior treatment needs to be differentiated between microbiological relapse and a paradoxical reaction. We searched all published literature on post-treatment PR, and present a synthesis of 30 studies, focusing on the epidemiology, diagnosis and management of this phenomenon. We report an additional case vignette. The majority of studies were of lymph node TB (LN-TB), followed by central nervous system TB (CNS-TB). A total of 112 confirmed and 42 possible post-treatment PR cases were reported. The incidence ranged between 3 and 14\\% in LN-TB and was more frequent than relapses, and between 0 and 2\\% in all TB. We found four reports of pulmonary or pleural TB post-treatment PR cases. The incidence did not differ by length of treatment, but was associated with younger age at initial diagnosis, and having had a PR (later) during treatment. Post-treatment PR developed mainly within the first 6 months after the end of TB treatment but has been reported many years later (longest report 10 years). The mainstays of diagnosis and management are negative mycobacterial cultures and anti-inflammatory treatment, respectively. Due to the favourable prognosis in LN-TB recurrent symptoms, a short period of observation is warranted to assess for spontaneous regression. In CNS-TB with recurrent symptoms, immediate investigation and anti-inflammatory treatment with the possibility of TB retreatment should be undertaken.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2025-06-24},\n\tjournal = {Infection},\n\tauthor = {Hermans, Sabine M. and Akkerman, Onno W. and Meintjes, Graeme and Grobusch, Martin P.},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {2083--2095},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Population Pharmacokinetics of Dolutegravir in African Children: Results From the CHAPAS-4 Trial.\n \n \n \n \n\n\n \n Waalewijn, H.; Wasmann, R. E; Bamford, A.; Gibb, D. M; McIlleron, H. M; Colbers, A.; Burger, D. M; Denti, P.; the CHAPAS-4 trial team; Gibb, D.; Walker, S.; Turkova, A.; Shakeshaft, C.; Spyer, M.; Thomason, M.; Griffiths, A.; Monkiewicz, L.; Massingham, S.; Szubert, A.; Bamford, A.; Doerholt, K.; Bigault, A.; Dudakia, N.; South, A.; Van Looy, N.; Au, C.; Sweeney, H.; Kityo, C. M; Musiime, V.; Natukunda, E.; Nambi, E.; Rutebarika Antonia, D.; Nazzinda, R.; Namyalo, I.; Nangiya, J.; Nabeeta, L.; Nakalyango, A.; Kobusingye, L.; Otike, C.; Namala, W.; Ampaire, P.; Edgar, A.; Nasaazi, C.; Ndigendawani, M.; Ociti, P.; Kyobutungi, P.; Mbabazi, R.; Mwesigwa Rubondo, P.; Ankunda, J.; Naabalamba, M.; Nannungi, M.; Musiime, A.; Mbasani, F.; Enoch Louis, B.; Namusanje, J.; Odoch, D.; Bagirigomwa, E.; Rubanga, E.; Mulima, D.; Oronon, P.; David Williams, E.; Baliruno, D.; Kobusingye, J.; Uyungrwoth, A.; Mukanza, B.; Okello, J.; Ninsiima, E.; Ezra, L.; Nambi, C.; Mangadalen, N.; Sharif, M.; Serunjogi, N. B; Thomas, O.; Lugemwa, A.; Makumbi, S.; Musumba, S.; Mawejje, E.; Yawe, I.; Jovia Kyomuhendo, L.; Kasozi, M.; Ankunda, R.; Kariisa, S.; Inyakuwa, C.; Ninsiima, E.; Atwine, L.; Tumusiime, B.; Ahuura, J.; Tukwasibwe, D.; Nagasha, V.; Kukundakwe, J.; Zahara Nakisekka, M.; Winnie Nambejja, R.; Tukamushaba, M.; Baker, R.; Keminyeto, E.; Ainebyoona, B.; Myalo, S.; Acen, J.; Jinta Wangwe, N.; Natuhurira, I.; Kananura Natukunatsa, G.; Mulenga, V.; Chabala, C.; Chipili Lungu, J.; Kapasa, M.; Zyambo, K.; Zimba, K.; Zangata, D.; Shingalili, E.; Mumba, N.; Kaonga, N.; Kabesha, M.; Mwenechanya, O.; Chipoya, T.; Manakalanga, F.; Malama, S.; Chola, D.; Nduna, B.; Mwamabazi, M.; Banda, K.; Kabamba, B.; Inambao, M.; Mahy Mukandila, P.; Nachamba, M.; Himabala, S.; Ngosa, S.; Sondashi, D.; Banda, C.; Munyangabe, M.; Mbewe Ngoma, G.; Chimfwembe, S.; Lukonde Malasha, M.; Kajimalwendo, M.; Musukwa, H.; Mumba, S.; Hakim, J.; Bwakura-Dangarembizi, M.; Nathoo, K.; Kamuzungu, T.; Chidziva, E.; Bhiri, J.; Choga, J.; Angela Mujuru, H.; Musoro, G.; Mumbiro, V.; Chitsamatanga, M.; Mutata, C.; Zimunhu, R.; Mudzingwa, S.; Gondo, S.; Moyo, C.; Nhema, R.; Boyd, K.; Matimba, F.; Kouamou, V.; Matarise, R.; Tangwena, Z.; Mudzviti, T.; Matubu, A.; Kateta, A.; Chinembiri, V.; Mukura, D.; Chimanzi, J.; Murungu, D.; Mapfumo, W.; Ngwaru, P.; Chivere, L.; Dube, P.; Mukanganiki, T.; Weza, S.; Gwenzi, T.; Mutsai, S.; Phiri, M.; Ndlovu, M.; Gwaze, T.; Chitongo, S.; Njaravani, W.; Musarurwa, S.; Langa, C.; Tafeni, S.; Ishemunyoro, W.; Mudzimirema, N.; Ndebele, W.; Nyathi, M.; Siziba, G.; Tawodzera, G.; Makuchete, T.; Chidarura, T.; Murangandi, S.; Mafaro, L.; Chivima, O.; Dumani, S.; Mampondo, B.; Maphosa, C.; Mwale, D.; Dhlamini, R.; Sibanda, T.; Madubeko, N.; Nyathi, S.; Matiwaza, Z.; Nabukenya, S.; Tibakabikoba, H.; Nakalanzi, S.; Williams, C.; Chandiwana, P.; Gozhora, W.; Dube, B.; Mulambo, S.; Mwanyungwi, H.; Burger, D.; Colbers, A.; Waalewijn, H.; Bevers, L.; Mohsenian-Naghani, S.; McIlleron, H.; Norman, J.; Wiesner, L.; Wasmann, R.; Denti, P.; Tsirizani Galileya, L.; Natukunda, E.; Musiime, V.; Musoke, P.; Revill, P.; Walker, S.; Kekitiinwa, A.; Mushavi, A.; Banda Kawamya, F.; Tindyebwa, D.; Lyall, H.; Weller, I.; Peto, T.; Musoke, P.; Siwale, M.; Kambarami, R.; Roth, J.; and Beattie, P.\n\n\n \n\n\n\n Journal of the Pediatric Infectious Diseases Society, 13(9): 496–500. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Population$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{waalewijn_population_2024,\n\ttitle = {Population {Pharmacokinetics} of {Dolutegravir} in {African} {Children}: {Results} {From} the {CHAPAS}-4 {Trial}},\n\tvolume = {13},\n\tcopyright = {https://creativecommons.org/licenses/by-nc-nd/4.0/},\n\tissn = {2048-7207},\n\tshorttitle = {Population {Pharmacokinetics} of {Dolutegravir} in {African} {Children}},\n\turl = {https://academic.oup.com/jpids/article/13/9/496/7721687},\n\tdoi = {10.1093/jpids/piae076},\n\tabstract = {Abstract \n            We characterized population pharmacokinetics in 42 African children receiving once-daily 25 mg (14 to \\&lt;20 kg) or 50 mg (\\&gt;20 kg) dolutegravir. Coadministration with emtricitabine and tenofovir alafenamide reduced dolutegravir bioavailability by 19.6\\% (95\\% confidence interval: 8.13\\%–30.8\\%) compared with zidovudine or abacavir with lamivudine. Nevertheless, concentrations remained above efficacy targets, confirming current dosing recommendations.},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {Journal of the Pediatric Infectious Diseases Society},\n\tauthor = {Waalewijn, Hylke and Wasmann, Roeland E and Bamford, Alasdair and Gibb, Diana M and McIlleron, Helen M and Colbers, Angela and Burger, David M and Denti, Paolo and {the CHAPAS-4 trial team} and Gibb, Di and Walker, Sarah and Turkova, Anna and Shakeshaft, Clare and Spyer, Moira and Thomason, Margaret and Griffiths, Anna and Monkiewicz, Lara and Massingham, Sue and Szubert, Alex and Bamford, Alasdair and Doerholt, Katja and Bigault, Amanda and Dudakia, Nimisha and South, Annabelle and Van Looy, Nadine and Au, Carly and Sweeney, Hannah and Kityo, Cissy M and Musiime, Victor and Natukunda, Eva and Nambi, Esether and Rutebarika Antonia, Diana and Nazzinda, Rashida and Namyalo, Imelda and Nangiya, Joan and Nabeeta, Lilian and Nakalyango, Aidah and Kobusingye, Lilian and Otike, Caroline and Namala, Winnie and Ampaire, Phionah and Edgar, Ayesiga and Nasaazi, Claire and Ndigendawani, Milly and Ociti, Paul and Kyobutungi, Priscilla and Mbabazi, Ritah and Mwesigwa Rubondo, Phyllis and Ankunda, Juliet and Naabalamba, Mariam and Nannungi, Mary and Musiime, Alex and Mbasani, Faith and Enoch Louis, Babu and Namusanje, Josephine and Odoch, Denis and Bagirigomwa, Edward and Rubanga, Eddie and Mulima, Disan and Oronon, Paul and David Williams, Eram and Baliruno, David and Kobusingye, Josephine and Uyungrwoth, Agnes and Mukanza, Barbara and Okello, Jimmy and Ninsiima, Emily and Ezra, Lutaro and Nambi, Christine and Mangadalen, Nansaigi and Sharif, Musumba and Serunjogi, Nobert B and Thomas, Otim and Lugemwa, Abbas and Makumbi, Shafic and Musumba, Sharif and Mawejje, Edward and Yawe, Ibrahim and Jovia Kyomuhendo, Linda and Kasozi, Mariam and Ankunda, Rogers and Kariisa, Samson and Inyakuwa, Christine and Ninsiima, Emily and Atwine, Lorna and Tumusiime, Beatrice and Ahuura, John and Tukwasibwe, Deogracious and Nagasha, Violet and Kukundakwe, Judith and Zahara Nakisekka, Mariam and Winnie Nambejja, Ritah and Tukamushaba, Mercy and Baker, Rubinga and Keminyeto, Edridah and Ainebyoona, Barbara and Myalo, Sula and Acen, Juliet and Jinta Wangwe, Nicholas and Natuhurira, Ian and Kananura Natukunatsa, Gershom and Mulenga, Veronica and Chabala, Chishala and Chipili Lungu, Joyce and Kapasa, Monica and Zyambo, Khonzya and Zimba, Kevin and Zangata, Dorothy and Shingalili, Ellen and Mumba, Naomi and Kaonga, Nayunda and Kabesha, Mukumbi and Mwenechanya, Oliver and Chipoya, Terrence and Manakalanga, Friday and Malama, Stephen and Chola, Daniel and Nduna, Bwendo and Mwamabazi, Mwate and Banda, Kabwe and Kabamba, Beatrice and Inambao, Muleya and Mahy Mukandila, Pauline and Nachamba, Mwizukanji and Himabala, Stella and Ngosa, Shadrick and Sondashi, Davies and Banda, Collins and Munyangabe, Mark and Mbewe Ngoma, Grace and Chimfwembe, Sarah and Lukonde Malasha, Mercy and Kajimalwendo, Mumba and Musukwa, Henry and Mumba, Shadrick and Hakim, James and Bwakura-Dangarembizi, Mutsa and Nathoo, Kusum and Kamuzungu, Taneal and Chidziva, Ennie and Bhiri, Joyline and Choga, Joshua and Angela Mujuru, Hilda and Musoro, Godfrey and Mumbiro, Vivian and Chitsamatanga, Moses and Mutata, Constantine and Zimunhu, Rudo and Mudzingwa, Shepherd and Gondo, Secrecy and Moyo, Columbus and Nhema, Ruth and Boyd, Kathryn and Matimba, Farai and Kouamou, Vinie and Matarise, Richard and Tangwena, Zorodzai and Mudzviti, Taona and Matubu, Allen and Kateta, Alfred and Chinembiri, Victor and Mukura, Dorinda and Chimanzi, Joy and Murungu, Dorothy and Mapfumo, Wendy and Ngwaru, Pia and Chivere, Lynette and Dube, Prosper and Mukanganiki, Trust and Weza, Sibusisiwe and Gwenzi, Tsitsi and Mutsai, Shirley and Phiri, Misheck and Ndlovu, Makhosonke and Gwaze, Tapiwa and Chitongo, Stuart and Njaravani, Winisayi and Musarurwa, Sandra and Langa, Cleopatra and Tafeni, Sue and Ishemunyoro, Wilbert and Mudzimirema, Nathalie and Ndebele, Wedu and Nyathi, Mary and Siziba, Grace and Tawodzera, Getrude and Makuchete, Tracey and Chidarura, Takudzwa and Murangandi, Shingaidzo and Mafaro, Lawrence and Chivima, Owen and Dumani, Sifiso and Mampondo, Beaullar and Maphosa, Constance and Mwale, Debra and Dhlamini, Rangarirai and Sibanda, Thabani and Madubeko, Nobukhosi and Nyathi, Silibaziso and Matiwaza, Zibusiso and Nabukenya, Sylvia and Tibakabikoba, Harriet and Nakalanzi, Sarah and Williams, Cynthia and Chandiwana, Precious and Gozhora, Winnie and Dube, Benedictor and Mulambo, Sylvia and Mwanyungwi, Hope and Burger, David and Colbers, Angela and Waalewijn, Hylke and Bevers, Lisanne and Mohsenian-Naghani, Shaghayegh and McIlleron, Helen and Norman, Jennifer and Wiesner, Lubbe and Wasmann, Roeland and Denti, Paolo and Tsirizani Galileya, Lufina and Natukunda, Eva and Musiime, Victor and Musoke, Phillipa and Revill, Paul and Walker, Simon and Kekitiinwa, Adeodata and Mushavi, Angela and Banda Kawamya, Febby and Tindyebwa, Denis and Lyall, Hermione and Weller, Ian and Peto, Tim and Musoke, Philippa and Siwale, Margaret and Kambarami, Rose and Roth, Johanna and Beattie, Pauline},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {496--500},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Testing novel strategies for patients hospitalised with HIV-associated disseminated tuberculosis (NewStrat-TB): protocol for a randomised controlled trial.\n \n \n \n \n\n\n \n Namale, P. E.; Boloko, L.; Vermeulen, M.; Haigh, K. A.; Bagula, F.; Maseko, A.; Sossen, B.; Lee-Jones, S.; Msomi, Y.; McIlleron, H.; Mnguni, A. T.; Crede, T.; Szymanski, P.; Naude, J.; Ebrahim, S.; Vallie, Y.; Moosa, M. S.; Bandeker, I.; Hoosain, S.; Nicol, M. P.; Samodien, N.; Centner, C.; Dowling, W.; Denti, P.; Gumedze, F.; Little, F.; Parker, A.; Price, B.; Schietekat, D.; Simmons, B.; Hill, A.; Wilkinson, R. J.; Oliphant, I.; Hlungulu, S.; Apolisi, I.; Toleni, M.; Asare, Z.; Mpalali, M. K.; Boshoff, E.; Prinsloo, D.; Lakay, F.; Bekiswa, A.; Jackson, A.; Barnes, A.; Johnson, R.; Wasserman, S.; Maartens, G.; Barr, D.; Schutz, C.; and Meintjes, G.\n\n\n \n\n\n\n Trials, 25(1): 311. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Testing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{namale_testing_2024,\n\ttitle = {Testing novel strategies for patients hospitalised with {HIV}-associated disseminated tuberculosis ({NewStrat}-{TB}): protocol for a randomised controlled trial},\n\tvolume = {25},\n\tissn = {1745-6215},\n\tshorttitle = {Testing novel strategies for patients hospitalised with {HIV}-associated disseminated tuberculosis ({NewStrat}-{TB})},\n\turl = {https://trialsjournal.biomedcentral.com/articles/10.1186/s13063-024-08119-4},\n\tdoi = {10.1186/s13063-024-08119-4},\n\tabstract = {Abstract \n             \n              Background \n              HIV-associated tuberculosis (TB) contributes disproportionately to global tuberculosis mortality. Patients hospitalised at the time of the diagnosis of HIV-associated disseminated TB are typically severely ill and have a high mortality risk despite initiation of tuberculosis treatment. The objective of the study is to assess the safety and efficacy of both intensified TB treatment (high dose rifampicin plus levofloxacin) and immunomodulation with corticosteroids as interventions to reduce early mortality in hospitalised patients with HIV-associated disseminated TB. \n             \n             \n              Methods \n              This is a phase III randomised controlled superiority trial, evaluating two interventions in a 2 × 2 factorial design: (1) high dose rifampicin (35 mg/kg/day) plus levofloxacin added to standard TB treatment for the first 14 days versus standard tuberculosis treatment and (2) adjunctive corticosteroids (prednisone 1.5 mg/kg/day) versus identical placebo for the first 14 days of TB treatment. The study population is HIV-positive patients diagnosed with disseminated TB (defined as being positive by at least one of the following assays: urine Alere LAM, urine Xpert MTB/RIF Ultra or blood Xpert MTB/RIF Ultra) during a hospital admission. The primary endpoint is all-cause mortality at 12 weeks comparing, first, patients receiving intensified TB treatment to standard of care and, second, patients receiving corticosteroids to those receiving placebo. Analysis of the primary endpoint will be by intention to treat. Secondary endpoints include all-cause mortality at 2 and 24 weeks. Safety and tolerability endpoints include hepatoxicity evaluations and corticosteroid-related adverse events. \n             \n             \n              Discussion \n              Disseminated TB is characterised by a high mycobacterial load and patients are often critically ill at presentation, with features of sepsis, which carries a high mortality risk. Interventions that reduce this high mycobacterial load or modulate associated immune activation could potentially reduce mortality. If found to be safe and effective, the interventions being evaluated in this trial could be easily implemented in clinical practice. \n             \n             \n              Trial registration \n              ClinicalTrials.gov NCT04951986. Registered on 7 July 2021 \n               \n                https://clinicaltrials.gov/study/NCT04951986},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Trials},\n\tauthor = {Namale, Phiona E. and Boloko, Linda and Vermeulen, Marcia and Haigh, Kate A. and Bagula, Fortuna and Maseko, Alexis and Sossen, Bianca and Lee-Jones, Scott and Msomi, Yoliswa and McIlleron, Helen and Mnguni, Ayanda Trevor and Crede, Thomas and Szymanski, Patryk and Naude, Jonathan and Ebrahim, Sakeena and Vallie, Yakoob and Moosa, Muhammed Shiraz and Bandeker, Ismail and Hoosain, Shakeel and Nicol, Mark P. and Samodien, Nazlee and Centner, Chad and Dowling, Wentzel and Denti, Paolo and Gumedze, Freedom and Little, Francesca and Parker, Arifa and Price, Brendon and Schietekat, Denzil and Simmons, Bryony and Hill, Andrew and Wilkinson, Robert J. and Oliphant, Ida and Hlungulu, Siphokazi and Apolisi, Ivy and Toleni, Monica and Asare, Zimkhitha and Mpalali, Mkanyiseli Kenneth and Boshoff, Erica and Prinsloo, Denise and Lakay, Francisco and Bekiswa, Abulele and Jackson, Amanda and Barnes, Ashleigh and Johnson, Ryan and Wasserman, Sean and Maartens, Gary and Barr, David and Schutz, Charlotte and Meintjes, Graeme},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {311},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Background HIV-associated tuberculosis (TB) contributes disproportionately to global tuberculosis mortality. Patients hospitalised at the time of the diagnosis of HIV-associated disseminated TB are typically severely ill and have a high mortality risk despite initiation of tuberculosis treatment. The objective of the study is to assess the safety and efficacy of both intensified TB treatment (high dose rifampicin plus levofloxacin) and immunomodulation with corticosteroids as interventions to reduce early mortality in hospitalised patients with HIV-associated disseminated TB. Methods This is a phase III randomised controlled superiority trial, evaluating two interventions in a 2 × 2 factorial design: (1) high dose rifampicin (35 mg/kg/day) plus levofloxacin added to standard TB treatment for the first 14 days versus standard tuberculosis treatment and (2) adjunctive corticosteroids (prednisone 1.5 mg/kg/day) versus identical placebo for the first 14 days of TB treatment. The study population is HIV-positive patients diagnosed with disseminated TB (defined as being positive by at least one of the following assays: urine Alere LAM, urine Xpert MTB/RIF Ultra or blood Xpert MTB/RIF Ultra) during a hospital admission. The primary endpoint is all-cause mortality at 12 weeks comparing, first, patients receiving intensified TB treatment to standard of care and, second, patients receiving corticosteroids to those receiving placebo. Analysis of the primary endpoint will be by intention to treat. Secondary endpoints include all-cause mortality at 2 and 24 weeks. Safety and tolerability endpoints include hepatoxicity evaluations and corticosteroid-related adverse events. Discussion Disseminated TB is characterised by a high mycobacterial load and patients are often critically ill at presentation, with features of sepsis, which carries a high mortality risk. Interventions that reduce this high mycobacterial load or modulate associated immune activation could potentially reduce mortality. If found to be safe and effective, the interventions being evaluated in this trial could be easily implemented in clinical practice. Trial registration ClinicalTrials.gov NCT04951986. Registered on 7 July 2021 https://clinicaltrials.gov/study/NCT04951986\n

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\n \n\n \n \n \n \n \n \n Author Correction: High monoclonal neutralization titers reduced breakthrough HIV-1 viral loads in the Antibody Mediated Prevention trials.\n \n \n \n \n\n\n \n Reeves, D. B.; Mayer, B. T.; deCamp , A. C.; Huang, Y.; Zhang, B.; Carpp, L. N.; Magaret, C. A.; Juraska, M.; Gilbert, P. B.; Montefiori, D. C.; Bar, K. J.; Cardozo-Ojeda, E. F.; Schiffer, J. T.; Rossenkhan, R.; Edlefsen, P.; Morris, L.; Mkhize, N. N.; Williamson, C.; Mullins, J. I.; Seaton, K. E.; Tomaras, G. D.; Andrew, P.; Mgodi, N.; Ledgerwood, J. E.; Cohen, M. S.; Corey, L.; Naidoo, L.; Orrell, C.; Goepfert, P. A.; Casapia, M.; Sobieszczyk, M. E.; Karuna, S. T.; and Edupuganti, S.\n\n\n \n\n\n\n Nature Communications, 15(1): 2575. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Author$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{reeves_author_2024,\n\ttitle = {Author {Correction}: {High} monoclonal neutralization titers reduced breakthrough {HIV}-1 viral loads in the {Antibody} {Mediated} {Prevention} trials},\n\tvolume = {15},\n\tissn = {2041-1723},\n\tshorttitle = {Author {Correction}},\n\turl = {https://www.nature.com/articles/s41467-024-46805-8},\n\tdoi = {10.1038/s41467-024-46805-8},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Reeves, Daniel B. and Mayer, Bryan T. and deCamp, Allan C. and Huang, Yunda and Zhang, Bo and Carpp, Lindsay N. and Magaret, Craig A. and Juraska, Michal and Gilbert, Peter B. and Montefiori, David C. and Bar, Katharine J. and Cardozo-Ojeda, E. Fabian and Schiffer, Joshua T. and Rossenkhan, Raabya and Edlefsen, Paul and Morris, Lynn and Mkhize, Nonhlanhla N. and Williamson, Carolyn and Mullins, James I. and Seaton, Kelly E. and Tomaras, Georgia D. and Andrew, Philip and Mgodi, Nyaradzo and Ledgerwood, Julie E. and Cohen, Myron S. and Corey, Lawrence and Naidoo, Logashvari and Orrell, Catherine and Goepfert, Paul A. and Casapia, Martin and Sobieszczyk, Magdalena E. and Karuna, Shelly T. and Edupuganti, Srilatha},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {2575},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n HIV-1 subtype A1, D, and recombinant proviral genome landscapes during long-term suppressive therapy.\n \n \n \n \n\n\n \n Lee, G. Q.; Khadka, P.; Gowanlock, S. N.; Copertino, D. C.; Duncan, M. C.; Omondi, F. H.; Kinloch, N. N.; Kasule, J.; Kityamuweesi, T.; Buule, P.; Jamiru, S.; Tomusange, S.; Anok, A.; Chen, Z.; Jones, R. B.; Galiwango, R. M.; Reynolds, S. J.; Quinn, T. C.; Brumme, Z. L.; Redd, A. D.; and Prodger, J. L.\n\n\n \n\n\n\n Nature Communications, 15(1): 5480. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"HIV-1$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{lee_hiv-1_2024,\n\ttitle = {{HIV}-1 subtype {A1}, {D}, and recombinant proviral genome landscapes during long-term suppressive therapy},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-48985-9},\n\tdoi = {10.1038/s41467-024-48985-9},\n\tabstract = {Abstract \n             \n              The primary obstacle to curing HIV-1 is a reservoir of CD4+ cells that contain stably integrated provirus. Previous studies characterizing the proviral landscape, which have been predominantly conducted in males in the United States and Europe living with HIV-1 subtype B, have revealed that most proviruses that persist during antiretroviral therapy (ART) are defective. In contrast, less is known about proviral landscapes in females with non-B subtypes, which represents the largest group of individuals living with HIV-1. Here, we analyze genomic DNA from resting CD4+ T-cells from 16 female and seven male Ugandans with HIV-1 receiving suppressive ART ( \n              n \n               = 23). We perform near-full-length proviral sequencing at limiting dilution to examine the proviral genetic landscape, yielding 607 HIV-1 subtype A1, D, and recombinant proviral sequences (mean 26/person). We observe that intact genomes are relatively rare and clonal expansion occurs in both intact and defective genomes. Our modification of the primers and probes of the Intact Proviral DNA Assay (IPDA), developed for subtype B, rescues intact provirus detection in Ugandan samples for which the original IPDA fails. This work will facilitate research on HIV-1 persistence and cure strategies in Africa, where the burden of HIV-1 is heaviest.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Lee, Guinevere Q. and Khadka, Pragya and Gowanlock, Sarah N. and Copertino, Dennis C. and Duncan, Maggie C. and Omondi, F. Harrison and Kinloch, Natalie N. and Kasule, Jingo and Kityamuweesi, Taddeo and Buule, Paul and Jamiru, Samiri and Tomusange, Stephen and Anok, Aggrey and Chen, Zhengming and Jones, R. Brad and Galiwango, Ronald M. and Reynolds, Steven J. and Quinn, Thomas C. and Brumme, Zabrina L. and Redd, Andrew D. and Prodger, Jessica L.},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {5480},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Use of electron microscopy to determine presence of coal dust in a neighborhood bordering an open-air coal terminal in Curtis Bay, Baltimore, Maryland, USA.\n \n \n \n \n\n\n \n Aubourg, M. A.; Livi, K. J.; Sawtell, G. G.; Sanchez-Gonzalez, C. C.; Spada, N. J.; Dickerson, R. R.; Chiou, W.; Kamanzi, C.; Ramachandran, G.; Rule, A. M.; and Heaney, C. D.\n\n\n \n\n\n\n Science of The Total Environment, 957: 176842. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Use$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{aubourg_use_2024,\n\ttitle = {Use of electron microscopy to determine presence of coal dust in a neighborhood bordering an open-air coal terminal in {Curtis} {Bay}, {Baltimore}, {Maryland}, {USA}},\n\tvolume = {957},\n\tissn = {00489697},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0048969724069997},\n\tdoi = {10.1016/j.scitotenv.2024.176842},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Science of The Total Environment},\n\tauthor = {Aubourg, Matthew A. and Livi, Kenneth J.T. and Sawtell, Gregory G. and Sanchez-Gonzalez, Carlos C. and Spada, Nicholas J. and Dickerson, Russell R. and Chiou, Wen-An and Kamanzi, Conchita and Ramachandran, Gurumurthy and Rule, Ana M. and Heaney, Christopher D.},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {176842},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Behavioural and social drivers of human papillomavirus vaccination in eThekwini District of KwaZulu-Natal Province, South Africa.\n \n \n \n \n\n\n \n Bhengu, P.; Ndwandwe, D.; Cooper, S.; Katoto, P. D. M. C.; Wiysonge, C. S.; and Shey, M.\n\n\n \n\n\n\n PLOS ONE, 19(12): e0311509. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Behavioural$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{bhengu_behavioural_2024,\n\ttitle = {Behavioural and social drivers of human papillomavirus vaccination in {eThekwini} {District} of {KwaZulu}-{Natal} {Province}, {South} {Africa}},\n\tvolume = {19},\n\tissn = {1932-6203},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0311509},\n\tdoi = {10.1371/journal.pone.0311509},\n\tabstract = {Background \n              Cervical cancer is the second most common cancer in women in South Africa. Infection with high-risk types of human papillomavirus (HPV) is the cause of cervical cancer, which can be prevented by HPV vaccination. However, there is wide variation in HPV vaccination coverage among the urban districts of South Africa; with the lowest coverage being 40\\% in eThekwini, KwaZulu-Natal. There could be many factors which affect HPV vaccine uptake in eThekwini District. Thus, this research aims to investigate the behaviourial and social drivers of HPV vaccination in this district. \n             \n             \n              Methods \n              The study will consist of two phases. We will apply a convergent parallel mixed methods approach, including a quantitative survey (phase 1) and in-depth interviews (phase 2) among caregivers and frontline healthcare workers to determine the drivers of HPV vaccination uptake. \n             \n             \n              Discussion \n              The study will provide knowledge on the main barriers facing HPV vaccination and provide contextually-tailored solutions for how these barriers might be addressed. A policy brief will be formulated from this study aimed at government policymakers and other stakeholders who formulate or influence policy, respectively. In addition, we will disseminate the findings through peer-reviewed publications in scientific journals.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {PLOS ONE},\n\tauthor = {Bhengu, P. and Ndwandwe, D. and Cooper, S. and Katoto, P. D. M. C. and Wiysonge, C. S. and Shey, M.},\n\teditor = {Adebamowo, Clement A.},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {e0311509},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Protocol to phenotype and quantify mycobacteria-specific myeloid cells from human airways by mass cytometry.\n \n \n \n \n\n\n \n Kiravu, A.; Rozot, V.; Cruywagen, L.; Gutschmidt, A.; DuPlessis, N.; Nemes, E.; Tameris, M.; Scriba, T.; Conradie, A.; Kafaar, F.; Van Rensburg, I. C.; Walzl, G.; Malherbe, S.; Shabangu, A.; and Middelkoop, K.\n\n\n \n\n\n\n STAR Protocols, 5(4): 103463. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Protocol$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kiravu_protocol_2024,\n\ttitle = {Protocol to phenotype and quantify mycobacteria-specific myeloid cells from human airways by mass cytometry},\n\tvolume = {5},\n\tissn = {26661667},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666166724006282},\n\tdoi = {10.1016/j.xpro.2024.103463},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {STAR Protocols},\n\tauthor = {Kiravu, Agano and Rozot, Virgine and Cruywagen, Lauren and Gutschmidt, Andrea and DuPlessis, Nelita and Nemes, Elisa and Tameris, Michele and Scriba, Thomas and Conradie, Arina and Kafaar, Fazlin and Van Rensburg, Ilana C. and Walzl, Gerhard and Malherbe, Stephanus and Shabangu, Ayanda and Middelkoop, Keren},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {103463},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Metabolic modelling as a powerful tool to identify critical components of Pneumocystis growth medium.\n \n \n \n \n\n\n \n Nev, O. A.; Zamaraeva, E.; De Oliveira, R.; Ryzhkov, I.; Duvenage, L.; Abou-Jaoudé, W.; Ouattara, D. A.; Hoving, J. C.; Gudelj, I.; and Brown, A. J. P.\n\n\n \n\n\n\n PLOS Computational Biology, 20(10): e1012545. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Metabolic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{nev_metabolic_2024,\n\ttitle = {Metabolic modelling as a powerful tool to identify critical components of {Pneumocystis} growth medium},\n\tvolume = {20},\n\tissn = {1553-7358},\n\turl = {https://dx.plos.org/10.1371/journal.pcbi.1012545},\n\tdoi = {10.1371/journal.pcbi.1012545},\n\tabstract = {Establishing suitable \n              in vitro \n              culture conditions for microorganisms is crucial for dissecting their biology and empowering potential applications. However, a significant number of bacterial and fungal species, including \n              Pneumocystis jirovecii \n              , remain unculturable, hampering research efforts. \n              P \n              . \n              jirovecii \n              is a deadly pathogen of humans that causes life-threatening pneumonia in immunocompromised individuals and transplant patients. Despite the major impact of \n              Pneumocystis \n              on human health, limited progress has been made in dissecting the pathobiology of this fungus. This is largely due to the fact that its experimental dissection has been constrained by the inability to culture the organism \n              in vitro \n              . We present a comprehensive \n              in silico \n              genome-scale metabolic model of \n              Pneumocystis \n              growth and metabolism, to identify metabolic requirements and imbalances that hinder growth \n              in vitro \n              . We utilise recently published genome data and available information in the literature as well as bioinformatics and software tools to develop and validate the model. In addition, we employ relaxed Flux Balance Analysis and Reinforcement Learning approaches to make predictions regarding metabolic fluxes and to identify critical components of the \n              Pneumocystis \n              growth medium. Our findings offer insights into the biology of \n              Pneumocystis \n              and provide a novel strategy to overcome the longstanding challenge of culturing this pathogen \n              in vitro \n              .},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Computational Biology},\n\tauthor = {Nev, Olga A. and Zamaraeva, Elena and De Oliveira, Romain and Ryzhkov, Ilia and Duvenage, Lucian and Abou-Jaoudé, Wassim and Ouattara, Djomangan Adama and Hoving, Jennifer Claire and Gudelj, Ivana and Brown, Alistair J. P.},\n\teditor = {Kaleta, Christoph},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {e1012545},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n WHO global research priorities for antimicrobial resistance in human health.\n \n \n \n \n\n\n \n Bertagnolio, S.; Dobreva, Z.; Centner, C. M; Olaru, I. D.; Donà, D.; Burzo, S.; Huttner, B. D; Chaillon, A.; Gebreselassie, N.; Wi, T.; Hasso-Agopsowicz, M.; Allegranzi, B.; Sati, H.; Ivanovska, V.; Kothari, K. U; Balkhy, H. H; Cassini, A.; Hamers, R. L; Weezenbeek, K. V.; Aanensen, D.; Alanio, A.; Alastruey-Izquierdo, A.; Alemayehu, T.; Al-Hasan, M.; Allegaert, K.; Al-Maani, A. S.; Al-Salman, J.; Alshukairi, A. N.; Amir, A.; Applegate, T.; Araj, G. F; Villalobos, M. A.; Årdal, C.; Ashiru-Oredope, D.; Ashley, E. A; Babin, F.; Bachmann, L. H; Bachmann, T.; Baker, K. S.; Balasegaram, M.; Bamford, C.; Baquero, F.; Barcelona, L. I.; Bassat, Q.; Bassetti, M.; Basu, S.; Beardsley, J.; Vásquez, G. B.; Berkley, J. A; Bhatnagar, A. K; Bielicki, J.; Bines, J.; Bongomin, F.; Bonomo, R. A; Bradley, J. S; Bradshaw, C.; Brett, A.; Brink, A.; Brown, C.; Brown, J.; Buising, K.; Carson, C.; Carvalho, A. C.; Castagnola, E.; Cavaleri, M.; Cecchini, M.; Chabala, C.; Chaisson, R. E; Chakrabarti, A.; Chandler, C.; Chandy, S. J.; Charani, E.; Chen, L.; Chiara, F.; Chowdhary, A.; Chua, A.; Chuki, P.; Chun, D. R.; Churchyard, G.; Cirillo, D.; Clack, L.; Coffin, S. E; Cohn, J.; Cole, M.; Conly, J.; Cooper, B.; Corso, A.; Cosgrove, S. E; Cox, H.; Daley, C. L; Darboe, S.; Darton, T.; Davies, G.; De Egea, V.; Dedeić-Ljubović, A.; Deeves, M.; Denkinger, C.; Dillon, J. R; Dramowski, A.; Eley, B.; Roberta Esposito, S. M.; Essack, S. Y; Farida, H.; Farooqi, J.; Feasey, N.; Ferreyra, C.; Fifer, H.; Finlayson, H.; Frick, M.; Gales, A. C.; Galli, L.; Gandra, S.; Gerber, J. S; Giske, C.; Gordon, B.; Govender, N.; Guessennd, N.; Guindo, I.; Gurbanova, E.; Gwee, A.; Hagen, F.; Harbarth, S.; Haze, J.; Heim, J.; Hendriksen, R.; Heyderman, R. S.; Holt, K. E.; Hönigl, M.; Hook, E. W; Hope, W.; Hopkins, H.; Hughes, G.; Ismail, G.; Issack, M. I.; Jacobs, J.; Jasovský, D.; Jehan, F.; Pearson, A. J.; Jones, M.; Joshi, M. P; Kapil, A.; Kariuki, S.; Karkey, A.; Kearns, G. L; Keddy, K. H.; Khanna, N.; Kitamura, A.; Kolho, K.; Kontoyiannis, D. P; Kotwani, A.; Kozlov, R. S; Kranzer, K.; Kularatne, R.; Lahra, M. M; Langford, B. J; Laniado-Laborin, R.; Larsson, D G J.; Lass-Flörl, C.; Le Doare, K.; Lee, H.; Lessa, F.; Levin, A. S; Limmathurotsakul, D.; Lincopan, N.; Lo Vecchio, A.; Lodha, R.; Loeb, M.; Longtin, Y.; Lye, D. C.; Mahmud, A. M.; Manaia, C.; Manderson, L.; Mareković, I.; Marimuthu, K.; Martin, I.; Mashe, T.; Mei, Z.; Meis, J. F; Lyra Tavares De Melo, F. A.; Mendelson, M.; Miranda, A. E.; Moore, D.; Morel, C.; Moremi, N.; Moro, M. L.; Moussy, F.; Mshana, S.; Mueller, A.; Ndow, F. J; Nicol, M.; Nunn, A.; Obaro, S.; Obiero, C. W; Okeke, I. N; Okomo, U.; Okwor, T. J; Oladele, R.; Omulo, S.; Ondoa, P.; Ortellado De Canese, J. M.; Ostrosky-Zeichner, L.; Padoveze, M. C.; Pai, M.; Park, B.; Parkhill, J.; Parry, C. M; Peeling, R.; Sobreira Vieira Peixe, L. M.; Perovic, O.; Pettigrew, M. M; Principi, N.; Pulcini, C.; Puspandari, N.; Rawson, T.; Reddy, D. L.; Reddy, K.; Redner, P.; Rodríguez Tudela, J. L.; Rodríguez-Baño, J.; Van Katwyk, S. R.; Roilides, E.; Rollier, C.; Rollock, L.; Ronat, J.; Ruppe, E.; Sadarangani, M.; Salisbury, D.; Salou, M.; Samison, L. H.; Sanguinetti, M.; Sartelli, M.; Schellack, N.; Schouten, J.; Schwaber, M. J; Seni, J.; Senok, A.; Shafer, W. M; Shakoor, S.; Sheppard, D.; Shin, J.; Sia, S.; Sievert, D.; Singh, I.; Singla, R.; Skov, R. L.; Soge, O. O; Sprute, R.; Srinivasan, A.; Srinivasan, S.; Sundsfjord, A.; Tacconelli, E.; Tahseen, S.; Tangcharoensathien, V.; Tängdén, T.; Thursky, K.; Thwaites, G.; Tigulini De Souza Peral, R.; Tong, D.; Tootla, H. D.; Tsioutis, C.; Turner, K. M; Turner, P.; Omar, S. V.; Van De Sande, W. W.; Van Den Hof, S.; Van Doorn, R.; Veeraraghavan, B.; Verweij, P.; Wahyuningsih, R.; Wang, H.; Warris, A.; Weinstock, H.; Wesangula, E.; Whiley, D.; White, P. J; Williams, P.; Xiao, Y.; Moscoso, M. Y.; Yang, H. L.; Yoshida, S.; Yu, Y.; Żabicka, D.; Zignol, M.; and Rudan, I.\n\n\n \n\n\n\n The Lancet Microbe, 5(11): 100902. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"WHO$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{bertagnolio_who_2024,\n\ttitle = {{WHO} global research priorities for antimicrobial resistance in human health},\n\tvolume = {5},\n\tissn = {26665247},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524724001344},\n\tdoi = {10.1016/S2666-5247(24)00134-4},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Bertagnolio, Silvia and Dobreva, Zlatina and Centner, Chad M and Olaru, Ioana Diana and Donà, Daniele and Burzo, Stefano and Huttner, Benedikt D and Chaillon, Antoine and Gebreselassie, Nebiat and Wi, Teodora and Hasso-Agopsowicz, Mateusz and Allegranzi, Benedetta and Sati, Hatim and Ivanovska, Verica and Kothari, Kavita U and Balkhy, Hanan H and Cassini, Alessandro and Hamers, Raph L and Weezenbeek, Kitty Van and Aanensen, David and Alanio, Alexandre and Alastruey-Izquierdo, Ana and Alemayehu, Tinsae and Al-Hasan, Majdi and Allegaert, Karel and Al-Maani, Amal Saif and Al-Salman, Jameela and Alshukairi, Abeer Nizar and Amir, Afreenish and Applegate, Tanya and Araj, George F and Villalobos, Marlen Arce and Årdal, Christine and Ashiru-Oredope, Diane and Ashley, Elizabeth A and Babin, François-Xavier and Bachmann, Laura H and Bachmann, Till and Baker, Kate Susan and Balasegaram, Manica and Bamford, Colleen and Baquero, Fernando and Barcelona, Laura Isabel and Bassat, Quique and Bassetti, Matteo and Basu, Sulagna and Beardsley, Justin and Vásquez, Grey Benoit and Berkley, James A and Bhatnagar, Anuj K and Bielicki, Julia and Bines, Julie and Bongomin, Felix and Bonomo, Robert A and Bradley, John S and Bradshaw, Catriona and Brett, Ana and Brink, Adrian and Brown, Colin and Brown, Jeremy and Buising, Kirsty and Carson, Carolee and Carvalho, Anna Cristina and Castagnola, Elio and Cavaleri, Marco and Cecchini, Michele and Chabala, Chishala and Chaisson, Richard E and Chakrabarti, Arunaloke and Chandler, Clare and Chandy, Sujith John and Charani, Esmita and Chen, Lisa and Chiara, Francesca and Chowdhary, Anuradha and Chua, Arlene and Chuki, Pem and Chun, Doo Ryeon and Churchyard, Gavin and Cirillo, Daniela and Clack, Lauren and Coffin, Susan E and Cohn, Jennifer and Cole, Michelle and Conly, John and Cooper, Ben and Corso, Alejandra and Cosgrove, Sara E and Cox, Helen and Daley, Charles L and Darboe, Saffiatou and Darton, Tom and Davies, Gerry and De Egea, Viviana and Dedeić-Ljubović, Amela and Deeves, Miranda and Denkinger, Claudia and Dillon, Jo-Anne R and Dramowski, Angela and Eley, Brian and Roberta Esposito, Susanna Maria and Essack, Sabiha Y and Farida, Helmia and Farooqi, Joveria and Feasey, Nicholas and Ferreyra, Cecilia and Fifer, Helen and Finlayson, Heather and Frick, Mike and Gales, Ana Cristina and Galli, Luisa and Gandra, Sumanth and Gerber, Jeffrey S and Giske, Christian and Gordon, Bruce and Govender, Nelesh and Guessennd, Nathalie and Guindo, Ibrehima and Gurbanova, Elmira and Gwee, Amanda and Hagen, Ferry and Harbarth, Stephan and Haze, John and Heim, Jutta and Hendriksen, Rene and Heyderman, Robert Simon and Holt, Kathryn Elizabeth and Hönigl, Martin and Hook, Edward W and Hope, William and Hopkins, Heidi and Hughes, Gwenda and Ismail, Ghada and Issack, Mohammad Iqbal and Jacobs, Jan and Jasovský, Dušan and Jehan, Fyeza and Pearson, Antonieta Jimenez and Jones, Makoto and Joshi, Mohan P and Kapil, Arti and Kariuki, Samuel and Karkey, Abhilasha and Kearns, Gregory L and Keddy, Karen Helena and Khanna, Nina and Kitamura, Akiko and Kolho, Kaija-Leena and Kontoyiannis, Dimitrios P and Kotwani, Anita and Kozlov, Roman S and Kranzer, Katharina and Kularatne, Ranmini and Lahra, Monica M and Langford, Bradley J and Laniado-Laborin, Rafael and Larsson, D G Joakim and Lass-Flörl, Cornelia and Le Doare, Kirsty and Lee, Hyukmin and Lessa, Fernanda and Levin, Anna S and Limmathurotsakul, Direk and Lincopan, Nilton and Lo Vecchio, Andrea and Lodha, Rakesh and Loeb, Mark and Longtin, Yves and Lye, David Chien and Mahmud, Asif Mujtaba and Manaia, Célia and Manderson, Lenore and Mareković, Ivana and Marimuthu, Kalisvar and Martin, Irene and Mashe, Tapfumanei and Mei, Zeng and Meis, Jacques F and Lyra Tavares De Melo, Flávio Augusto and Mendelson, Marc and Miranda, Angelica Espinosa and Moore, David and Morel, Chantal and Moremi, Nyambura and Moro, Maria Luisa and Moussy, Francis and Mshana, Stephen and Mueller, Arno and Ndow, Francis J and Nicol, Mark and Nunn, Andrew and Obaro, Stephen and Obiero, Christina W and Okeke, Iruka N and Okomo, Uduak and Okwor, Tochi J and Oladele, Rita and Omulo, Sylvia and Ondoa, Pascale and Ortellado De Canese, Juana Medarda and Ostrosky-Zeichner, Luis and Padoveze, Maria Clara and Pai, Madhukar and Park, Benjamin and Parkhill, Julian and Parry, Christopher M and Peeling, Rosanna and Sobreira Vieira Peixe, Luísa Maria and Perovic, Olga and Pettigrew, Melinda M and Principi, Nicola and Pulcini, Céline and Puspandari, Nelly and Rawson, Timothy and Reddy, Denasha Lavanya and Reddy, Kessendri and Redner, Paulo and Rodríguez Tudela, Juan Luis and Rodríguez-Baño, Jesús and Van Katwyk, Susan Rogers and Roilides, Emmanuel and Rollier, Christine and Rollock, Leslie and Ronat, Jean-Baptiste and Ruppe, Etienne and Sadarangani, Manish and Salisbury, David and Salou, Mounerou and Samison, Luc Hervé and Sanguinetti, Maurizio and Sartelli, Massimo and Schellack, Natalie and Schouten, Jeroen and Schwaber, Mitchell J and Seni, Jeremiah and Senok, Abiola and Shafer, William M and Shakoor, Sadia and Sheppard, Donald and Shin, Jong-Hee and Sia, Sonia and Sievert, Dawn and Singh, Ishwar and Singla, Rupak and Skov, Robert Leo and Soge, Olusegun O and Sprute, Rosanne and Srinivasan, Arjun and Srinivasan, Subasree and Sundsfjord, Arnfinn and Tacconelli, Evelina and Tahseen, Sabira and Tangcharoensathien, Viroj and Tängdén, Thomas and Thursky, Karin and Thwaites, Guy and Tigulini De Souza Peral, Renata and Tong, Deborah and Tootla, Hafsah Deepa and Tsioutis, Constantinos and Turner, Katy M and Turner, Paul and Omar, Shaheed Vally and Van De Sande, Wendy Wj and Van Den Hof, Susan and Van Doorn, Rogier and Veeraraghavan, Balaji and Verweij, Paul and Wahyuningsih, Retno and Wang, Hui and Warris, Adilia and Weinstock, Hillard and Wesangula, Evelyn and Whiley, David and White, Peter J and Williams, Phoebe and Xiao, Yonghong and Moscoso, Martin Yagui and Yang, Hsu Li and Yoshida, Sachiyo and Yu, Yunsong and Żabicka, Dorota and Zignol, Matteo and Rudan, Igor},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {100902},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Premature skewing of T cell receptor clonality and delayed memory expansion in HIV-exposed infants.\n \n \n \n \n\n\n \n Dzanibe, S.; Wilk, A. J.; Canny, S.; Ranganath, T.; Alinde, B.; Rubelt, F.; Huang, H.; Davis, M. M.; Holmes, S. P.; Jaspan, H. B.; Blish, C. A.; and Gray, C. M.\n\n\n \n\n\n\n Nature Communications, 15(1): 4080. May 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Premature$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{dzanibe_premature_2024,\n\ttitle = {Premature skewing of {T} cell receptor clonality and delayed memory expansion in {HIV}-exposed infants},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-47955-5},\n\tdoi = {10.1038/s41467-024-47955-5},\n\tabstract = {Abstract \n             \n              While preventing vertical HIV transmission has been very successful, HIV-exposed uninfected infants (iHEU) experience an elevated risk to infections compared to HIV-unexposed and uninfected infants (iHUU). Here we present a longitudinal multimodal analysis of infant immune ontogeny that highlights the impact of HIV/ARV exposure. Using mass cytometry, we show alterations in T cell memory differentiation between iHEU and iHUU being significant from week 15 of life. The altered memory T cell differentiation in iHEU was preceded by lower TCR Vβ clonotypic diversity and linked to TCR clonal depletion within the naïve T cell compartment. Compared to iHUU, iHEU had elevated CD56 \n              lo \n              CD16 \n              lo \n              Perforin \n              + \n              CD38 \n              + \n              CD45RA \n              + \n              FcεRIγ \n              + \n              NK cells at 1 month postpartum and whose abundance pre-vaccination were predictive of vaccine-induced pertussis and rotavirus antibody responses post 3 months of life. Collectively, HIV/ARV exposure disrupted the trajectory of innate and adaptive immunity from birth which may underlie relative vulnerability to infections in iHEU.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Dzanibe, Sonwabile and Wilk, Aaron J. and Canny, Susan and Ranganath, Thanmayi and Alinde, Berenice and Rubelt, Florian and Huang, Huang and Davis, Mark M. and Holmes, Susan P. and Jaspan, Heather B. and Blish, Catherine A. and Gray, Clive M.},\n\tmonth = may,\n\tyear = {2024},\n\tpages = {4080},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Corrigendum to “In vitro antiplasmodium and antitrypanosomal activities, β-haematin formation inhibition, molecular docking and DFT computational studies of quinoline-urea-benzothiazole hybrids” [Heliyon Volume 10, Issue 19, October 2024, Article e38434].\n \n \n \n \n\n\n \n Oyeneyin, O. E.; Moodley, R.; Mashaba, C.; Garnie, L. F.; Omoboyowa, D. A.; Rakodi, G. H.; Maphoru, M. V.; Balogun, M. O.; Hoppe, H. C.; Egan, T. J.; and Tukulula, M.\n\n\n \n\n\n\n Heliyon, 10(23): e40195. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Corrigendum$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{oyeneyin_corrigendum_2024,\n\ttitle = {Corrigendum to “{In} vitro antiplasmodium and antitrypanosomal activities, β-haematin formation inhibition, molecular docking and {DFT} computational studies of quinoline-urea-benzothiazole hybrids” [{Heliyon} {Volume} 10, {Issue} 19, {October} 2024, {Article} e38434]},\n\tvolume = {10},\n\tissn = {24058440},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2405844024162263},\n\tdoi = {10.1016/j.heliyon.2024.e40195},\n\tlanguage = {en},\n\tnumber = {23},\n\turldate = {2025-06-24},\n\tjournal = {Heliyon},\n\tauthor = {Oyeneyin, Oluwatoba E. and Moodley, Rashmika and Mashaba, Chakes and Garnie, Larnelle F. and Omoboyowa, Damilola A. and Rakodi, Goitsemodimo H. and Maphoru, Mabuatsela V. and Balogun, Mohamed O. and Hoppe, Heinrich C. and Egan, Timothy J. and Tukulula, Matshawandile},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {e40195},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Influence of Genetic Polymorphisms on the Age at Cancer Diagnosis in a Homogenous Lynch Syndrome Cohort of Individuals Carrying the MLH1:c.1528C\\textgreaterT South African Founder Variant.\n \n \n \n \n\n\n \n Ndou, L.; Chambuso, R.; Algar, U.; Goldberg, P.; Boutall, A.; and Ramesar, R.\n\n\n \n\n\n\n Biomedicines, 12(10): 2201. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Influence$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{ndou_influence_2024,\n\ttitle = {Influence of {Genetic} {Polymorphisms} on the {Age} at {Cancer} {Diagnosis} in a {Homogenous} {Lynch} {Syndrome} {Cohort} of {Individuals} {Carrying} the {MLH1}:c.{1528C}{\\textgreater}{T} {South} {African} {Founder} {Variant}},\n\tvolume = {12},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2227-9059},\n\tshorttitle = {Influence of {Genetic} {Polymorphisms} on the {Age} at {Cancer} {Diagnosis} in a {Homogenous} {Lynch} {Syndrome} {Cohort} of {Individuals} {Carrying} the {MLH1}},\n\turl = {https://www.mdpi.com/2227-9059/12/10/2201},\n\tdoi = {10.3390/biomedicines12102201},\n\tabstract = {Background: High variability in the age at cancer diagnosis in Lynch syndrome (LS) patients is widely observed, even among relatives with the same germline pathogenic variant (PV) in the mismatch repair (MMR) genes. Genetic polymorphisms and lifestyle factors are thought to contribute to this variability. We investigated the influence of previously reported genetic polymorphisms on the age at cancer diagnosis in a homogenous LS cohort with a South African founder germline PV c.1528C{\\textgreater}T in the MLH1 gene. Methods: A total of 359 LS variant heterozygotes (LSVH) from 60 different families were genotyped for specific genetic polymorphisms in GSTM1, GSTT1, CYP1A1, CYP17, PPP2R2B, KIF20A, TGFB1, XRCC5, TNF, BCL2, CHFR, CDC25C, ATM, TTC28, CDC25C, HFE, and hTERT genes using Multiplex Polymerase Chain Reaction and MassArray methods. Kaplan–Meier survival analysis, univariate and multivariate Cox proportional hazards gamma shared frailty models adjusted for sex were used to estimate the association between age at cancer diagnosis and polymorphism genotypes. A p-value {\\textless} 0.05 after correcting for multiple testing using the Benjamini–Hochberg method was considered significant at a 95\\% confidence interval. Results: We identified three genotypes in the cell-cycle regulation, DNA repair, and xenobiotic-metabolism genes significantly associated with age at cancer diagnosis in this cohort. The CYP1A1 rs4646903 risk (GG) and CDC25C rs3734166 polymorphic (GA+AA) genotypes were significantly associated with an increased risk of a younger age at cancer diagnosis (Adj HR: 2.03 [1.01–4.08], p = 0.034 and Adj HR: 1.53 [1.09–2.14], p = 0.015, respectively). LSVH who were heterozygous for the XRCC5 rs1051685 SNP showed significant protection against younger age at cancer diagnosis (Adj HR: 0.69 [CI, 0.48–0.99], p = 0.043). The risk of a younger age at any cancer diagnosis was significantly high in LS carriers of one to two risk genotypes (Adj HR: 1.49 [CI: 1.06–2.09], corrected p = 0.030), while having one to two protective genotypes significantly reduced the risk of developing any cancer and CRC at a younger age (Adj HR: 0.52 [CI: 0.37–0.73], and Adj HR: 0.51 [CI: 0.36–0.74], both corrected p {\\textless} 0.001). Conclusions: Polymorphism genotypes in the cell-cycle regulation, DNA repair, and xenobiotic metabolizing genes may influence the age at cancer diagnosis in a homogenous LS cohort with a South African founder germline PV c.1528C{\\textgreater}T in the MLH1 gene.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {Biomedicines},\n\tauthor = {Ndou, Lutricia and Chambuso, Ramadhani and Algar, Ursula and Goldberg, Paul and Boutall, Adam and Ramesar, Raj},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {2201},\n}\n\n\n\n

\n

\n\n\n

\n Background: High variability in the age at cancer diagnosis in Lynch syndrome (LS) patients is widely observed, even among relatives with the same germline pathogenic variant (PV) in the mismatch repair (MMR) genes. Genetic polymorphisms and lifestyle factors are thought to contribute to this variability. We investigated the influence of previously reported genetic polymorphisms on the age at cancer diagnosis in a homogenous LS cohort with a South African founder germline PV c.1528C\\textgreaterT in the MLH1 gene. Methods: A total of 359 LS variant heterozygotes (LSVH) from 60 different families were genotyped for specific genetic polymorphisms in GSTM1, GSTT1, CYP1A1, CYP17, PPP2R2B, KIF20A, TGFB1, XRCC5, TNF, BCL2, CHFR, CDC25C, ATM, TTC28, CDC25C, HFE, and hTERT genes using Multiplex Polymerase Chain Reaction and MassArray methods. Kaplan–Meier survival analysis, univariate and multivariate Cox proportional hazards gamma shared frailty models adjusted for sex were used to estimate the association between age at cancer diagnosis and polymorphism genotypes. A p-value \\textless 0.05 after correcting for multiple testing using the Benjamini–Hochberg method was considered significant at a 95% confidence interval. Results: We identified three genotypes in the cell-cycle regulation, DNA repair, and xenobiotic-metabolism genes significantly associated with age at cancer diagnosis in this cohort. The CYP1A1 rs4646903 risk (GG) and CDC25C rs3734166 polymorphic (GA+AA) genotypes were significantly associated with an increased risk of a younger age at cancer diagnosis (Adj HR: 2.03 [1.01–4.08], p = 0.034 and Adj HR: 1.53 [1.09–2.14], p = 0.015, respectively). LSVH who were heterozygous for the XRCC5 rs1051685 SNP showed significant protection against younger age at cancer diagnosis (Adj HR: 0.69 [CI, 0.48–0.99], p = 0.043). The risk of a younger age at any cancer diagnosis was significantly high in LS carriers of one to two risk genotypes (Adj HR: 1.49 [CI: 1.06–2.09], corrected p = 0.030), while having one to two protective genotypes significantly reduced the risk of developing any cancer and CRC at a younger age (Adj HR: 0.52 [CI: 0.37–0.73], and Adj HR: 0.51 [CI: 0.36–0.74], both corrected p \\textless 0.001). Conclusions: Polymorphism genotypes in the cell-cycle regulation, DNA repair, and xenobiotic metabolizing genes may influence the age at cancer diagnosis in a homogenous LS cohort with a South African founder germline PV c.1528C\\textgreaterT in the MLH1 gene.\n

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\n \n\n \n \n \n \n \n \n Association between HIV and acquisition of rifamycin resistance with first-line TB treatment: a systematic review and meta-analysis.\n \n \n \n \n\n\n \n Zinyakatira, N.; Ford, N.; and Cox, H.\n\n\n \n\n\n\n BMC Infectious Diseases, 24(1): 657. July 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Association$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{zinyakatira_association_2024,\n\ttitle = {Association between {HIV} and acquisition of rifamycin resistance with first-line {TB} treatment: a systematic review and meta-analysis},\n\tvolume = {24},\n\tissn = {1471-2334},\n\tshorttitle = {Association between {HIV} and acquisition of rifamycin resistance with first-line {TB} treatment},\n\turl = {https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-024-09514-7},\n\tdoi = {10.1186/s12879-024-09514-7},\n\tabstract = {Abstract \n             \n              Background \n              Multi-drug or rifamycin-resistant tuberculosis (MDR/RR-TB) is an important public health concern, including in settings with high HIV prevalence. TB drug resistance can be directly transmitted or arise through resistance acquisition during first-line TB treatment. Limited evidence suggests that people living with HIV (PLHIV) might have an increased risk of acquired rifamycin-resistance (ARR). \n             \n             \n              Methods \n              To assess HIV as a risk factor for ARR during first-line TB treatment, a systematic review and meta-analysis was conducted. ARR was defined as rifamycin-susceptibility at treatment start with rifamycin-resistance diagnosed during or at the end of treatment, or at recurrence. PubMed/MEDLINE, CINAHL, Cochrane Library, and Google Scholar databases were searched from inception to 23 May 2024 for articles in English; conference abstracts were also searched from 2004 to 2021. The Mantel-Haenszel random-effects model was used to estimate the pooled odds ratio of any association between HIV and ARR among individuals receiving first-line TB treatment. \n             \n             \n              Results \n              Ten studies that included data collected between 1990 and 2014 were identified: five from the United States, two from South Africa and one each from Uganda, India and Moldova. A total of 97,564 individuals were included across all studies, with 13,359 (13.7\\%) PLHIV. Overall, 312 (0.32\\%) acquired rifamycin-resistance, among whom 115 (36.9\\%) were PLHIV. The weighted odds of ARR were 4.57 (95\\% CI, 2.01–10.42) times higher among PLHIV compared to HIV-negative individuals receiving first-line TB treatment. \n             \n             \n              Conclusion \n              The available data, suggest that PLHIV have an increased ARR risk during first-line TB treatment. Further research is needed to clarify specific risk factors, including advanced HIV disease and TB disease severity. Given the introduction of shorter, 4-month rifamycin-based regimens, there is an urgent need for additional data on ARR, particularly for PLHIV. \n             \n             \n              Systematic review registration \n              PROSPERO CRD42022327337.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {BMC Infectious Diseases},\n\tauthor = {Zinyakatira, Nesbert and Ford, Nathan and Cox, Helen},\n\tmonth = jul,\n\tyear = {2024},\n\tpages = {657},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Background Multi-drug or rifamycin-resistant tuberculosis (MDR/RR-TB) is an important public health concern, including in settings with high HIV prevalence. TB drug resistance can be directly transmitted or arise through resistance acquisition during first-line TB treatment. Limited evidence suggests that people living with HIV (PLHIV) might have an increased risk of acquired rifamycin-resistance (ARR). Methods To assess HIV as a risk factor for ARR during first-line TB treatment, a systematic review and meta-analysis was conducted. ARR was defined as rifamycin-susceptibility at treatment start with rifamycin-resistance diagnosed during or at the end of treatment, or at recurrence. PubMed/MEDLINE, CINAHL, Cochrane Library, and Google Scholar databases were searched from inception to 23 May 2024 for articles in English; conference abstracts were also searched from 2004 to 2021. The Mantel-Haenszel random-effects model was used to estimate the pooled odds ratio of any association between HIV and ARR among individuals receiving first-line TB treatment. Results Ten studies that included data collected between 1990 and 2014 were identified: five from the United States, two from South Africa and one each from Uganda, India and Moldova. A total of 97,564 individuals were included across all studies, with 13,359 (13.7%) PLHIV. Overall, 312 (0.32%) acquired rifamycin-resistance, among whom 115 (36.9%) were PLHIV. The weighted odds of ARR were 4.57 (95% CI, 2.01–10.42) times higher among PLHIV compared to HIV-negative individuals receiving first-line TB treatment. Conclusion The available data, suggest that PLHIV have an increased ARR risk during first-line TB treatment. Further research is needed to clarify specific risk factors, including advanced HIV disease and TB disease severity. Given the introduction of shorter, 4-month rifamycin-based regimens, there is an urgent need for additional data on ARR, particularly for PLHIV. Systematic review registration PROSPERO CRD42022327337.\n

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\n \n\n \n \n \n \n \n \n Association Between Mycobacterium tuberculosis Sensitization and Insulin Resistance Among US Adults Screened for Type 2 Diabetes Mellitus.\n \n \n \n \n\n\n \n Magodoro, I. M; Aluoch, A.; Claggett, B.; Nyirenda, M. J; Siedner, M. J; Wilkinson, K. A; Wilkinson, R. J; and Ntusi, N. A B\n\n\n \n\n\n\n Open Forum Infectious Diseases, 11(10): ofae568. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Association$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{magodoro_association_2024,\n\ttitle = {Association {Between} \\textit{{Mycobacterium} tuberculosis} {Sensitization} and {Insulin} {Resistance} {Among} {US} {Adults} {Screened} for {Type} 2 {Diabetes} {Mellitus}},\n\tvolume = {11},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2328-8957},\n\turl = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofae568/7826054},\n\tdoi = {10.1093/ofid/ofae568},\n\tabstract = {Abstract \n             \n              Background \n              Type 2 diabetes mellitus (T2DM) may be a long-term sequela of infection with Mycobacterium tuberculosis (Mtb) by mechanisms that remain to be fully explained. We evaluated the association between Mtb sensitization and T2DM and, via mediation analysis, the extent to which it is mediated by insulin resistance and/or β-cell failure. \n             \n             \n              Methods \n              Adults were assessed for T2DM by fasting plasma glucose, 2-hour oral glucose tolerance testing, and hemoglobin A1c; β-cell dysfunction and insulin resistance by homoeostasis model assessment 2; and Mtb sensitization by tuberculin skin testing. Associations between Mtb sensitization and T2DM were modeled with probit regression and decomposed into indirect effects of β-cell dysfunction and insulin resistance. Analyses were adjusted for sociodemographic, behavioral, and clinical characteristics. \n             \n             \n              Results \n              We included 1843 adults. Individuals with Mtb sensitization were older than those without Mtb (median [IQR], 54 [39–64] vs 47 [33–62] years). As compared with being uninfected, Mtb sensitization was associated with T2DM (adjusted absolute risk difference, 9.34\\% [95\\% CI, 2.38\\%–15.0\\%]; P \\&lt; .001) and increased insulin resistance (adjusted median difference, 0.16 [95\\% CI, .03–.29]; P = .014) but not β-cell dysfunction (adjusted median difference, −3.1 [95\\% CI, −10.4 to 4.3]; P = .42). In mediation analyses, insulin resistance mediated 18.3\\% (95\\% CI, 3.29\\%–36.0\\%; P = .020) of the total effect of the association between Mtb sensitization and T2DM. \n             \n             \n              Conclusions \n              Definitive prospective studies examining incident T2DM following tuberculosis are warranted. Notwithstanding, our findings suggest that exposure to Mtb may be a novel risk factor for T2DM, likely driven by an increase in insulin resistance.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {Open Forum Infectious Diseases},\n\tauthor = {Magodoro, Itai M and Aluoch, Aloice and Claggett, Brian and Nyirenda, Moffat J and Siedner, Mark J and Wilkinson, Katalina A and Wilkinson, Robert J and Ntusi, Ntobeko A B},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {ofae568},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Single-cell transcriptomics identifies the differentiation trajectory from inflammatory monocytes to pro-resolving macrophages in a mouse skin allergy model.\n \n \n \n \n\n\n \n Miyake, K.; Ito, J.; Takahashi, K.; Nakabayashi, J.; Brombacher, F.; Shichino, S.; Yoshikawa, S.; Miyake, S.; and Karasuyama, H.\n\n\n \n\n\n\n Nature Communications, 15(1): 1666. February 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Single-cell$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{miyake_single-cell_2024,\n\ttitle = {Single-cell transcriptomics identifies the differentiation trajectory from inflammatory monocytes to pro-resolving macrophages in a mouse skin allergy model},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-46148-4},\n\tdoi = {10.1038/s41467-024-46148-4},\n\tabstract = {Abstract \n             \n              Both monocytes and macrophages are heterogeneous populations. It was traditionally understood that Ly6C \n              hi \n              classical (inflammatory) monocytes differentiate into pro-inflammatory Ly6C \n              hi \n              macrophages. Accumulating evidence has suggested that Ly6C \n              hi \n              classical monocytes can also differentiate into Ly6C \n              lo \n              pro-resolving macrophages under certain conditions, while their differentiation trajectory remains to be fully elucidated. The present study with scRNA-seq and flow cytometric analyses reveals that Ly6C \n              hi \n              PD-L2 \n              lo \n              classical monocytes recruited to the allergic skin lesion sequentially differentiate into Ly6C \n              lo \n              PD-L2 \n              hi \n              pro-resolving macrophages, via intermediate Ly6C \n              hi \n              PD-L2 \n              hi \n              macrophages but not Ly6C \n              lo \n              non-classical monocytes, in an IL-4 receptor-dependent manner. Along the differentiation, classical monocyte-derived macrophages display anti-inflammatory signatures followed by metabolic rewiring concordant with their ability to phagocytose apoptotic neutrophils and allergens, therefore contributing to the resolution of inflammation. The failure in the generation of these pro-resolving macrophages drives the IL-1α-mediated cycle of inflammation with abscess-like accumulation of necrotic neutrophils. Thus, we clarify the stepwise differentiation trajectory from Ly6C \n              hi \n              classical monocytes toward Ly6C \n              lo \n              pro-resolving macrophages that restrain neutrophilic aggravation of skin allergic inflammation.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Miyake, Kensuke and Ito, Junya and Takahashi, Kazufusa and Nakabayashi, Jun and Brombacher, Frank and Shichino, Shigeyuki and Yoshikawa, Soichiro and Miyake, Sachiko and Karasuyama, Hajime},\n\tmonth = feb,\n\tyear = {2024},\n\tpages = {1666},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Eliminating malaria transmission requires targeting immature and mature gametocytes through lipoidal uptake of antimalarials.\n \n \n \n \n\n\n \n Naude, M.; Van Heerden, A.; Reader, J.; Van Der Watt, M.; Niemand, J.; Joubert, D.; Siciliano, G.; Alano, P.; Njoroge, M.; Chibale, K.; Herreros, E.; Leroy, D.; and Birkholtz, L.\n\n\n \n\n\n\n Nature Communications, 15(1): 9896. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Eliminating$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{naude_eliminating_2024,\n\ttitle = {Eliminating malaria transmission requires targeting immature and mature gametocytes through lipoidal uptake of antimalarials},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-54144-x},\n\tdoi = {10.1038/s41467-024-54144-x},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Naude, Mariska and Van Heerden, Ashleigh and Reader, Janette and Van Der Watt, Mariëtte and Niemand, Jandeli and Joubert, Dorè and Siciliano, Giulia and Alano, Pietro and Njoroge, Mathew and Chibale, Kelly and Herreros, Esperanza and Leroy, Didier and Birkholtz, Lyn-Marié},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {9896},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Clinical, pharmacological, and qualitative characterization of drug–drug interactions in pregnant women initiating HIV therapy in Sub-Saharan Africa.\n \n \n \n \n\n\n \n Kiiza, D.; Rostami-Hochaghan, D.; Alhassan, Y.; Seden, K.; Reynolds, H.; Kaboggoza, J. P; Taegtmeyer, M.; Chen, T.; Challenger, E.; Malaba, T.; Wang, D.; Else, L.; Hern, F.; Sharp, J.; Neary, M.; Dilly Penchala, S.; Waitt, C.; Orrell, C.; Colbers, A.; Myer, L.; Owen, A.; Rannard, S.; Khoo, S.; and Lamorde, M.\n\n\n \n\n\n\n Journal of Antimicrobial Chemotherapy, 79(9): 2334–2342. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Clinical,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kiiza_clinical_2024,\n\ttitle = {Clinical, pharmacological, and qualitative characterization of drug–drug interactions in pregnant women initiating {HIV} therapy in {Sub}-{Saharan} {Africa}},\n\tvolume = {79},\n\tcopyright = {https://academic.oup.com/pages/standard-publication-reuse-rights},\n\tissn = {0305-7453, 1460-2091},\n\turl = {https://academic.oup.com/jac/article/79/9/2334/7713049},\n\tdoi = {10.1093/jac/dkae232},\n\tabstract = {Abstract \n             \n              Background \n              We investigated the impact of Drug–Drug Interactions (DDIs) on virologic control among HIV-positive pregnant women initiating antiretroviral therapy while identifying drivers for Traditional Medicine (TM) use and exploring the nature and extent of TM-related DDIs. \n             \n             \n              Methods \n              Employing a three-pronged approach, we examined DDIs arising from comedication, including TM, in ART. The DolPHIN-2 trial (NCT03249181) randomized 268 HIV-positive pregnant women in Uganda and South Africa to dolutegravir (DTG)-based (135) or efavirenz-based (133) regimens while systematically recording comedications and screening for DDIs. We used Cox regression models to compare time-to-virologic control between participants with and without DDIs. We conducted in-depth interviews and focus group discussions among 37 and 67 women with and without HIV, respectively, to explore reasons for TM use during pregnancy. Additionally, in-vitro and in-vivo studies evaluated the composition and impact of clay-based TM, mumbwa, on DTG plasma exposure. \n             \n             \n              Results \n              The baseline prevalence of DDIs was 67.2\\%, with TM use prevalent in 34\\% of participants, with mumbwa being the most frequent (76\\%, 69/91). There was no difference in virologic response between participants with and without DDIs. Fetal health and cultural norms were among the reasons cited for TM use. Analysis of mumbwa rods confirmed significant amounts of aluminium (8.4\\%–13.9\\%) and iron (4\\%–6\\%). In Balb-C mice, coadministration of mumbwa led to a reduction in DTG exposure observed in the AUC0-24 (−21\\%; P = 0.0271) and C24 (−53\\%; P = 0.0028). \n             \n             \n              Conclusions \n              The widespread use of clay-based TM may compromise HIV treatment, necessitating medication screening and counselling to manage DDIs in pregnant women.},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Antimicrobial Chemotherapy},\n\tauthor = {Kiiza, Daniel and Rostami-Hochaghan, Danial and Alhassan, Yussif and Seden, Kay and Reynolds, Helen and Kaboggoza, Julian P and Taegtmeyer, Miriam and Chen, Tao and Challenger, Elizabeth and Malaba, Thokozile and Wang, Duolao and Else, Laura and Hern, Faye and Sharp, Jo and Neary, Megan and Dilly Penchala, Sujan and Waitt, Catriona and Orrell, Catherine and Colbers, Angela and Myer, Landon and Owen, Andrew and Rannard, Steve and Khoo, Saye and Lamorde, Mohammed},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {2334--2342},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Discovery of Non-Covalent Inhibitors for SARS-CoV-2 PLpro: Integrating Virtual Screening, Synthesis, and Experimental Validation.\n \n \n \n \n\n\n \n Sousa, B. K. P.; Mottin, M.; Seanego, D.; Jurisch, C. D.; Rodrigues, B. S. A.; Da Silva, V. L. S.; Andrade, M. A.; Morais, G. S.; Boerin, D. F.; Froes, T. Q.; Motta, F. N.; Nonato, M. C.; Bastos, I. D. M.; Chibale, K.; Gessner, R. K.; and Andrade, C. H.\n\n\n \n\n\n\n ACS Medicinal Chemistry Letters, 15(12): 2140–2149. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Discovery$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{sousa_discovery_2024,\n\ttitle = {Discovery of {Non}-{Covalent} {Inhibitors} for {SARS}-{CoV}-2 {PLpro}: {Integrating} {Virtual} {Screening}, {Synthesis}, and {Experimental} {Validation}},\n\tvolume = {15},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1948-5875, 1948-5875},\n\tshorttitle = {Discovery of {Non}-{Covalent} {Inhibitors} for {SARS}-{CoV}-2 {PLpro}},\n\turl = {https://pubs.acs.org/doi/10.1021/acsmedchemlett.4c00420},\n\tdoi = {10.1021/acsmedchemlett.4c00420},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {ACS Medicinal Chemistry Letters},\n\tauthor = {Sousa, Bruna K. P. and Mottin, Melina and Seanego, Donald and Jurisch, Christopher D. and Rodrigues, Beatriz S. A. and Da Silva, Verônica L. S. and Andrade, Milene Aparecida and Morais, Gilberto S. and Boerin, Diogo F. and Froes, Thamires Q. and Motta, Flávia Nader and Nonato, M. Cristina and Bastos, Izabela D. M. and Chibale, Kelly and Gessner, Richard K. and Andrade, Carolina Horta},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {2140--2149},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Cognitive performance, neuropsychiatric symptoms, and cerebrospinal fluid viral control following programmatic switch from efavirenz-based to dolutegravir-based antiretroviral therapy in South Africa (CONNECT): a prospective cohort study.\n \n \n \n \n\n\n \n Nightingale, S.; Dreyer, A. J; Thomas, K. G F; Van Zyl, G.; Decloedt, E.; Naude, P. J W; Orrell, C.; Sinxadi, P.; Winston, A.; Khoo, S.; and Joska, J. A\n\n\n \n\n\n\n The Lancet HIV, 11(10): e680–e689. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Cognitive$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{nightingale_cognitive_2024,\n\ttitle = {Cognitive performance, neuropsychiatric symptoms, and cerebrospinal fluid viral control following programmatic switch from efavirenz-based to dolutegravir-based antiretroviral therapy in {South} {Africa} ({CONNECT}): a prospective cohort study},\n\tvolume = {11},\n\tissn = {23523018},\n\tshorttitle = {Cognitive performance, neuropsychiatric symptoms, and cerebrospinal fluid viral control following programmatic switch from efavirenz-based to dolutegravir-based antiretroviral therapy in {South} {Africa} ({CONNECT})},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352301824002091},\n\tdoi = {10.1016/S2352-3018(24)00209-1},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet HIV},\n\tauthor = {Nightingale, Sam and Dreyer, Anna J and Thomas, Kevin G F and Van Zyl, Gert and Decloedt, Eric and Naude, Petrus J W and Orrell, Catherine and Sinxadi, Phumla and Winston, Alan and Khoo, Saye and Joska, John A},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {e680--e689},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Prospective antimicrobial stewardship interventions by multidisciplinary teams to reduce neonatal antibiotic use in South Africa: The Neonatal Antimicrobial Stewardship (NeoAMS) study.\n \n \n \n \n\n\n \n Dramowski, A.; Prusakov, P.; Goff, D. A.; Brink, A.; Govender, N. P.; Annor, A. S.; Balfour, L.; Bekker, A.; Cassim, A.; Gijzelaar, M.; Holgate, S. L.; Kolman, S.; Messina, A.; Tootla, H.; Schellack, N.; Van Jaarsveld, A.; Reddy, K.; Pillay, S.; Conradie, L.; Van Niekerk, A. M.; Bester, T.; Alexander, P.; Andrews, A.; Dippenaar, M.; Bamford, C.; Brits, S.; Chirwa, P.; Erasmus, H.; Ekermans, P.; Gounden, P.; Kriel, T.; Mawela, D.; Moncho, M.; Mphuthi, T.; Nhari, R.; Charani, E.; Sánchez, P. J.; and Bergh, D. V. D.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 146: 107158. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Prospective$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{dramowski_prospective_2024,\n\ttitle = {Prospective antimicrobial stewardship interventions by multidisciplinary teams to reduce neonatal antibiotic use in {South} {Africa}: {The} {Neonatal} {Antimicrobial} {Stewardship} ({NeoAMS}) study},\n\tvolume = {146},\n\tissn = {12019712},\n\tshorttitle = {Prospective antimicrobial stewardship interventions by multidisciplinary teams to reduce neonatal antibiotic use in {South} {Africa}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971224002297},\n\tdoi = {10.1016/j.ijid.2024.107158},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Dramowski, Angela and Prusakov, Pavel and Goff, Debra A. and Brink, Adrian and Govender, Nelesh P. and Annor, Ama Sakoa and Balfour, Liezl and Bekker, Adrie and Cassim, Azraa and Gijzelaar, Michelle and Holgate, Sandi L. and Kolman, Sonya and Messina, Angeliki and Tootla, Hafsah and Schellack, Natalie and Van Jaarsveld, Andriette and Reddy, Kessendri and Pillay, Shakti and Conradie, Lucinda and Van Niekerk, Anika M. and Bester, Tarina and Alexander, Pearl and Andrews, Antoinette and Dippenaar, Magdel and Bamford, Colleen and Brits, Sharnel and Chirwa, Pinky and Erasmus, Hannelie and Ekermans, Pieter and Gounden, Pebenita and Kriel, Teresa and Mawela, Dini and Moncho, Masego and Mphuthi, Tonia and Nhari, Ronald and Charani, Esmita and Sánchez, Pablo J. and Bergh, Dena Van Den},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {107158},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Development of a Two-Component Nanoparticle Vaccine Displaying an HIV-1 Envelope Glycoprotein that Elicits Tier 2 Neutralising Antibodies.\n \n \n \n \n\n\n \n Malebo, K.; Woodward, J.; Ximba, P.; Mkhize, Q.; Cingo, S.; Moyo-Gwete, T.; Moore, P. L.; Williamson, A.; and Chapman, R.\n\n\n \n\n\n\n Vaccines, 12(9): 1063. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Development$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{malebo_development_2024,\n\ttitle = {Development of a {Two}-{Component} {Nanoparticle} {Vaccine} {Displaying} an {HIV}-1 {Envelope} {Glycoprotein} that {Elicits} {Tier} 2 {Neutralising} {Antibodies}},\n\tvolume = {12},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2076-393X},\n\turl = {https://www.mdpi.com/2076-393X/12/9/1063},\n\tdoi = {10.3390/vaccines12091063},\n\tabstract = {Despite treatment and other interventions, an effective prophylactic HIV vaccine is still an essential goal in the control of HIV. Inducing robust and long-lasting antibody responses is one of the main targets of an HIV vaccine. The delivery of HIV envelope glycoproteins (Env) using nanoparticle (NP) platforms has been shown to elicit better immunogenicity than soluble HIV Env. In this paper, we describe the development of a nanoparticle-based vaccine decorated with HIV Env using the SpyCatcher/SpyTag system. The Env utilised in this study, CAP255, was derived from a transmitted founder virus isolated from a patient who developed broadly neutralising antibodies. Negative stain and cryo-electron microscopy analyses confirmed the assembly and stability of the mi3 into uniform icosahedral NPs surrounded by regularly spaced CAP255 gp140 Env trimers. A three-dimensional reconstruction of CAP255 gp140 SpyTag–SpyCatcher mi3 clearly showed Env trimers projecting from the centre of each of the pentagonal dodecahedral faces of the NP. To our knowledge, this is the first study to report the formation of SpyCatcher pentamers on the dodecahedral faces of mi3 NPs. To investigate the immunogenicity, rabbits were primed with two doses of DNA vaccines expressing the CAP255 gp150 and a mosaic subtype C Gag and boosted with three doses of the NP-developed autologous Tier 2 CAP255 neutralising antibodies (Nabs) and low levels of heterologous CAP256SU NAbs.},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {Vaccines},\n\tauthor = {Malebo, Kegomoditswe and Woodward, Jeremy and Ximba, Phindile and Mkhize, Qiniso and Cingo, Sanele and Moyo-Gwete, Thandeka and Moore, Penny L. and Williamson, Anna-Lise and Chapman, Rosamund},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {1063},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Treatment adherence and clinical outcomes amongst in people with drug-susceptible tuberculosis using medication monitor and differentiated care approach compared with standard of care in South Africa: a cluster randomized trial.\n \n \n \n \n\n\n \n Charalambous, S.; Maraba, N.; Jennings, L.; Rabothata, I.; Cogill, D.; Mukora, R.; Hippner, P.; Naidoo, P.; Xaba, N.; Mchunu, L.; Velen, K.; Orrell, C.; and Fielding, K. L.\n\n\n \n\n\n\n eClinicalMedicine, 75: 102745. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Treatment$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{charalambous_treatment_2024,\n\ttitle = {Treatment adherence and clinical outcomes amongst in people with drug-susceptible tuberculosis using medication monitor and differentiated care approach compared with standard of care in {South} {Africa}: a cluster randomized trial},\n\tvolume = {75},\n\tissn = {25895370},\n\tshorttitle = {Treatment adherence and clinical outcomes amongst in people with drug-susceptible tuberculosis using medication monitor and differentiated care approach compared with standard of care in {South} {Africa}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2589537024003249},\n\tdoi = {10.1016/j.eclinm.2024.102745},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {eClinicalMedicine},\n\tauthor = {Charalambous, Salome and Maraba, Noriah and Jennings, Lauren and Rabothata, Israel and Cogill, Dolphina and Mukora, Rachel and Hippner, Piotr and Naidoo, Pren and Xaba, Nokhanyo and Mchunu, Lihle and Velen, Kavindhran and Orrell, Catherine and Fielding, Katherine L.},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {102745},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Meta-analysis of genome-wide association studies of stable warfarin dose in patients of African ancestry.\n \n \n \n \n\n\n \n Asiimwe, I. G.; Blockman, M.; Cavallari, L. H.; Cohen, K.; Cupido, C.; Dandara, C.; Davis, B. H.; Jacobson, B.; Johnson, J. A.; Lamorde, M.; Limdi, N. A.; Morgan, J.; Mouton, J. P.; Muyambo, S.; Nakagaayi, D.; Ndadza, A.; Okello, E.; Perera, M. A.; Schapkaitz, E.; Sekaggya-Wiltshire, C.; Semakula, J. R.; Tatz, G.; Waitt, C.; Yang, G.; Zhang, E. J.; Jorgensen, A. L.; and Pirmohamed, M.\n\n\n \n\n\n\n Blood Advances, 8(20): 5248–5261. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Meta-analysis$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{asiimwe_meta-analysis_2024,\n\ttitle = {Meta-analysis of genome-wide association studies of stable warfarin dose in patients of {African} ancestry},\n\tvolume = {8},\n\tissn = {2473-9529, 2473-9537},\n\turl = {https://ashpublications.org/bloodadvances/article/8/20/5248/517477/Meta-analysis-of-genome-wide-association-studies},\n\tdoi = {10.1182/bloodadvances.2024014227},\n\tabstract = {Abstract \n              Warfarin dose requirements are highly variable because of clinical and genetic factors. Although genetic variants influencing warfarin dose have been identified in European and East Asian populations, more work is needed to identify African-specific genetic variants to help optimize warfarin dosing. We performed genome-wide association studies (GWASs) in 4 African cohorts from Uganda, South Africa, and Zimbabwe, totaling 989 warfarin-treated participants who reached stable dose and had international normalized ratios within therapeutic ranges. We also included 2 African American cohorts recruited by the International Warfarin Pharmacogenetics Consortium (n = 316) and the University of Alabama at Birmingham (n = 199). After the GWAS, we performed standard error-weighted meta-analyses and then conducted stepwise conditional analyses to account for known loci in chromosomes 10 and 16. The genome-wide significance threshold was set at P \\&lt; 5 × 10−8. The meta-analysis, comprising 1504 participants, identified 242 significant SNPs across 3 genomic loci, with 99.6\\% of these located within known loci on chromosomes 10 (top SNP: rs58800757, P = 4.27 × 10−13) and 16 (top SNP: rs9925964, P = 9.97 × 10−16). Adjustment for the VKORC1 SNP -1639G\\&gt;A revealed an additional locus on chromosome 2 (top SNPs rs116057875/rs115254730/rs115240773, P = 3.64 × 10−8), implicating the MALL gene, that could indirectly influence warfarin response through interactions with caveolin-1. In conclusion, we reaffirmed the importance of CYP2C9 and VKORC1 in influencing warfarin dose requirements, and identified a new locus (MALL), that still requires direct evidence of biological plausibility.},\n\tlanguage = {en},\n\tnumber = {20},\n\turldate = {2025-06-24},\n\tjournal = {Blood Advances},\n\tauthor = {Asiimwe, Innocent G. and Blockman, Marc and Cavallari, Larisa H. and Cohen, Karen and Cupido, Clint and Dandara, Collet and Davis, Brittney H. and Jacobson, Barry and Johnson, Julie A. and Lamorde, Mohammed and Limdi, Nita A. and Morgan, Jennie and Mouton, Johannes P. and Muyambo, Sarudzai and Nakagaayi, Doreen and Ndadza, Arinao and Okello, Emmy and Perera, Minoli A. and Schapkaitz, Elise and Sekaggya-Wiltshire, Christine and Semakula, Jerome R. and Tatz, Gayle and Waitt, Catriona and Yang, Guang and Zhang, Eunice J. and Jorgensen, Andrea L. and Pirmohamed, Munir},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {5248--5261},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Announcing the Early Career Board of ACS Medicinal Chemistry Letters.\n \n \n \n \n\n\n \n Baranczak, A.; Bigi-Botterill, S. V.; Borsari, C.; Dombrowski, A. W.; Estrada, M. A.; Farrell, M. P.; Riley, A. P.; and Woodland, J. G.\n\n\n \n\n\n\n ACS Medicinal Chemistry Letters, 15(9): 1403–1406. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Announcing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{baranczak_announcing_2024,\n\ttitle = {Announcing the {Early} {Career} {Board} of \\textit{{ACS} {Medicinal} {Chemistry} {Letters}}},\n\tvolume = {15},\n\tcopyright = {https://doi.org/10.15223/policy-001},\n\tissn = {1948-5875, 1948-5875},\n\turl = {https://pubs.acs.org/doi/10.1021/acsmedchemlett.4c00294},\n\tdoi = {10.1021/acsmedchemlett.4c00294},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {ACS Medicinal Chemistry Letters},\n\tauthor = {Baranczak, Aleksandra and Bigi-Botterill, Simone V. and Borsari, Chiara and Dombrowski, Amanda W. and Estrada, Michelle A. and Farrell, Mark P. and Riley, Andrew P. and Woodland, John G.},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {1403--1406},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Clearance of persistent SARS-CoV-2 associates with increased neutralizing antibodies in advanced HIV disease post-ART initiation.\n \n \n \n \n\n\n \n Karim, F.; Riou, C.; Bernstein, M.; Jule, Z.; Lustig, G.; Van Graan, S.; Keeton, R. S.; Upton, J.; Ganga, Y.; Khan, K.; Reedoy, K.; Mazibuko, M.; Govender, K.; Thambu, K.; Ngcobo, N.; Venter, E.; Makhado, Z.; Hanekom, W.; Von Gottberg, A.; Hoque, M.; Karim, Q. A.; Abdool Karim, S. S.; Manickchund, N.; Magula, N.; Gosnell, B. I.; Lessells, R. J.; Moore, P. L.; Burgers, W. A.; De Oliveira, T.; Moosa, M. S.; and Sigal, A.\n\n\n \n\n\n\n Nature Communications, 15(1): 2360. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Clearance$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{karim_clearance_2024,\n\ttitle = {Clearance of persistent {SARS}-{CoV}-2 associates with increased neutralizing antibodies in advanced {HIV} disease post-{ART} initiation},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-46673-2},\n\tdoi = {10.1038/s41467-024-46673-2},\n\tabstract = {Abstract \n             \n              SARS-CoV-2 clearance requires adaptive immunity but the contribution of neutralizing antibodies and T cells in different immune states is unclear. Here we ask which adaptive immune responses associate with clearance of long-term SARS-CoV-2 infection in HIV-mediated immunosuppression after suppressive antiretroviral therapy (ART) initiation. We assembled a cohort of SARS-CoV-2 infected people in South Africa ( \n              n \n               = 994) including participants with advanced HIV disease characterized by immunosuppression due to T cell depletion. Fifty-four percent of participants with advanced HIV disease had prolonged SARS-CoV-2 infection ({\\textgreater}1 month). In the five vaccinated participants with advanced HIV disease tested, SARS-CoV-2 clearance associates with emergence of neutralizing antibodies but not SARS-CoV-2 specific CD8 T cells, while CD4 T cell responses were not determined due to low cell numbers. Further, complete HIV suppression is not required for clearance, although it is necessary for an effective vaccine response. Persistent SARS-CoV-2 infection led to SARS-CoV-2 evolution, including virus with extensive neutralization escape in a Delta variant infected participant. The results provide evidence that neutralizing antibodies are required for SARS-CoV-2 clearance in HIV-mediated immunosuppression recovery, and that suppressive ART is necessary to curtail evolution of co-infecting pathogens to reduce individual health consequences as well as public health risk linked with generation of escape mutants.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Karim, Farina and Riou, Catherine and Bernstein, Mallory and Jule, Zesuliwe and Lustig, Gila and Van Graan, Strauss and Keeton, Roanne S. and Upton, Janine-Lee and Ganga, Yashica and Khan, Khadija and Reedoy, Kajal and Mazibuko, Matilda and Govender, Katya and Thambu, Kershnee and Ngcobo, Nokuthula and Venter, Elizabeth and Makhado, Zanele and Hanekom, Willem and Von Gottberg, Anne and Hoque, Monjurul and Karim, Quarraisha Abdool and Abdool Karim, Salim S. and Manickchund, Nithendra and Magula, Nombulelo and Gosnell, Bernadett I. and Lessells, Richard J. and Moore, Penny L. and Burgers, Wendy A. and De Oliveira, Tulio and Moosa, Mahomed-Yunus S. and Sigal, Alex},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {2360},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Influence of vitamin D supplementation on muscle strength and exercise capacity in South African schoolchildren: secondary outcomes from a randomised controlled trial (ViDiKids).\n \n \n \n \n\n\n \n Middelkoop, K.; Micklesfield, L.; Hemmings, S.; Walker, N.; Stewart, J.; Jolliffe, D. A; Mendham, A. E; Tang, J. C Y; Cooper, C.; Harvey, N. C; Wilkinson, R. J; and Martineau, A. R\n\n\n \n\n\n\n BMJ Open Sport & Exercise Medicine, 10(3): e002019. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Influence$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{middelkoop_influence_2024,\n\ttitle = {Influence of vitamin {D} supplementation on muscle strength and exercise capacity in {South} {African} schoolchildren: secondary outcomes from a randomised controlled trial ({ViDiKids})},\n\tvolume = {10},\n\tissn = {2055-7647},\n\tshorttitle = {Influence of vitamin {D} supplementation on muscle strength and exercise capacity in {South} {African} schoolchildren},\n\turl = {https://bmjopensem.bmj.com/lookup/doi/10.1136/bmjsem-2024-002019},\n\tdoi = {10.1136/bmjsem-2024-002019},\n\tabstract = {Objective \n              To determine whether vitamin D supplementation influences grip strength, explosive leg power, cardiorespiratory fitness and risk of exercise-induced bronchoconstriction (EIB) in South African schoolchildren. \n             \n             \n              Methods \n               \n                Substudy (n=450) in Cape Town schoolchildren aged 8–11 years nested within a phase 3 randomised placebo-controlled trial (ViDiKids). The intervention was weekly oral doses of 10 000 IU vitamin D \n                3 \n                (n=228) or placebo (n=222) for 3 years. Outcome measures were serum 25-hydroxyvitamin D \n                3 \n                (25(OH)D \n                3 \n                ) concentrations, grip strength, standing long jump distance, peak oxygen uptake (VO \n                2peak \n                , determined using 20 m multistage shuttle run tests) and the proportion of children with EIB, measured at end-study. \n               \n             \n             \n              Results \n               \n                64.7\\% of participants had serum 25(OH)D \n                3 \n                concentrations {\\textless}75 nmol/L at baseline. At 3-year follow-up, children randomised to vitamin D versus placebo had higher mean serum 25(OH)D \n                3 \n                concentrations (97.6 vs 58.8 nmol/L, respectively; adjusted mean difference 39.9 nmol/L, 95\\% CI 36.1 to 43.6). However, this was not associated with end-study differences in grip strength, standing long jump distance, VO \n                2peak \n                or risk of EIB. \n               \n             \n             \n              Conclusion \n               \n                A 3-year course of weekly oral supplementation with 10 000 IU vitamin D \n                3 \n                elevated serum 25(OH)D \n                3 \n                concentrations in South African schoolchildren but did not influence muscle strength, exercise capacity or risk of EIB.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {BMJ Open Sport \\& Exercise Medicine},\n\tauthor = {Middelkoop, Keren and Micklesfield, Lisa and Hemmings, Stephanie and Walker, Neil and Stewart, Justine and Jolliffe, David A and Mendham, Amy E and Tang, Jonathan C Y and Cooper, Cyrus and Harvey, Nicholas C and Wilkinson, Robert J and Martineau, Adrian R},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {e002019},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Association between a large change between the minimum and maximum monthly values of solar insolation and a history of suicide attempts in bipolar I disorder.\n \n \n \n \n\n\n \n Ritter, P.; Glenn, T.; Achtyes, E. D.; Alda, M.; Agaoglu, E.; Altınbaş, K.; Andreassen, O. A.; Angelopoulos, E.; Ardau, R.; Aydin, M.; Ayhan, Y.; Baethge, C.; Bauer, R.; Baune, B. T.; Balaban, C.; Becerra-Palars, C.; Behere, A. P.; Behere, P. B.; Belete, H.; Belete, T.; Belizario, G. O.; Bellivier, F.; Belmaker, R. H.; Benedetti, F.; Berk, M.; Bersudsky, Y.; Bicakci, Ş.; Birabwa-Oketcho, H.; Bjella, T. D.; Brady, C.; Cabrera, J.; Cappucciati, M.; Castro, A. M. P.; Chen, W.; Cheung, E. Y. W.; Chiesa, S.; Chanopoulou, M.; Crowe, M.; Cuomo, A.; Dallaspezia, S.; Desai, P.; Dodd, S.; Etain, B.; Fagiolini, A.; Fellendorf, F. T.; Ferensztajn-Rochowiak, E.; Fiedorowicz, J. G.; Fountoulakis, K. N.; Frye, M. A.; Geoffroy, P. A.; Gitlin, M. J.; Gonzalez-Pinto, A.; Gottlieb, J. F.; Grof, P.; Haarman, B. C. M.; Harima, H.; Hasse-Sousa, M.; Henry, C.; Hoffding, L.; Houenou, J.; Imbesi, M.; Isometsä, E. T.; Ivkovic, M.; Janno, S.; Johnsen, S.; Kapczinski, F.; Karakatsoulis, G. N.; Kardell, M.; Kessing, L. V.; Kim, S. J.; König, B.; Kot, T. L.; Koval, M.; Kunz, M.; Lafer, B.; Landén, M.; Larsen, E. R.; Licht, R. W.; Ludwig, V. M.; Lopez-Jaramillo, C.; MacKenzie, A.; Madsen, H. Ø.; Madsen, S. A. K. A.; Mahadevan, J.; Mahardika, A.; Manchia, M.; Marsh, W.; Martinez-Cengotitabengoa, M.; Martini, J.; Martiny, K.; Mashima, Y.; McLoughlin, D. M.; Meesters, A. N. R.; Meesters, Y.; Melle, I.; Meza-Urzúa, F.; Michaelis, E.; Mikolas, P.; Mok, Y. M.; Monteith, S.; Moorthy, M.; Morken, G.; Mosca, E.; Mozzhegorov, A. A.; Munoz, R.; Mythri, S. V.; Nacef, F.; Nadella, R. K.; Nakanotani, T.; Nielsen, R. E.; O’Donovan, C.; Omrani, A.; Osher, Y.; Ouali, U.; Pantovic-Stefanovic, M.; Pariwatcharakul, P.; Petite, J.; Petzold, J.; Pfennig, A.; Pilhatsch, M.; Ruiz, Y. P.; Pinna, M.; Pompili, M.; Porter, R.; Quiroz, D.; Rabelo-da-Ponte, F. D.; Ramesar, R.; Rasgon, N.; Ratta-apha, W.; Redahan, M.; Reddy, M. S.; Reif, A.; Reininghaus, E. Z.; Richards, J. G.; Rybakowski, J. K.; Sathyaputri, L.; Scippa, A. M.; Simhandl, C.; Smith, D.; Smith, J.; Stackhouse, P. W.; Stein, D. J.; Stilwell, K.; Strejilevich, S.; Su, K.; Subramaniam, M.; Sulaiman, A. H.; Suominen, K.; Tanra, A. J.; Tatebayashi, Y.; Teh, W. L.; Tondo, L.; Torrent, C.; Tuinstra, D.; Uchida, T.; Vaaler, A. E.; Vieta, E.; Viswanath, B.; Volf, C.; Yang, K.; Yoldi-Negrete, M.; Yalcinkaya, O. K.; Young, A. H.; Zgueb, Y.; Whybrow, P. C.; and Bauer, M.\n\n\n \n\n\n\n International Journal of Bipolar Disorders, 12(1): 43. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Association$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{ritter_association_2024,\n\ttitle = {Association between a large change between the minimum and maximum monthly values of solar insolation and a history of suicide attempts in bipolar {I} disorder},\n\tvolume = {12},\n\tissn = {2194-7511},\n\turl = {https://journalbipolardisorders.springeropen.com/articles/10.1186/s40345-024-00364-5},\n\tdoi = {10.1186/s40345-024-00364-5},\n\tabstract = {Abstract \n \n Background \n The rate of suicide attempts by patients with bipolar disorder is high. In addition to patient and country specific factors, environmental factors may contribute to suicidal behavior. Sunlight has multiple diverse impacts on human physiology and behavior. Solar insolation is defined as the electromagnetic energy from the sun striking a surface area on earth. We previously found that a large change in solar insolation between the minimum and maximum monthly values was associated with an increased risk of suicide attempts in patients with bipolar I disorder. \n \n \n Methods \n The association between solar insolation and a history of suicide attempts in bipolar disorder was again investigated using an international database with 15\\% more data and more sites at diverse locations and countries. \n \n \n Results \n Data were available from 5641 patients with bipolar I disorder living at a wide range of latitudes in 41 countries in both hemispheres. A large change in solar insolation between the minimum and maximum monthly values was associated with a history of suicide attempts in patients with bipolar I disorder, a replication of our prior analysis. The estimated model also associated state sponsored religion in the onset country, female gender, a history of alcohol or substance abuse, and being part of a younger birth cohort with a history of suicide attempts. \n \n \n Conclusions \n A large change between the minimum and maximum monthly values of solar insolation was associated with a history of suicide attempts in bipolar I disorder, replicating our prior research. Physicians should be aware that daylight has wide ranging physiological and psychiatric impacts, and that living with large changes in solar insolation may be associated with an increased suicide risk.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {International Journal of Bipolar Disorders},\n\tauthor = {Ritter, Philipp and Glenn, Tasha and Achtyes, Eric D. and Alda, Martin and Agaoglu, Esen and Altınbaş, Kürsat and Andreassen, Ole A. and Angelopoulos, Elias and Ardau, Raffaella and Aydin, Memduha and Ayhan, Yavuz and Baethge, Christopher and Bauer, Rita and Baune, Bernhard T. and Balaban, Ceylan and Becerra-Palars, Claudia and Behere, Aniruddh P. and Behere, Prakash B. and Belete, Habte and Belete, Tilahun and Belizario, Gabriel Okawa and Bellivier, Frank and Belmaker, Robert H. and Benedetti, Francesco and Berk, Michael and Bersudsky, Yuly and Bicakci, Şule and Birabwa-Oketcho, Harriet and Bjella, Thomas D. and Brady, Conan and Cabrera, Jorge and Cappucciati, Marco and Castro, Angela Marianne Paredes and Chen, Wei-Ling and Cheung, Eric Y. W. and Chiesa, Silvia and Chanopoulou, Margarita and Crowe, Marie and Cuomo, Alessandro and Dallaspezia, Sara and Desai, Pratikkumar and Dodd, Seetal and Etain, Bruno and Fagiolini, Andrea and Fellendorf, Frederike T. and Ferensztajn-Rochowiak, Ewa and Fiedorowicz, Jess G. and Fountoulakis, Kostas N. and Frye, Mark A. and Geoffroy, Pierre A. and Gitlin, Michael J. and Gonzalez-Pinto, Ana and Gottlieb, John F. and Grof, Paul and Haarman, Bartholomeus C. M. and Harima, Hirohiko and Hasse-Sousa, Mathias and Henry, Chantal and Hoffding, Lone and Houenou, Josselin and Imbesi, Massimiliano and Isometsä, Erkki T. and Ivkovic, Maja and Janno, Sven and Johnsen, Simon and Kapczinski, Flávio and Karakatsoulis, Grigorios N. and Kardell, Mathias and Kessing, Lars Vedel and Kim, Seong Jae and König, Barbara and Kot, Timur L. and Koval, Michael and Kunz, Mauricio and Lafer, Beny and Landén, Mikael and Larsen, Erik R. and Licht, Rasmus W. and Ludwig, Vera M. and Lopez-Jaramillo, Carlos and MacKenzie, Alan and Madsen, Helle Østergaard and Madsen, Simone Alberte Kongstad A. and Mahadevan, Jayant and Mahardika, Agustine and Manchia, Mirko and Marsh, Wendy and Martinez-Cengotitabengoa, Monica and Martini, Julia and Martiny, Klaus and Mashima, Yuki and McLoughlin, Declan M. and Meesters, Alie N. R. and Meesters, Ybe and Melle, Ingrid and Meza-Urzúa, Fátima and Michaelis, Elisabeth and Mikolas, Pavol and Mok, Yee Ming and Monteith, Scott and Moorthy, Muthukumaran and Morken, Gunnar and Mosca, Enrica and Mozzhegorov, Anton A. and Munoz, Rodrigo and Mythri, Starlin V. and Nacef, Fethi and Nadella, Ravi K. and Nakanotani, Takako and Nielsen, René Ernst and O’Donovan, Claire and Omrani, Adel and Osher, Yamima and Ouali, Uta and Pantovic-Stefanovic, Maja and Pariwatcharakul, Pornjira and Petite, Joanne and Petzold, Johannes and Pfennig, Andrea and Pilhatsch, Maximilian and Ruiz, Yolanda Pica and Pinna, Marco and Pompili, Maurizio and Porter, Richard and Quiroz, Danilo and Rabelo-da-Ponte, Francisco Diego and Ramesar, Raj and Rasgon, Natalie and Ratta-apha, Woraphat and Redahan, Maria and Reddy, M. S. and Reif, Andreas and Reininghaus, Eva Z. and Richards, Jenny Gringer and Rybakowski, Janusz K. and Sathyaputri, Leela and Scippa, Angela M. and Simhandl, Christian and Smith, Daniel and Smith, José and Stackhouse, Paul W. and Stein, Dan J. and Stilwell, Kellen and Strejilevich, Sergio and Su, Kuan-Pin and Subramaniam, Mythily and Sulaiman, Ahmad Hatim and Suominen, Kirsi and Tanra, Andi J. and Tatebayashi, Yoshitaka and Teh, Wen Lin and Tondo, Leonardo and Torrent, Carla and Tuinstra, Daniel and Uchida, Takahito and Vaaler, Arne E. and Vieta, Eduard and Viswanath, Biju and Volf, Carlo and Yang, Kai-Jie and Yoldi-Negrete, Maria and Yalcinkaya, Oguz Kaan and Young, Allan H. and Zgueb, Yosra and Whybrow, Peter C. and Bauer, Michael},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {43},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The epidemiology, transmission, diagnosis, and management of drug-resistant tuberculosis—lessons from the South African experience.\n \n \n \n \n\n\n \n Naidoo, K.; Perumal, R.; Cox, H.; Mathema, B.; Loveday, M.; Ismail, N.; Omar, S. V.; Georghiou, S. B; Daftary, A.; O'Donnell, M.; and Ndjeka, N.\n\n\n \n\n\n\n The Lancet Infectious Diseases, 24(9): e559–e575. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{naidoo_epidemiology_2024,\n\ttitle = {The epidemiology, transmission, diagnosis, and management of drug-resistant tuberculosis—lessons from the {South} {African} experience},\n\tvolume = {24},\n\tissn = {14733099},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1473309924001440},\n\tdoi = {10.1016/S1473-3099(24)00144-0},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Infectious Diseases},\n\tauthor = {Naidoo, Kogieleum and Perumal, Rubeshan and Cox, Helen and Mathema, Barun and Loveday, Marian and Ismail, Nazir and Omar, Shaheed Vally and Georghiou, Sophia B and Daftary, Amrita and O'Donnell, Max and Ndjeka, Norbert},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {e559--e575},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Postinfectious Pulmonary Complications: Establishing Research Priorities to Advance the Field: An Official American Thoracic Society Workshop Report.\n \n \n \n \n\n\n \n Auld, S. C.; Sheshadri, A.; Alexander-Brett, J.; Aschner, Y.; Barczak, A. K.; Basil, M. C.; Cohen, K. A.; Dela Cruz, C.; McGroder, C.; Restrepo, M. I.; Ridge, K. M.; Schnapp, L. M.; Traber, K.; Wunderink, R. G.; Zhang, D.; Ziady, A.; Attia, E. F.; Carter, J.; Chalmers, J. D.; Crothers, K.; Feldman, C.; Jones, B. E.; Kaminski, N.; Keane, J.; Lewinsohn, D.; Metersky, M.; Mizgerd, J. P.; Morris, A.; Ramirez, J.; Samarasinghe, A. E.; Staitieh, B. S.; Stek, C.; Sun, J.; and Evans, S. E.\n\n\n \n\n\n\n Annals of the American Thoracic Society, 21(9): 1219–1237. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Postinfectious$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{auld_postinfectious_2024,\n\ttitle = {Postinfectious {Pulmonary} {Complications}: {Establishing} {Research} {Priorities} to {Advance} the {Field}: {An} {Official} {American} {Thoracic} {Society} {Workshop} {Report}},\n\tvolume = {21},\n\tissn = {2329-6933, 2325-6621},\n\tshorttitle = {Postinfectious {Pulmonary} {Complications}},\n\turl = {https://www.atsjournals.org/doi/10.1513/AnnalsATS.202406-651ST},\n\tdoi = {10.1513/AnnalsATS.202406-651ST},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {Annals of the American Thoracic Society},\n\tauthor = {Auld, Sara C. and Sheshadri, Ajay and Alexander-Brett, Jennifer and Aschner, Yael and Barczak, Amy K. and Basil, Maria C. and Cohen, Keira A. and Dela Cruz, Charles and McGroder, Claire and Restrepo, Marcos I. and Ridge, Karen M. and Schnapp, Lynn M. and Traber, Katrina and Wunderink, Richard G. and Zhang, David and Ziady, Assem and Attia, Engi F. and Carter, Jane and Chalmers, James D. and Crothers, Kristina and Feldman, Charles and Jones, Barbara E. and Kaminski, Naftali and Keane, Joseph and Lewinsohn, David and Metersky, Mark and Mizgerd, Joseph P. and Morris, Alison and Ramirez, Julio and Samarasinghe, Amali E. and Staitieh, Bashar S. and Stek, Cari and Sun, Jie and Evans, Scott E.},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {1219--1237},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Transcriptomic Signatures of Progression to Tuberculosis Disease Among Close Contacts in Brazil.\n \n \n \n \n\n\n \n Mendelsohn, S. C; Andrade, B. B; Mbandi, S. K.; Andrade, A. M S; Muwanga, V. M; Figueiredo, M. C; Erasmus, M.; Rolla, V. C; Thami, P. K; Cordeiro-Santos, M.; Penn-Nicholson, A.; Kritski, A. L; Hatherill, M.; Sterling, T. R; Scriba, T. J; the RePORT–South Africa; Consortia, R.; Bilek, N.; Cloete, Y.; Erasmus, M.; Fisher, M.; Hadley, K.; Hassiem, R.; Hatherill, M.; Jaxa, L.; Mbandi, S. K.; Mendelsohn, S. C; Meyer, F.; Muwanga, V. M; Nombida, O.; Penn-Nicholson, A.; Raphela, R.; Scriba, T. J; September, A.; Sterling, T. R; Thami, P. K; Veldsman, A.; Andrade, A.; Andrade, B. B; Carvalho, B.; Cordeiro-Santos, M.; Figueiredo, M. C.; Gomes, A.; Kritski, A. L; Rolla, V. C; and Sterling, T. R\n\n\n \n\n\n\n The Journal of Infectious Diseases, 230(6): e1355–e1365. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Transcriptomic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{mendelsohn_transcriptomic_2024,\n\ttitle = {Transcriptomic {Signatures} of {Progression} to {Tuberculosis} {Disease} {Among} {Close} {Contacts} in {Brazil}},\n\tvolume = {230},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/230/6/e1355/7665574},\n\tdoi = {10.1093/infdis/jiae237},\n\tabstract = {Abstract \n             \n              Background \n              Approximately 5\\% of people infected with Mycobacterium tuberculosis progress to tuberculosis (TB) disease without preventive therapy. There is a need for a prognostic test to identify those at highest risk of incident TB so that therapy can be targeted. We evaluated host blood transcriptomic signatures for progression to TB disease. \n             \n             \n              Methods \n              Close contacts (≥4 hours of exposure per week) of adult patients with culture-confirmed pulmonary TB were enrolled in Brazil. Investigation for incident, microbiologically confirmed, or clinically diagnosed pulmonary or extrapulmonary TB disease through 24 months of follow-up was symptom triggered. Twenty previously validated blood TB transcriptomic signatures were measured at baseline by real-time quantitative polymerase chain reaction. Prognostic performance for incident TB was tested by receiver operating characteristic curve analysis at 6, 9, 12, and 24 months of follow-up. \n             \n             \n              Results \n              Between June 2015 and June 2019, 1854 close contacts were enrolled. Twenty-five progressed to incident TB, of whom 13 had microbiologically confirmed disease. Baseline transcriptomic signature scores were measured in 1789 close contacts. Prognostic performance for all signatures was best within 6 months of diagnosis. Seven signatures (Gliddon4, Suliman4, Roe3, Roe1, Penn-Nicholson6, Francisco2, and Rajan5) met the minimum World Health Organization target product profile for a prognostic test through 6 months and 3 signatures (Gliddon4, Rajan5, and Duffy9) through 9 months. None met the target product profile threshold through ≥12 months of follow-up. \n             \n             \n              Conclusions \n              Blood transcriptomic signatures may be useful for predicting TB risk within 9 months of measurement among TB-exposed contacts to target preventive therapy administration.},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Mendelsohn, Simon C and Andrade, Bruno B and Mbandi, Stanley Kimbung and Andrade, Alice M S and Muwanga, Vanessa M and Figueiredo, Marina C and Erasmus, Mzwandile and Rolla, Valeria C and Thami, Prisca K and Cordeiro-Santos, Marcelo and Penn-Nicholson, Adam and Kritski, Afranio L and Hatherill, Mark and Sterling, Timothy R and Scriba, Thomas J and {the RePORT–South Africa and RePORT–Brazil Consortia} and Bilek, Nicole and Cloete, Yolundi and Erasmus, Mzwandile and Fisher, Michelle and Hadley, Katie and Hassiem, Rieyaat and Hatherill, Mark and Jaxa, Lungisa and Mbandi, Stanley Kimbung and Mendelsohn, Simon C and Meyer, Faheemah and Muwanga, Vanessa M and Nombida, Onke and Penn-Nicholson, Adam and Raphela, Rodney and Scriba, Thomas J and September, Alison and Sterling, Timothy R and Thami, Prisca K and Veldsman, Ashley and Andrade, Alice and Andrade, Bruno B and Carvalho, Brenda and Cordeiro-Santos, Marcelo and Figueiredo, Marina Cruvinel and Gomes, Adriano and Kritski, Afranio L and Rolla, Valeria C and Sterling, Timothy R},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {e1355--e1365},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Multi-level tuberculosis of the spine identified by 18 F-FDG-PET/CT and concomitant urogenital tuberculosis: a case report from the spinal TB X cohort.\n \n \n \n \n\n\n \n Scherer, J.; Mukasa, S. L.; Wolmarans, K.; Guler, R.; Kotze, T.; Song, T.; Dunn, R.; Laubscher, M.; Pape, H.; Held, M.; and Thienemann, F.\n\n\n \n\n\n\n Infection, 52(6): 2507–2519. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Multi-level$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{scherer_multi-level_2024,\n\ttitle = {Multi-level tuberculosis of the spine identified by 18 {F}-{FDG}-{PET}/{CT} and concomitant urogenital tuberculosis: a case report from the spinal {TB} {X} cohort},\n\tvolume = {52},\n\tissn = {0300-8126, 1439-0973},\n\tshorttitle = {Multi-level tuberculosis of the spine identified by 18 {F}-{FDG}-{PET}/{CT} and concomitant urogenital tuberculosis},\n\turl = {https://link.springer.com/10.1007/s15010-024-02327-5},\n\tdoi = {10.1007/s15010-024-02327-5},\n\tabstract = {Abstract \n             \n              Background \n               \n                Tuberculosis (TB) is caused by \n                Mycobacterium tuberculosis \n                ( \n                Mtb \n                ) and typically infects the lungs. However, extrapulmonary forms of TB can be found in approximately 20\\% of cases. It is suggested, that up to 10\\% of extrapulmonary TB affects the musculoskeletal system, in which spinal elements (spinal tuberculosis, STB) are involved in approximately 50\\% of the cases. STB is a debilitating disease with nonspecific symptoms and diagnosis is often delayed for months to years. In our Spinal TB X Cohort, we aim to describe the clinical phenotype of STB using whole-body 18 F-fluorodeoxyglucose positron emission tomography computed tomography (PET/CT) and to identify a specific gene expression profile for the different stages of dissemination on PET/CT. Here we report on the first patient recruited into our cohort who underwent PET/CT before treatment initiation, at 6-months and at 12-months - time of TB treatment completion. \n               \n             \n             \n              Case presentation \n               \n                A 27-year-old immunocompetent male presented with severe thoracolumbar back pain for 9 months with severe antalgic gait and night sweats. Magnetic resonance imaging (MRI) of the whole spine revealed multilevel spinal disease (T5/6, T11/12, L3/4) in keeping with STB. After informed consent and recruitment into the Spinal TB X Cohort, the patient underwent PET/CT as per protocol, which revealed isolated multilevel STB (T4-7, T11/12, L3/4) with no concomitant lung or urogenital lesion. However, sputum and urine were Xpert MTB/RIF Ultra positive and \n                Mtb \n                was cultured from the urine sample. CT-guided biopsy of the T11/12 lesion confirmed drug-sensitive \n                Mtb \n                on Xpert MTB/RIF Ultra and the patient was started on TB treatment according to local guidelines for 12 months. The 6-month follow-up PET/CT revealed new and existing spinal lesions with increased FDG-uptake despite significant improvement of clinical features and laboratory markers. After 9 months of treatment, the patient developed an acute urethral stricture, most likely due to urogenital TB, and a suprapubic catheter was inserted. The 12-month PET/CT showed significantly decreased PET/CT values of all lesions, however, significant persistent spinal inflammation was present at the end of TB treatment. Clinically, the patient was considered cured by the TB control program and currently awaits urethroplasty. \n               \n             \n             \n              Conclusions \n              In our case, PET/CT emerged as a valuable imaging modality for the initial assessment, surpassing MRI by revealing more comprehensive extensive disease. Subsequent PET/CT scans at 6-month uncovered new lesions and increased inflammation in existing ones, while by the end of TB treatment, all lesions exhibited improvement. However, the interpretation of FDG avidity remains ambiguous, whether it correlates with active infection and viable Mtb. or fibro- and osteoblast activity indicative of the healing process. Additionally, the absence of extraspinal TB lesions on PET/CT despite positive microbiology from sputum and urine maybe explained by paucibacillary, subclinical infection of extraspinal organs. The Spinal TB X Cohort endeavours to shed light on whole-body imaging patterns at diagnosis, their evolution midway through TB treatment, and upon treatment completion. Ultimately, this study aims to advance our understanding of the biology of this complex disease.},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {Infection},\n\tauthor = {Scherer, Julian and Mukasa, Sandra L. and Wolmarans, Karen and Guler, Reto and Kotze, Tessa and Song, Taeksun and Dunn, Robert and Laubscher, Maritz and Pape, Hans-Christoph and Held, Michael and Thienemann, Friedrich},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {2507--2519},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Background Tuberculosis (TB) is caused by Mycobacterium tuberculosis ( Mtb ) and typically infects the lungs. However, extrapulmonary forms of TB can be found in approximately 20% of cases. It is suggested, that up to 10% of extrapulmonary TB affects the musculoskeletal system, in which spinal elements (spinal tuberculosis, STB) are involved in approximately 50% of the cases. STB is a debilitating disease with nonspecific symptoms and diagnosis is often delayed for months to years. In our Spinal TB X Cohort, we aim to describe the clinical phenotype of STB using whole-body 18 F-fluorodeoxyglucose positron emission tomography computed tomography (PET/CT) and to identify a specific gene expression profile for the different stages of dissemination on PET/CT. Here we report on the first patient recruited into our cohort who underwent PET/CT before treatment initiation, at 6-months and at 12-months - time of TB treatment completion. Case presentation A 27-year-old immunocompetent male presented with severe thoracolumbar back pain for 9 months with severe antalgic gait and night sweats. Magnetic resonance imaging (MRI) of the whole spine revealed multilevel spinal disease (T5/6, T11/12, L3/4) in keeping with STB. After informed consent and recruitment into the Spinal TB X Cohort, the patient underwent PET/CT as per protocol, which revealed isolated multilevel STB (T4-7, T11/12, L3/4) with no concomitant lung or urogenital lesion. However, sputum and urine were Xpert MTB/RIF Ultra positive and Mtb was cultured from the urine sample. CT-guided biopsy of the T11/12 lesion confirmed drug-sensitive Mtb on Xpert MTB/RIF Ultra and the patient was started on TB treatment according to local guidelines for 12 months. The 6-month follow-up PET/CT revealed new and existing spinal lesions with increased FDG-uptake despite significant improvement of clinical features and laboratory markers. After 9 months of treatment, the patient developed an acute urethral stricture, most likely due to urogenital TB, and a suprapubic catheter was inserted. The 12-month PET/CT showed significantly decreased PET/CT values of all lesions, however, significant persistent spinal inflammation was present at the end of TB treatment. Clinically, the patient was considered cured by the TB control program and currently awaits urethroplasty. Conclusions In our case, PET/CT emerged as a valuable imaging modality for the initial assessment, surpassing MRI by revealing more comprehensive extensive disease. Subsequent PET/CT scans at 6-month uncovered new lesions and increased inflammation in existing ones, while by the end of TB treatment, all lesions exhibited improvement. However, the interpretation of FDG avidity remains ambiguous, whether it correlates with active infection and viable Mtb. or fibro- and osteoblast activity indicative of the healing process. Additionally, the absence of extraspinal TB lesions on PET/CT despite positive microbiology from sputum and urine maybe explained by paucibacillary, subclinical infection of extraspinal organs. The Spinal TB X Cohort endeavours to shed light on whole-body imaging patterns at diagnosis, their evolution midway through TB treatment, and upon treatment completion. Ultimately, this study aims to advance our understanding of the biology of this complex disease.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Screening of Inherited Retinal Disease Patients in a Low‐Resource Setting Using an Augmented Next‐Generation Sequencing Panel.\n \n \n \n \n\n\n \n Midgley, N.; Rebello, G.; Holtes, L. K.; Ramesar, R.; and Roberts, L.\n\n\n \n\n\n\n Molecular Genetics & Genomic Medicine, 12(12): e70046. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Screening$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{midgley_screening_2024,\n\ttitle = {Screening of {Inherited} {Retinal} {Disease} {Patients} in a {Low}‐{Resource} {Setting} {Using} an {Augmented} {Next}‐{Generation} {Sequencing} {Panel}},\n\tvolume = {12},\n\tissn = {2324-9269, 2324-9269},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/mgg3.70046},\n\tdoi = {10.1002/mgg3.70046},\n\tabstract = {ABSTRACT \n             \n              Background \n              Inherited retinal diseases (IRDs) are a clinically and genetically heterogeneous group of disorders affecting millions worldwide. Despite the widespread adoption of next‐generation sequencing (NGS) panels, there remains a critical gap in the genetically diverse and understudied African populations. \n             \n             \n              Methods \n               \n                One hundred and thirty‐five South African patients affected by various IRDs underwent NGS using a custom‐targeted panel sequencing over 100 known genes. The panel was supplemented by \n                in silico \n                screening for a \n                MAK \n                ‐Alu insertion and screening of seven functionally established deep intronic variants. \n               \n             \n             \n              Results \n              Through our combined screening strategy, we obtained a probable genetic diagnosis for 56\\% of the cohort. We identified 83 unique variants in 29 IRD genes underlying the disease, including 16 putative novel variants. Molecular findings prompted recommendations for clinical re‐examination in ten patients. Resolution rates varied across clinical classifications and population groups. \n             \n             \n              Conclusions \n              This study reports the first use of a targeted NGS panel for IRDs in southern Africa, demonstrating a cost‐effective, customisable approach that optimises both diagnostic yield and resource efficiency, making it a valuable tool for IRD molecular characterisation in resource‐limited settings. Augmenting the panel by screening for variants relevant to South African patients allowed us to achieve a resolution rate in line with international studies. Our study underscores the importance of investigating diverse populations to bridge disparities in genomic research and improve diagnostic outcomes for underrepresented population groups.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {Molecular Genetics \\& Genomic Medicine},\n\tauthor = {Midgley, Nicole and Rebello, George and Holtes, Lara K. and Ramesar, Raj and Roberts, Lisa},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {e70046},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The curious case of the hypothalamic–pituitary–gonadal axis dysfunction in subordinate female naked mole‐rats ( Heterocephalus glaber ): No apparent role of opioids and glucocorticoids.\n \n \n \n \n\n\n \n Hart, D. W.; Roberts, E.; O'Riain, M. J.; Millar, R. P.; and Bennett, N. C.\n\n\n \n\n\n\n Journal of Neuroendocrinology, 36(10): e13444. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{hart_curious_2024,\n\ttitle = {The curious case of the hypothalamic–pituitary–gonadal axis dysfunction in subordinate female naked mole‐rats ( \\textit{{Heterocephalus} glaber} ): {No} apparent role of opioids and glucocorticoids},\n\tvolume = {36},\n\tissn = {0953-8194, 1365-2826},\n\tshorttitle = {The curious case of the hypothalamic–pituitary–gonadal axis dysfunction in subordinate female naked mole‐rats ( \\textit{{Heterocephalus} glaber} )},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/jne.13444},\n\tdoi = {10.1111/jne.13444},\n\tabstract = {Abstract \n             \n              The naked mole‐rat ( \n              Heterocephalus glaber \n              ) is a unique model mammal in which to study socially induced inhibition of the hypothalamic–pituitary–gonadal (HPG) axis. Naked mole‐rat groups exhibit a high degree of reproductive bias in which breeding is restricted to one female (the queen) and one male, with subordinate non‐breeding colony members rarely, if ever, having the opportunity to reproduce due to a dysfunctional HPG axis. It is posited that aggression directed at subordinates by the queen suppresses reproduction in these subordinates, yet the underlying physiological mechanisms causing this dysfunction are unknown. This study aimed to investigate the possible factors contributing to the dysfunction of the HPG axis in subordinate female naked mole‐rats with a specific focus on the role of ovarian feedback and stress‐related factors such as circulating glucocorticoid and endogenous opioid peptides. The results showed that stress‐related factors appear to not mediate the suppression of reproductive function in subordinate female naked mole rats. Indeed, in some cases, the activation of the stress axis may lead to reproductive activation instead of deactivation. At the same time, the role of ovarian sex steroid feedback in reproductive suppression is likely limited and not clearly delineated. This study highlights the need for detailed studies to elucidate the mechanism of reproductive suppression in this unique model mammalian species which may shed light on, and reveal novel mechanisms, in the social regulation of reproduction.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Neuroendocrinology},\n\tauthor = {Hart, Daniel W. and Roberts, E. and O'Riain, M. J. and Millar, R. P. and Bennett, N. C.},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {e13444},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Expanding Xpert MTB/RIF Ultra® and LF-LAM testing for diagnosis of tuberculosis among HIV-positive adults admitted to hospitals in Tanzania and Mozambique: a randomized controlled trial (the EXULTANT trial).\n \n \n \n \n\n\n \n Mangu, C.; Cossa, M.; Ndege, R.; Khosa, C.; Leukes, V.; De La Torre-Pérez, L.; Machiana, A.; Kivuma, B.; Mnzava, D.; Zachariah, C.; Manjate, P.; Tagliani, E.; Schacht, C.; Buech, J.; Singh, S.; Ehrlich, J.; Riess, F.; Sanz, S.; Kranzer, K.; Cox, H.; Sabi, I.; Nguenha, D.; Meggi, B.; Weisser, M.; Ntinginya, N.; Schumacher, S.; Ruhwald, M.; Penn-Nicholson, A.; Garcia-Basteiro, A. L.; TB-CAPT Consortium; Erkosar, B.; Nuru, M.; Mahmud, M.; Shija, N.; Bulime, D.; Sabuni, P.; Temba, H.; Siru, J.; Hella, J.; Msafiri, J.; Mbaruku, M.; Sasamalo, M.; Leonard, A.; Malango, A.; Alexander, A.; Komakoma, F.; Msigala, G.; Johaness, K.; Mhalu, G.; Hamis, M.; Mlay, P.; Barasa, S.; Masoud, S.; Byakuzana, T.; Lwilla, A.; Sylvester, P.; Sichone, E.; Wailes, S.; Mtafya, B.; Kisinda, A.; Martine, M.; Mgaya, R.; Manyama, C.; Mbunda, T.; Siyame, E.; Mwaipopo, L.; Ntinginya, N. E.; Edom, R.; Olomi, W.; Elisio, D.; Edson Mambuque; Cossa, J.; Gomes, N.; Munguambe, S.; Acacio, S.; Chiconela, H.; Ribeiro, K.; Madeira, C.; Machavae, D.; Manhiça, E.; Guiliche, O.; Malamule, D.; Viegas, S.; Saavedra, B.; Fernández-Escobar, C.; Hoelscher, M.; Heinrich, N.; Larsson, L.; Del Mar Castro Noriega, M.; Denkinger, C.; Arif, S.; Cirillo, D. M.; Di Marco, F.; Batignani, V.; Malhotra, A.; Dowdy, D.; Stöhr, C.; Loembé, M. M.; Ondoa, P.; Ndlovu, N.; Brown, F.; Ghebrekristos, Y.; Hayes, C.; Vanderwalt, I.; Abrahams, S.; Marokane, P.; Radebe, M.; Martinson, N.; David, A.; Scott, L.; Ngwenya, L.; Da Silva, P.; Munir, R.; Stevens, W.; Abongomera, C.; Reither, K.; Stieger, L.; Brink, A.; Centner, C.; Van Heerden, J.; Nicol, M.; Hapeela, N.; Brown, P.; Solomon, R.; Zemanay, W.; and Dolby, T.\n\n\n \n\n\n\n BMC Infectious Diseases, 24(1): 831. August 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Expanding$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{mangu_expanding_2024,\n\ttitle = {Expanding {Xpert} {MTB}/{RIF} {Ultra}® and {LF}-{LAM} testing for diagnosis of tuberculosis among {HIV}-positive adults admitted to hospitals in {Tanzania} and {Mozambique}: a randomized controlled trial (the {EXULTANT} trial)},\n\tvolume = {24},\n\tissn = {1471-2334},\n\tshorttitle = {Expanding {Xpert} {MTB}/{RIF} {Ultra}® and {LF}-{LAM} testing for diagnosis of tuberculosis among {HIV}-positive adults admitted to hospitals in {Tanzania} and {Mozambique}},\n\turl = {https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-024-09651-z},\n\tdoi = {10.1186/s12879-024-09651-z},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {BMC Infectious Diseases},\n\tauthor = {Mangu, Chacha and Cossa, Marta and Ndege, Robert and Khosa, Celso and Leukes, Vinzeigh and De La Torre-Pérez, Laura and Machiana, Antonio and Kivuma, Bernard and Mnzava, Dorcas and Zachariah, Craysophy and Manjate, Patricia and Tagliani, Elisa and Schacht, Claudia and Buech, Julia and Singh, Sunita and Ehrlich, Joanna and Riess, Friedrich and Sanz, Sergi and Kranzer, Katharina and Cox, Helen and Sabi, Issa and Nguenha, Dinis and Meggi, Bindiya and Weisser, Maja and Ntinginya, Nyanda and Schumacher, Samuel and Ruhwald, Morten and Penn-Nicholson, Adam and Garcia-Basteiro, Alberto L. and {TB-CAPT Consortium} and Erkosar, Berra and Nuru, Muhuminu and Mahmud, Mahmud and Shija, Neema and Bulime, Deogratias and Sabuni, Petro and Temba, Hosiana and Siru, Jamali and Hella, Jerry and Msafiri, Jonathan and Mbaruku, Mohamed and Sasamalo, Mohamed and Leonard, Alice and Malango, Ambilikile and Alexander, Annastazia and Komakoma, Faith and Msigala, Gloria and Johaness, Kasmir and Mhalu, Grace and Hamis, Mwajabu and Mlay, Priscilla and Barasa, Sera and Masoud, Swalehe and Byakuzana, Theonestina and Lwilla, Anange and Sylvester, Pauline and Sichone, Emanuel and Wailes, Subira and Mtafya, Bariki and Kisinda, Abisai and Martine, Malendeja and Mgaya, Regino and Manyama, Christina and Mbunda, Theodora and Siyame, Elimina and Mwaipopo, Last and Ntinginya, Nyanda Elias and Edom, Raphael and Olomi, Willyhelmina and Elisio, Delio and {Edson Mambuque} and Cossa, Joaquim and Gomes, Neide and Munguambe, Shilzia and Acacio, Sozinho and Chiconela, Helio and Ribeiro, Katia and Madeira, Carla and Machavae, Daniel and Manhiça, Emelva and Guiliche, Onelia and Malamule, Diosdélio and Viegas, Sofia and Saavedra, Belén and Fernández-Escobar, Carlos and Hoelscher, Michael and Heinrich, Norbert and Larsson, Leyla and Del Mar Castro Noriega, Maria and Denkinger, Claudia and Arif, Saima and Cirillo, Daniela Maria and Di Marco, Federico and Batignani, Virginia and Malhotra, Akash and Dowdy, David and Stöhr, Caroline and Loembé, Marguerite Massinga and Ondoa, Pascale and Ndlovu, Nqobile and Brown, Fumbani and Ghebrekristos, Yonas and Hayes, Cindy and Vanderwalt, Ilse and Abrahams, Shareef and Marokane, Puleng and Radebe, Mbuti and Martinson, Neil and David, Anura and Scott, Lesley and Ngwenya, Lucky and Da Silva, Pedro and Munir, Riffat and Stevens, Wendy and Abongomera, Charles and Reither, Klaus and Stieger, Leon and Brink, Adrian and Centner, Chad and Van Heerden, Judi and Nicol, Mark and Hapeela, Nchimunya and Brown, Parveen and Solomon, Reyhana and Zemanay, Widaad and Dolby, Tania},\n\tmonth = aug,\n\tyear = {2024},\n\tpages = {831},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Safety, effectiveness and immunogenicity of heterologous mRNA-1273 boost after prime with Ad26.COV2.S among healthcare workers in South Africa: The single-arm, open-label, phase 3 SHERPA study.\n \n \n \n \n\n\n \n Garrett, N.; Reddy, T.; Yende-Zuma, N.; Takalani, A.; Woeber, K.; Bodenstein, A.; Jonas, P.; Engelbrecht, I.; Jassat, W.; Moultrie, H.; Bradshaw, D.; Seocharan, I.; Odhiambo, J.; Khuto, K.; Richardson, S. I.; Omondi, M. A.; Nesamari, R.; Keeton, R. S.; Riou, C.; Moyo-Gwete, T.; Innes, C.; Zwane, Z.; Mngadi, K.; Brumskine, W.; Naicker, N.; Potloane, D.; Badal-Faesen, S.; Innes, S.; Barnabas, S.; Lombaard, J.; Gill, K.; Nchabeleng, M.; Snyman, E.; Petrick, F.; Spooner, E.; Naidoo, L.; Kalonji, D.; Naicker, V.; Singh, N.; Maboa, R.; Mda, P.; Malan, D.; Nana, A.; Malahleha, M.; Kotze, P.; Allagappen, J. J.; Diacon, A. H.; Kruger, G. M.; Patel, F.; Moore, P. L.; Burgers, W. A.; Anteyi, K.; Leav, B.; Bekker, L.; Gray, G. E.; Goga, A.; and the SHERPA study team\n\n\n \n\n\n\n PLOS Global Public Health, 4(12): e0003260. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Safety,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{garrett_safety_2024,\n\ttitle = {Safety, effectiveness and immunogenicity of heterologous {mRNA}-1273 boost after prime with {Ad26}.{COV2}.{S} among healthcare workers in {South} {Africa}: {The} single-arm, open-label, phase 3 {SHERPA} study},\n\tvolume = {4},\n\tissn = {2767-3375},\n\tshorttitle = {Safety, effectiveness and immunogenicity of heterologous {mRNA}-1273 boost after prime with {Ad26}.{COV2}.{S} among healthcare workers in {South} {Africa}},\n\turl = {https://dx.plos.org/10.1371/journal.pgph.0003260},\n\tdoi = {10.1371/journal.pgph.0003260},\n\tabstract = {Limited studies have been conducted on the safety and effectiveness of heterologous COVID-19 vaccine boosting in lower income settings, especially those with high-HIV prevalence., The Sisonke Heterologous mRNA-1273 boost after prime with Ad26.COV2.S (SHERPA) trial evaluated a mRNA-1273 boost after Ad26.COV2.S priming in South Africa. SHERPA was a single-arm, open-label, phase 3 study nested in the Sisonke implementation trial of 500000 healthcare workers (HCWs). Sisonke participants were offered mRNA-1273 boosters between May and November 2022, when Omicron sub-lineages were circulating. Adverse events (AE) were self-reported, and co-primary endpoints (SARS-CoV-2 infections and COVID-19 hospitalizations or deaths) were collected through national databases. We used Cox regression models with booster status as a time-varying covariate to determine the relative vaccine effectiveness (rVE) of the mRNA-1273 booster among SHERPA versus unboosted Sisonke participants. Of 11248 SHERPA participants in the rVE analysis cohort (79.3\\% female, median age 41), 45.4\\% had received one and 54.6\\% two Ad26.COV2.S doses. Self-reported comorbidities included HIV (18.7\\%), hypertension (12.9\\%) and diabetes (4.6\\%). In multivariable analysis including 413161 unboosted Sisonke participants, rVE of the booster was 59\\% (95\\%CI 29–76\\%) against SARS-CoV-2 infection: 77\\% (95\\%CI 9–94\\%) in the one-Ad26.COV2.S dose group and 52\\% (95\\%CI 13–73\\%) in the two-dose group. Severe COVID-19 was identified in 148 unboosted Sisonke participants, and only one SHERPA participant with severe HIV-related immunosuppression. Of 11798 participants in the safety analysis, 228 (1.9\\%) participants reported 575 reactogenicity events within 7 days of the booster (most commonly injection site pain, malaise, myalgia, swelling, induration and fever). More reactogenicity events were reported among those with prior SARS-CoV-2 infections (adjusted odds ratio [aOR] 2.03, 95\\%CI 1.59–2.59) and less among people living with HIV (PLWH) (aOR 0.49, 95\\%CI 0.34–0.69). There were 115 unsolicited adverse events (AEs) within 28 days of vaccination. No related serious AEs were reported. In an immunogenicity sub-study, mRNA-1273 increased binding and neutralizing antibody titres and spike-specific T-cell responses 4 weeks after boosting regardless of the number of prior Ad26.COV2.S doses, or HIV status, and generated Omicron spike-specific cross-reactive responses. mRNA-1273 boosters after one or two Ad26.COV2.S doses were well-tolerated, safe and effective against Omicron SARS-CoV-2 infections among HCWs and PLWH. \n             \n              Trial registration: \n              The SHERPA study is registered in the Pan African Clinical Trials Registry (PACTR): \n              PACTR202310615330649 \n              and the South African National Clinical Trial Registry (SANCTR): DOH-27-052022-5778.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {PLOS Global Public Health},\n\tauthor = {Garrett, Nigel and Reddy, Tarylee and Yende-Zuma, Nonhlanhla and Takalani, Azwidhwi and Woeber, Kubashni and Bodenstein, Annie and Jonas, Phumeza and Engelbrecht, Imke and Jassat, Waasila and Moultrie, Harry and Bradshaw, Debbie and Seocharan, Ishen and Odhiambo, Jackline and Khuto, Kentse and Richardson, Simone I. and Omondi, Millicent A. and Nesamari, Rofhiwa and Keeton, Roanne S. and Riou, Catherine and Moyo-Gwete, Thandeka and Innes, Craig and Zwane, Zwelethu and Mngadi, Kathy and Brumskine, William and Naicker, Nivashnee and Potloane, Disebo and Badal-Faesen, Sharlaa and Innes, Steve and Barnabas, Shaun and Lombaard, Johan and Gill, Katherine and Nchabeleng, Maphoshane and Snyman, Elizma and Petrick, Friedrich and Spooner, Elizabeth and Naidoo, Logashvari and Kalonji, Dishiki and Naicker, Vimla and Singh, Nishanta and Maboa, Rebone and Mda, Pamela and Malan, Daniel and Nana, Anusha and Malahleha, Mookho and Kotze, Philip and Allagappen, Jon J. and Diacon, Andreas H. and Kruger, Gertruida M. and Patel, Faeezah and Moore, Penny L. and Burgers, Wendy A. and Anteyi, Kate and Leav, Brett and Bekker, Linda-Gail and Gray, Glenda E. and Goga, Ameena and {the SHERPA study team}},\n\teditor = {Wagner, Abram L.},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {e0003260},\n}\n\n\n\n

\n

\n\n\n

\n Limited studies have been conducted on the safety and effectiveness of heterologous COVID-19 vaccine boosting in lower income settings, especially those with high-HIV prevalence., The Sisonke Heterologous mRNA-1273 boost after prime with Ad26.COV2.S (SHERPA) trial evaluated a mRNA-1273 boost after Ad26.COV2.S priming in South Africa. SHERPA was a single-arm, open-label, phase 3 study nested in the Sisonke implementation trial of 500000 healthcare workers (HCWs). Sisonke participants were offered mRNA-1273 boosters between May and November 2022, when Omicron sub-lineages were circulating. Adverse events (AE) were self-reported, and co-primary endpoints (SARS-CoV-2 infections and COVID-19 hospitalizations or deaths) were collected through national databases. We used Cox regression models with booster status as a time-varying covariate to determine the relative vaccine effectiveness (rVE) of the mRNA-1273 booster among SHERPA versus unboosted Sisonke participants. Of 11248 SHERPA participants in the rVE analysis cohort (79.3% female, median age 41), 45.4% had received one and 54.6% two Ad26.COV2.S doses. Self-reported comorbidities included HIV (18.7%), hypertension (12.9%) and diabetes (4.6%). In multivariable analysis including 413161 unboosted Sisonke participants, rVE of the booster was 59% (95%CI 29–76%) against SARS-CoV-2 infection: 77% (95%CI 9–94%) in the one-Ad26.COV2.S dose group and 52% (95%CI 13–73%) in the two-dose group. Severe COVID-19 was identified in 148 unboosted Sisonke participants, and only one SHERPA participant with severe HIV-related immunosuppression. Of 11798 participants in the safety analysis, 228 (1.9%) participants reported 575 reactogenicity events within 7 days of the booster (most commonly injection site pain, malaise, myalgia, swelling, induration and fever). More reactogenicity events were reported among those with prior SARS-CoV-2 infections (adjusted odds ratio [aOR] 2.03, 95%CI 1.59–2.59) and less among people living with HIV (PLWH) (aOR 0.49, 95%CI 0.34–0.69). There were 115 unsolicited adverse events (AEs) within 28 days of vaccination. No related serious AEs were reported. In an immunogenicity sub-study, mRNA-1273 increased binding and neutralizing antibody titres and spike-specific T-cell responses 4 weeks after boosting regardless of the number of prior Ad26.COV2.S doses, or HIV status, and generated Omicron spike-specific cross-reactive responses. mRNA-1273 boosters after one or two Ad26.COV2.S doses were well-tolerated, safe and effective against Omicron SARS-CoV-2 infections among HCWs and PLWH. Trial registration: The SHERPA study is registered in the Pan African Clinical Trials Registry (PACTR): PACTR202310615330649 and the South African National Clinical Trial Registry (SANCTR): DOH-27-052022-5778.\n

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\n \n\n \n \n \n \n \n \n An Oxford Nanopore Technology-Based Hepatitis B Virus Sequencing Protocol Suitable for Genomic Surveillance Within Clinical Diagnostic Settings.\n \n \n \n \n\n\n \n Tshiabuila, D.; Choga, W.; San, J. E.; Maponga, T.; Van Zyl, G.; Giandhari, J.; Pillay, S.; Preiser, W.; Naidoo, Y.; Baxter, C.; Martin, D. P.; and De Oliveira, T.\n\n\n \n\n\n\n International Journal of Molecular Sciences, 25(21): 11702. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"An$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{tshiabuila_oxford_2024,\n\ttitle = {An {Oxford} {Nanopore} {Technology}-{Based} {Hepatitis} {B} {Virus} {Sequencing} {Protocol} {Suitable} for {Genomic} {Surveillance} {Within} {Clinical} {Diagnostic} {Settings}},\n\tvolume = {25},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1422-0067},\n\turl = {https://www.mdpi.com/1422-0067/25/21/11702},\n\tdoi = {10.3390/ijms252111702},\n\tabstract = {Chronic Hepatitis B Virus (HBV) infection remains a significant public health concern, particularly in Africa, where the burden is substantial. HBV is an enveloped virus, classified into ten phylogenetically distinct genotypes (A–J). Tests to determine HBV genotypes are based on full-genome sequencing or reverse hybridization. In practice, both approaches have limitations. Whereas diagnostic sequencing, generally using the Sanger approach, tends to focus only on the S-gene and yields little or no information on intra-patient HBV genetic diversity, reverse hybridization detects only known genotype-specific mutations. To resolve these limitations, we developed an Oxford Nanopore Technology (ONT)-based HBV diagnostic sequencing protocol suitable for clinical virology that yields both complete genome sequences and extensive intra-patient HBV diversity data. Specifically, the protocol involves tiling-based PCR amplification of HBV sequences, library preparation using the ONT Rapid Barcoding Kit (Oxford nanopore Technologies, Oxford, OX4 4DQ, UK), ONT GridION sequencing, genotyping using genome detective software v1.132/1.133, a recombination analysis using jpHMM (26 October 2011 version) and RDP5.61 software, and drug resistance profiling using Geno2pheno v2.0 software. We prove the utility of our protocol by efficiently generating and characterizing high-quality near full-length HBV genomes from 148 residual diagnostic samples from HBV-infected patients in the Western Cape province of South Africa, providing valuable insights into the genetic diversity and epidemiology of HBV in this region of the world.},\n\tlanguage = {en},\n\tnumber = {21},\n\turldate = {2025-06-24},\n\tjournal = {International Journal of Molecular Sciences},\n\tauthor = {Tshiabuila, Derek and Choga, Wonderful and San, James E. and Maponga, Tongai and Van Zyl, Gert and Giandhari, Jennifer and Pillay, Sureshnee and Preiser, Wolfgang and Naidoo, Yeshnee and Baxter, Cheryl and Martin, Darren P. and De Oliveira, Tulio},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {11702},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Mtb-Specific HLA-E-Restricted T Cells Are Induced during Mtb Infection but Not after BCG Administration in Non-Human Primates and Humans.\n \n \n \n \n\n\n \n Voogd, L.; Van Wolfswinkel, M.; Satti, I.; White, A.; Dijkman, K.; Gela, A.; Van Meijgaarden, K.; Franken, K.; Marshall, J.; Ottenhoff, T.; Scriba, T.; McShane, H.; Sharpe, S.; Verreck, F.; and Joosten, S.\n\n\n \n\n\n\n Vaccines, 12(10): 1129. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Mtb-Specific$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{voogd_mtb-specific_2024,\n\ttitle = {Mtb-{Specific} {HLA}-{E}-{Restricted} {T} {Cells} {Are} {Induced} during {Mtb} {Infection} but {Not} after {BCG} {Administration} in {Non}-{Human} {Primates} and {Humans}},\n\tvolume = {12},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2076-393X},\n\turl = {https://www.mdpi.com/2076-393X/12/10/1129},\n\tdoi = {10.3390/vaccines12101129},\n\tabstract = {Background: Novel vaccines targeting the world’s deadliest pathogen Mycobacterium tuberculosis (Mtb) are urgently needed as the efficacy of the Bacillus Calmette–Guérin (BCG) vaccine in its current use is limited. HLA-E is a virtually monomorphic unconventional antigen presentation molecule, and HLA-E-restricted Mtb-specific CD8+ T cells can control intracellular Mtb growth, making HLA-E a promising vaccine target for Mtb. Methods: In this study, we evaluated the frequency and phenotype of HLA-E-restricted Mtb-specific CD4+/CD8+ T cells in the circulation and bronchoalveolar lavage fluid of two independent non-human primate (NHP) studies and from humans receiving BCG either intradermally or mucosally. Results: BCG vaccination followed by Mtb challenge in NHPs did not affect the frequency of circulating and local HLA-E–Mtb CD4+ and CD8+ T cells, and we saw the same in humans receiving BCG. HLA-E–Mtb T cell frequencies were significantly increased after Mtb challenge in unvaccinated NHPs, which was correlated with higher TB pathology. Conclusions: Together, HLA-E–Mtb-restricted T cells are minimally induced by BCG in humans and rhesus macaques (RMs) but can be elicited after Mtb infection in unvaccinated RMs. These results give new insights into targeting HLA-E as a potential immune mechanism against TB.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {Vaccines},\n\tauthor = {Voogd, Linda and Van Wolfswinkel, Marjolein and Satti, Iman and White, Andrew and Dijkman, Karin and Gela, Anele and Van Meijgaarden, Krista and Franken, Kees and Marshall, Julia and Ottenhoff, Tom and Scriba, Thomas and McShane, Helen and Sharpe, Sally and Verreck, Frank and Joosten, Simone},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {1129},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Characterization of bacterial and viral pathogens in the respiratory tract of children with HIV-associated chronic lung disease: a case–control study.\n \n \n \n \n\n\n \n Mushunje, P. K.; Dube, F. S.; Olwagen, C.; Madhi, S.; Odland, J. Ø; Ferrand, R. A.; Nicol, M. P.; Abotsi, R. E.; The BREATHE study team; Bandason, T.; Dauya, E.; Madanhire, T.; Corbett, E. L.; Kranzer, K.; Majonga, E. D.; Simms, V.; Rehman, A. M.; A.Weiss, H.; Mujuru, H.; Bowen, D.; Yindom, L.; Rowland-Jones, S. L.; Flaegstad, T.; Gutteberg, T. J.; Cavanagh, J. P.; Flygel, T. T.; Sovarashaeva, E.; Chikwana, J.; Mapurisa, G. N.; Gonzalez-Martinez, C.; Semphere, R.; Moyo, B. W.; Ngwira, L. G.; and Mbhele, S.\n\n\n \n\n\n\n BMC Infectious Diseases, 24(1): 637. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Characterization$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{mushunje_characterization_2024,\n\ttitle = {Characterization of bacterial and viral pathogens in the respiratory tract of children with {HIV}-associated chronic lung disease: a case–control study},\n\tvolume = {24},\n\tissn = {1471-2334},\n\tshorttitle = {Characterization of bacterial and viral pathogens in the respiratory tract of children with {HIV}-associated chronic lung disease},\n\turl = {https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-024-09540-5},\n\tdoi = {10.1186/s12879-024-09540-5},\n\tabstract = {Abstract \n             \n              Introduction \n              Chronic lung disease is a major cause of morbidity in African children with HIV infection; however, the microbial determinants of HIV-associated chronic lung disease (HCLD) remain poorly understood. We conducted a case–control study to investigate the prevalence and densities of respiratory microbes among pneumococcal conjugate vaccine (PCV)-naive children with (HCLD +) and without HCLD (HCLD-) established on antiretroviral treatment (ART). \n             \n             \n              Methods \n               \n                Nasopharyngeal swabs collected from HCLD + (defined as forced-expiratory-volume/second {\\textless} -1.0 without reversibility postbronchodilation) and age-, site-, and duration-of-ART-matched HCLD- participants aged between 6–19 years enrolled in Zimbabwe and Malawi (BREATHE trial-NCT02426112) were tested for 94 pneumococcal serotypes together with twelve bacteria, including \n                Streptococcus pneumoniae \n                (SP), \n                Staphylococcus aureus \n                (SA), \n                Haemophilus influenzae \n                (HI), \n                Moraxella catarrhalis \n                (MC), and eight viruses, including human rhinovirus (HRV), respiratory syncytial virus A or B, and human metapneumovirus, using nanofluidic qPCR (Standard BioTools formerly known as Fluidigm). Fisher's exact test and logistic regression analysis were used for between-group comparisons and risk factors associated with common respiratory microbes, respectively. \n               \n             \n             \n              Results \n               \n                A total of 345 participants (287 HCLD + , 58 HCLD-; median age, 15.5 years [IQR = 12.8–18], females, 52\\%) were included in the final analysis. The prevalence of SP (40\\%[116/287] \n                vs. \n                21\\%[12/58], \n                p \n                 = 0.005) and HRV (7\\%[21/287] \n                vs. \n                0\\%[0/58], \n                p \n                 = 0.032) were higher in HCLD + participants compared to HCLD- participants. Of the participants positive for SP (116 HCLD + \\& 12 HCLD-), 66\\% [85/128] had non-PCV-13 serotypes detected. Overall, PCV-13 serotypes (4, 19A, 19F: 16\\% [7/43] each) and NVT 13 and 21 (9\\% [8/85] each) predominated. The densities of HI (2 × 10 \n                4 \n                genomic equivalents [GE/ml] \n                vs. \n                3 × 10 \n                2 \n                GE/ml, \n                p \n                 = 0.006) and MC (1 × 10 \n                4 \n                GE/ml \n                vs. \n                1 × 10 \n                3 \n                GE/ml \n                , p \n                 = 0.031) were higher in HCLD + compared to HCLD-. Bacterial codetection (≥ any 2 bacteria) was higher in the HCLD + group (36\\% [114/287] \n                vs. \n                (19\\% [11/58]), ( \n                p \n                 = 0.014), with SP and HI codetection (HCLD + : 30\\% [86/287] \n                vs. \n                HCLD-: 12\\% [7/58], \n                p \n                 = 0.005) predominating. Viruses (predominantly HRV) were detected only in HCLD + participants. Lastly, participants with a history of previous tuberculosis treatment were more likely to carry SP (adjusted odds ratio (aOR): 1.9 [1.1 -3.2], \n                p \n                 = 0.021) or HI (aOR: 2.0 [1.2 – 3.3], \n                p \n                 = 0.011), while those who used ART for ≥ 2 years were less likely to carry HI (aOR: 0.3 [0.1 – 0.8], \n                p \n                 = 0.005) and MC (aOR: 0.4 [0.1 – 0.9], \n                p \n                 = 0.039). \n               \n             \n             \n              Conclusion \n              Children with HCLD + were more likely to be colonized by SP and HRV and had higher HI and MC bacterial loads in their nasopharynx. The role of SP, HI, and HRV in the pathogenesis of CLD, including how they influence the risk of acute exacerbations, should be studied further. \n             \n             \n              Trial registration \n               \n                The BREATHE trial (ClinicalTrials.gov Identifier: \n                NCT02426112 \n                , registered date: 24 April 2015).},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {BMC Infectious Diseases},\n\tauthor = {Mushunje, Prince K. and Dube, Felix S. and Olwagen, Courtney and Madhi, Shabir and Odland, Jon Ø and Ferrand, Rashida A. and Nicol, Mark P. and Abotsi, Regina E. and {The BREATHE study team} and Bandason, Tsitsi and Dauya, Ethel and Madanhire, Tafadzwa and Corbett, Elizabeth L. and Kranzer, Katharina and Majonga, Edith D. and Simms, Victoria and Rehman, Andrea M. and A.Weiss, Helen and Mujuru, Hilda and Bowen, Dan and Yindom, Louis-Marie and Rowland-Jones, Sarah L. and Flaegstad, Trond and Gutteberg, Tore J. and Cavanagh, Jorunn Pauline and Flygel, Trym Thune and Sovarashaeva, Evegeniya and Chikwana, Jessica and Mapurisa, Gugulethu Newton and Gonzalez-Martinez, Carmen and Semphere, Robina and Moyo, Brewster Wisdom and Ngwira, Lucky Gift and Mbhele, Slindile},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {637},\n}\n\n\n\n

\n

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\n Abstract Introduction Chronic lung disease is a major cause of morbidity in African children with HIV infection; however, the microbial determinants of HIV-associated chronic lung disease (HCLD) remain poorly understood. We conducted a case–control study to investigate the prevalence and densities of respiratory microbes among pneumococcal conjugate vaccine (PCV)-naive children with (HCLD +) and without HCLD (HCLD-) established on antiretroviral treatment (ART). Methods Nasopharyngeal swabs collected from HCLD + (defined as forced-expiratory-volume/second \\textless -1.0 without reversibility postbronchodilation) and age-, site-, and duration-of-ART-matched HCLD- participants aged between 6–19 years enrolled in Zimbabwe and Malawi (BREATHE trial-NCT02426112) were tested for 94 pneumococcal serotypes together with twelve bacteria, including Streptococcus pneumoniae (SP), Staphylococcus aureus (SA), Haemophilus influenzae (HI), Moraxella catarrhalis (MC), and eight viruses, including human rhinovirus (HRV), respiratory syncytial virus A or B, and human metapneumovirus, using nanofluidic qPCR (Standard BioTools formerly known as Fluidigm). Fisher's exact test and logistic regression analysis were used for between-group comparisons and risk factors associated with common respiratory microbes, respectively. Results A total of 345 participants (287 HCLD + , 58 HCLD-; median age, 15.5 years [IQR = 12.8–18], females, 52%) were included in the final analysis. The prevalence of SP (40%[116/287] vs. 21%[12/58], p = 0.005) and HRV (7%[21/287] vs. 0%[0/58], p = 0.032) were higher in HCLD + participants compared to HCLD- participants. Of the participants positive for SP (116 HCLD + & 12 HCLD-), 66% [85/128] had non-PCV-13 serotypes detected. Overall, PCV-13 serotypes (4, 19A, 19F: 16% [7/43] each) and NVT 13 and 21 (9% [8/85] each) predominated. The densities of HI (2 × 10 4 genomic equivalents [GE/ml] vs. 3 × 10 2 GE/ml, p = 0.006) and MC (1 × 10 4 GE/ml vs. 1 × 10 3 GE/ml , p = 0.031) were higher in HCLD + compared to HCLD-. Bacterial codetection (≥ any 2 bacteria) was higher in the HCLD + group (36% [114/287] vs. (19% [11/58]), ( p = 0.014), with SP and HI codetection (HCLD + : 30% [86/287] vs. HCLD-: 12% [7/58], p = 0.005) predominating. Viruses (predominantly HRV) were detected only in HCLD + participants. Lastly, participants with a history of previous tuberculosis treatment were more likely to carry SP (adjusted odds ratio (aOR): 1.9 [1.1 -3.2], p = 0.021) or HI (aOR: 2.0 [1.2 – 3.3], p = 0.011), while those who used ART for ≥ 2 years were less likely to carry HI (aOR: 0.3 [0.1 – 0.8], p = 0.005) and MC (aOR: 0.4 [0.1 – 0.9], p = 0.039). Conclusion Children with HCLD + were more likely to be colonized by SP and HRV and had higher HI and MC bacterial loads in their nasopharynx. The role of SP, HI, and HRV in the pathogenesis of CLD, including how they influence the risk of acute exacerbations, should be studied further. Trial registration The BREATHE trial (ClinicalTrials.gov Identifier: NCT02426112 , registered date: 24 April 2015).\n

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\n \n\n \n \n \n \n \n \n Impact of Variable Sampling on Estimates of HIV-1 Reservoir Formation Dates.\n \n \n \n \n\n\n \n Kankaka, E. N; Poon, A. F Y; Quinn, T. C; Chang, L. W; Prodger, J. L; and Redd, A. D\n\n\n \n\n\n\n The Journal of Infectious Diseases, 230(4): 928–932. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Impact$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kankaka_impact_2024,\n\ttitle = {Impact of {Variable} {Sampling} on {Estimates} of {HIV}-1 {Reservoir} {Formation} {Dates}},\n\tvolume = {230},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/230/4/928/7685857},\n\tdoi = {10.1093/infdis/jiae294},\n\tabstract = {Abstract \n            Timing of human immunodeficiency virus-1 (HIV-1) reservoir formation is important for informing HIV cure efforts. It is unclear how much of the variability seen in dating reservoir formation is due to sampling and gene-specific differences. We used a Bayesian extension of root to tip regression (bayroot) to reestimate formation date distributions in participants from Swedish and South African cohorts, and assessed the impact of variable timing, frequency, and depth of sampling on these estimates. Significant shifts in formation date distributions were only observed with use of faster-evolving genes, while timing, frequency, and depth of sampling had minor or no significant effect on estimates.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Kankaka, Edward N and Poon, Art F Y and Quinn, Thomas C and Chang, Larry W and Prodger, Jessica L and Redd, Andrew D},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {928--932},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The Tuberculosis Drug Candidate SQ109 and Its Analogs Have Multistage Activity against Plasmodium falciparum.\n \n \n \n \n\n\n \n Watson, S. J.; Van Der Watt, M. E.; Theron, A.; Reader, J.; Tshabalala, S.; Erlank, E.; Koekemoer, L. L.; Naude, M.; Stampolaki, M.; Adewole, F.; Sadowska, K.; Pérez-Lozano, P.; Turcu, A. L.; Vázquez, S.; Ko, J.; Mazurek, B.; Singh, D.; Malwal, S. R.; Njoroge, M.; Chibale, K.; Onajole, O. K.; Kolocouris, A.; Oldfield, E.; and Birkholtz, L.\n\n\n \n\n\n\n ACS Infectious Diseases, 10(9): 3358–3367. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{watson_tuberculosis_2024,\n\ttitle = {The {Tuberculosis} {Drug} {Candidate} {SQ109} and {Its} {Analogs} {Have} {Multistage} {Activity} against \\textit{{Plasmodium} falciparum}},\n\tvolume = {10},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2373-8227, 2373-8227},\n\turl = {https://pubs.acs.org/doi/10.1021/acsinfecdis.4c00461},\n\tdoi = {10.1021/acsinfecdis.4c00461},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2025-06-24},\n\tjournal = {ACS Infectious Diseases},\n\tauthor = {Watson, Savannah J. and Van Der Watt, Mariëtte E. and Theron, Anjo and Reader, Janette and Tshabalala, Sizwe and Erlank, Erica and Koekemoer, Lizette L. and Naude, Mariska and Stampolaki, Marianna and Adewole, Feyisola and Sadowska, Katie and Pérez-Lozano, Pilar and Turcu, Andreea L. and Vázquez, Santiago and Ko, Jihee and Mazurek, Ben and Singh, Davinder and Malwal, Satish R. and Njoroge, Mathew and Chibale, Kelly and Onajole, Oluseye K. and Kolocouris, Antonios and Oldfield, Eric and Birkholtz, Lyn-Marié},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {3358--3367},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n In vitro antiplasmodium and antitrypanosomal activities, β-haematin formation inhibition, molecular docking and DFT computational studies of quinoline-urea-benzothiazole hybrids.\n \n \n \n \n\n\n \n Oyeneyin, O. E.; Moodley, R.; Mashaba, C.; Garnie, L. F.; Omoboyowa, D. A.; Rakodi, G. H.; Maphoru, M. V.; Balogun, M. O.; Hoppe, H. C.; Egan, T. J.; and Tukulula, M.\n\n\n \n\n\n\n Heliyon, 10(19): e38434. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"In$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{oyeneyin_vitro_2024,\n\ttitle = {In vitro antiplasmodium and antitrypanosomal activities, β-haematin formation inhibition, molecular docking and {DFT} computational studies of quinoline-urea-benzothiazole hybrids},\n\tvolume = {10},\n\tissn = {24058440},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2405844024144659},\n\tdoi = {10.1016/j.heliyon.2024.e38434},\n\tlanguage = {en},\n\tnumber = {19},\n\turldate = {2025-06-24},\n\tjournal = {Heliyon},\n\tauthor = {Oyeneyin, Oluwatoba E. and Moodley, Rashmika and Mashaba, Chakes and Garnie, Larnelle F. and Omoboyowa, Damilola A. and Rakodi, Goitsemodimo H. and Maphoru, Mabuatsela V. and Balogun, Mohamed O. and Hoppe, Heinrich C. and Egan, Timothy J. and Tukulula, Matshawandile},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {e38434},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Spatiotemporal dynamics of the oropharyngeal microbiome in a cohort of Ivorian school children.\n \n \n \n \n\n\n \n Diallo, K.; Missa, K. F.; Tuo, K. J.; Tiemele, L. S.; Ouattara, A. F.; Gboko, K. D. T.; Gragnon, B. G.; Bla, K. B.; Ngoi, J. M.; Wilkinson, R. J.; Awandare, G. A.; and Bonfoh, B.\n\n\n \n\n\n\n Scientific Reports, 14(1): 30895. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Spatiotemporal$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{diallo_spatiotemporal_2024,\n\ttitle = {Spatiotemporal dynamics of the oropharyngeal microbiome in a cohort of {Ivorian} school children},\n\tvolume = {14},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-024-81829-6},\n\tdoi = {10.1038/s41598-024-81829-6},\n\tabstract = {Abstract \n             \n              The respiratory tract harbours microorganisms of the normal host microbiota which are also capable of causing invasive disease. Among these, \n              Neisseria \n              meningitidis a commensal bacterium of the oropharynx can cause meningitis, a disease with epidemic potential. The oral microbiome plays a crucial role in maintaining respiratory health. An imbalance in its composition is associated with increased risk of invasive disease. The main objective of this study was to evaluate changes in the spatio-temporal dynamics of the oropharyngeal microbiota considering meningococcal carriage in a cohort of 8–12-year-old school children within (Korhogo) and outside (Abidjan) of the meningitis belt of Côte d’Ivoire. A significant geographic difference in the oropharyngeal microbiome was identified between the two study sites in terms of bacterial abundance and diversity ( \n              p \n               {\\textless} 0.001), with greater diversity in children in Abidjan than in Korhogo. Meningococcal carriage was low in the cohort with eight \n              Neisseria \n              carriers identified in Korhogo (3.64\\%) including one \n              Neisseria meningit \n              idis (0.45\\%). No \n              Neisseria \n              were detected in Abidjan indicating geographical differences in carriage ( \n              p \n               = 0.006). Negative correlations were also found between \n              Neisseria \n              abundance and humidity. Meningococcal carriage was very low during the study; however, \n              Neisseria \n              carriage differed between the two study areas, with a higher frequency in children in Korhogo. Analysis of the oropharyngeal microbiome showed significant differences between children followed in Abidjan and Korhogo with higher microbial diversity in Abidjan, which is generally associated with better health status. Significant correlations between \n              Neisseria \n              or other pathogens carriage and climatic variables (Temperature, Relative humidity, and Wind speed) were also demonstrated, indicating an important role of climate in the carriage of these bacteria; an important element to note in the current context of climate change.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Scientific Reports},\n\tauthor = {Diallo, K. and Missa, K. F. and Tuo, K. J. and Tiemele, L. S. and Ouattara, A. F. and Gboko, K. D. T. and Gragnon, B. G. and Bla, K. B. and Ngoi, J. M. and Wilkinson, R. J. and Awandare, G. A. and Bonfoh, B.},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {30895},\n}\n\n\n\n

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\n Abstract The respiratory tract harbours microorganisms of the normal host microbiota which are also capable of causing invasive disease. Among these, Neisseria meningitidis a commensal bacterium of the oropharynx can cause meningitis, a disease with epidemic potential. The oral microbiome plays a crucial role in maintaining respiratory health. An imbalance in its composition is associated with increased risk of invasive disease. The main objective of this study was to evaluate changes in the spatio-temporal dynamics of the oropharyngeal microbiota considering meningococcal carriage in a cohort of 8–12-year-old school children within (Korhogo) and outside (Abidjan) of the meningitis belt of Côte d’Ivoire. A significant geographic difference in the oropharyngeal microbiome was identified between the two study sites in terms of bacterial abundance and diversity ( p \\textless 0.001), with greater diversity in children in Abidjan than in Korhogo. Meningococcal carriage was low in the cohort with eight Neisseria carriers identified in Korhogo (3.64%) including one Neisseria meningit idis (0.45%). No Neisseria were detected in Abidjan indicating geographical differences in carriage ( p = 0.006). Negative correlations were also found between Neisseria abundance and humidity. Meningococcal carriage was very low during the study; however, Neisseria carriage differed between the two study areas, with a higher frequency in children in Korhogo. Analysis of the oropharyngeal microbiome showed significant differences between children followed in Abidjan and Korhogo with higher microbial diversity in Abidjan, which is generally associated with better health status. Significant correlations between Neisseria or other pathogens carriage and climatic variables (Temperature, Relative humidity, and Wind speed) were also demonstrated, indicating an important role of climate in the carriage of these bacteria; an important element to note in the current context of climate change.\n

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\n \n\n \n \n \n \n \n \n Pharmacokinetics of once-daily darunavir/ritonavir in second-line treatment in African children with HIV.\n \n \n \n \n\n\n \n Tsirizani, L.; Mohsenian Naghani, S.; Waalewijn, H.; Szubert, A.; Mulenga, V.; Chabala, C.; Bwakura-Dangarembizi, M.; Chitsamatanga, M.; Rutebarika, D. A; Musiime, V.; Kasozi, M.; Lugemwa, A.; Monkiewicz, L. N; McIlleron, H. M; Burger, D. M; Gibb, D. M; Denti, P.; Wasmann, R. E; and Colbers, A.\n\n\n \n\n\n\n Journal of Antimicrobial Chemotherapy, 79(11): 2990–2998. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Pharmacokinetics$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{tsirizani_pharmacokinetics_2024,\n\ttitle = {Pharmacokinetics of once-daily darunavir/ritonavir in second-line treatment in {African} children with {HIV}},\n\tvolume = {79},\n\tcopyright = {https://creativecommons.org/licenses/by-nc/4.0/},\n\tissn = {0305-7453, 1460-2091},\n\turl = {https://academic.oup.com/jac/article/79/11/2990/7762808},\n\tdoi = {10.1093/jac/dkae319},\n\tabstract = {Abstract \n             \n              Background \n              Darunavir is a potent HIV protease inhibitor with a high barrier to resistance. We conducted a nested pharmacokinetic sub-study within CHAPAS-4 to evaluate darunavir exposure in African children with HIV, taking once-daily darunavir/ritonavir for second-line treatment. \n             \n             \n              Methods \n              We used data from the CHAPAS-4 pharmacokinetic sub-study treating children with once-daily darunavir/ritonavir (600/100 mg if 14–24.9 kg and 800/100 mg if ≥25 kg) with either tenofovir alafenamide fumarate (TAF)/emtricitabine (FTC), abacavir/lamivudine or zidovudine/lamivudine. Steady-state pharmacokinetic sampling was done at 0, 1, 2, 4, 6, 8, 12 and 24 hours after observed darunavir/ritonavir intake. Non-compartmental and population pharmacokinetic analyses were used to describe the data and identify significant covariates. Reference adult pharmacokinetic data were used for comparison. We simulated the World Health Organization (WHO) recommended 600/100 mg darunavir/ritonavir dose for the 25–34.9 kg weight band. \n             \n             \n              Results \n              Data from 59 children with median age and weight 10.9 (range 3.8–14.7) years and 26.0 (14.5–47.0) kg, respectively, were available. A two-compartment disposition model with transit absorption compartments and weight-based allometric scaling of clearance and volume best described darunavir data. Our population achieved geometric mean (\\%CV) darunavir AUC0–24h, 94.3(50) mg·h/L and Cmax, 9.1(35) mg/L, above adult reference values and Ctrough, 1.5(111) mg/L, like adult values. The nucleoside reverse-transcriptase inhibitor backbone was not found to affect darunavir concentrations. Simulated WHO-recommended darunavir/ritonavir doses showed exposures equivalent to adults. Higher alpha-1-acid glycoprotein increased binding to darunavir and decreased apparent clearance of darunavir. \n             \n             \n              Conclusions \n              Darunavir exposures achieved in our trial are within safe range. Darunavir/ritonavir can safely be co-administered with TAF/FTC. Both WHO-recommended 600/100 mg and CHAPAS-4 800/100 mg darunavir/ritonavir doses for the 25–34.9 kg weight band offer favourable exposures. The choice between them can depend on tablet availability.},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Antimicrobial Chemotherapy},\n\tauthor = {Tsirizani, Lufina and Mohsenian Naghani, Shaghayegh and Waalewijn, Hylke and Szubert, Alexander and Mulenga, Veronica and Chabala, Chishala and Bwakura-Dangarembizi, Mutsa and Chitsamatanga, Moses and Rutebarika, Diana A and Musiime, Victor and Kasozi, Mariam and Lugemwa, Abbas and Monkiewicz, Lara N and McIlleron, Helen M and Burger, David M and Gibb, Diana M and Denti, Paolo and Wasmann, Roeland E and Colbers, Angela},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {2990--2998},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Background Darunavir is a potent HIV protease inhibitor with a high barrier to resistance. We conducted a nested pharmacokinetic sub-study within CHAPAS-4 to evaluate darunavir exposure in African children with HIV, taking once-daily darunavir/ritonavir for second-line treatment. Methods We used data from the CHAPAS-4 pharmacokinetic sub-study treating children with once-daily darunavir/ritonavir (600/100 mg if 14–24.9 kg and 800/100 mg if ≥25 kg) with either tenofovir alafenamide fumarate (TAF)/emtricitabine (FTC), abacavir/lamivudine or zidovudine/lamivudine. Steady-state pharmacokinetic sampling was done at 0, 1, 2, 4, 6, 8, 12 and 24 hours after observed darunavir/ritonavir intake. Non-compartmental and population pharmacokinetic analyses were used to describe the data and identify significant covariates. Reference adult pharmacokinetic data were used for comparison. We simulated the World Health Organization (WHO) recommended 600/100 mg darunavir/ritonavir dose for the 25–34.9 kg weight band. Results Data from 59 children with median age and weight 10.9 (range 3.8–14.7) years and 26.0 (14.5–47.0) kg, respectively, were available. A two-compartment disposition model with transit absorption compartments and weight-based allometric scaling of clearance and volume best described darunavir data. Our population achieved geometric mean (%CV) darunavir AUC0–24h, 94.3(50) mg·h/L and Cmax, 9.1(35) mg/L, above adult reference values and Ctrough, 1.5(111) mg/L, like adult values. The nucleoside reverse-transcriptase inhibitor backbone was not found to affect darunavir concentrations. Simulated WHO-recommended darunavir/ritonavir doses showed exposures equivalent to adults. Higher alpha-1-acid glycoprotein increased binding to darunavir and decreased apparent clearance of darunavir. Conclusions Darunavir exposures achieved in our trial are within safe range. Darunavir/ritonavir can safely be co-administered with TAF/FTC. Both WHO-recommended 600/100 mg and CHAPAS-4 800/100 mg darunavir/ritonavir doses for the 25–34.9 kg weight band offer favourable exposures. The choice between them can depend on tablet availability.\n

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\n \n\n \n \n \n \n \n \n Implications of subclinical tuberculosis for vaccine trial design and global effect.\n \n \n \n \n\n\n \n Churchyard, G. J; Houben, R. M G J; Fielding, K.; Fiore-Gartland, A. L; Esmail, H.; Grant, A. D; Rangaka, M. X; Behr, M.; Garcia-Basteiro, A. L; Wong, E. B; Hatherill, M.; Mave, V.; Dagnew, A. F; Schmidt, A. C; Hanekom, W. A; Cobelens, F.; and White, R. G\n\n\n \n\n\n\n The Lancet Microbe, 5(10): 100895. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Implications$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{churchyard_implications_2024,\n\ttitle = {Implications of subclinical tuberculosis for vaccine trial design and global effect},\n\tvolume = {5},\n\tissn = {26665247},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524724001277},\n\tdoi = {10.1016/S2666-5247(24)00127-7},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Churchyard, Gavin J and Houben, Rein M G J and Fielding, Katherine and Fiore-Gartland, Andrew L and Esmail, Hanif and Grant, Alison D and Rangaka, Molebogeng X and Behr, Marcel and Garcia-Basteiro, Alberto L and Wong, Emily B and Hatherill, Mark and Mave, Vidya and Dagnew, Alemnew F and Schmidt, Alexander C and Hanekom, Willem A and Cobelens, Frank and White, Richard G},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {100895},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Pathogenesis of Post-Tuberculosis Lung Disease: Defining Knowledge Gaps and Research Priorities at the Second International Post-Tuberculosis Symposium.\n \n \n \n \n\n\n \n Auld, S. C.; Barczak, A. K.; Bishai, W.; Coussens, A. K.; Dewi, I. M. W.; Mitini-Nkhoma, S. C.; Muefong, C.; Naidoo, T.; Pooran, A.; Stek, C.; Steyn, A. J. C.; Tezera, L.; and Walker, N. F.\n\n\n \n\n\n\n American Journal of Respiratory and Critical Care Medicine, 210(8): 979–993. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Pathogenesis$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{auld_pathogenesis_2024,\n\ttitle = {Pathogenesis of {Post}-{Tuberculosis} {Lung} {Disease}: {Defining} {Knowledge} {Gaps} and {Research} {Priorities} at the {Second} {International} {Post}-{Tuberculosis} {Symposium}},\n\tvolume = {210},\n\tissn = {1073-449X, 1535-4970},\n\tshorttitle = {Pathogenesis of {Post}-{Tuberculosis} {Lung} {Disease}},\n\turl = {https://www.atsjournals.org/doi/10.1164/rccm.202402-0374SO},\n\tdoi = {10.1164/rccm.202402-0374SO},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2025-06-24},\n\tjournal = {American Journal of Respiratory and Critical Care Medicine},\n\tauthor = {Auld, Sara C. and Barczak, Amy K. and Bishai, William and Coussens, Anna K. and Dewi, Intan M. W. and Mitini-Nkhoma, Steven C. and Muefong, Caleb and Naidoo, Threnesan and Pooran, Anil and Stek, Cari and Steyn, Adrie J. C. and Tezera, Liku and Walker, Naomi F.},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {979--993},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Frequency, kinetics and determinants of viable SARS-CoV-2 in bioaerosols from ambulatory COVID-19 patients infected with the Beta, Delta or Omicron variants.\n \n \n \n \n\n\n \n Jaumdally, S.; Tomasicchio, M.; Pooran, A.; Esmail, A.; Kotze, A.; Meier, S.; Wilson, L.; Oelofse, S.; Van Der Merwe, C.; Roomaney, A.; Davids, M.; Suliman, T.; Joseph, R.; Perumal, T.; Scott, A.; Shaw, M.; Preiser, W.; Williamson, C.; Goga, A.; Mayne, E.; Gray, G.; Moore, P.; Sigal, A.; Limberis, J.; Metcalfe, J.; and Dheda, K.\n\n\n \n\n\n\n Nature Communications, 15(1): 2003. March 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Frequency,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{jaumdally_frequency_2024,\n\ttitle = {Frequency, kinetics and determinants of viable {SARS}-{CoV}-2 in bioaerosols from ambulatory {COVID}-19 patients infected with the {Beta}, {Delta} or {Omicron} variants},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-45400-1},\n\tdoi = {10.1038/s41467-024-45400-1},\n\tabstract = {Abstract \n            Airborne transmission of SARS-CoV-2 aerosol remains contentious. Importantly, whether cough or breath-generated bioaerosols can harbor viable and replicating virus remains largely unclarified. We performed size-fractionated aerosol sampling (Andersen cascade impactor) and evaluated viral culturability in human cell lines (infectiousness), viral genetics, and host immunity in ambulatory participants with COVID-19. Sixty-one percent (27/44) and 50\\% (22/44) of participants emitted variant-specific culture-positive aerosols {\\textless}10μm and {\\textless}5μm, respectively, for up to 9 days after symptom onset. Aerosol culturability is significantly associated with lower neutralizing antibody titers, and suppression of transcriptomic pathways related to innate immunity and the humoral response. A nasopharyngeal Ct {\\textless}17 rules-in {\\textasciitilde}40\\% of aerosol culture-positives and identifies those who are probably highly infectious. A parsimonious three transcript blood-based biosignature is highly predictive of infectious aerosol generation (PPV {\\textgreater} 95\\%). There is considerable heterogeneity in potential infectiousness i.e., only 29\\% of participants were probably highly infectious (produced culture-positive aerosols {\\textless}5μm at {\\textasciitilde}6 days after symptom onset). These data, which comprehensively confirm variant-specific culturable SARS-CoV-2 in aerosol, inform the targeting of transmission-related interventions and public health containment strategies emphasizing improved ventilation.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Jaumdally, S. and Tomasicchio, M. and Pooran, A. and Esmail, A. and Kotze, A. and Meier, S. and Wilson, L. and Oelofse, S. and Van Der Merwe, C. and Roomaney, A. and Davids, M. and Suliman, T. and Joseph, R. and Perumal, T. and Scott, A. and Shaw, M. and Preiser, W. and Williamson, C. and Goga, A. and Mayne, E. and Gray, G. and Moore, P. and Sigal, A. and Limberis, J. and Metcalfe, J. and Dheda, K.},\n\tmonth = mar,\n\tyear = {2024},\n\tpages = {2003},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The influence of fixation and cryopreservation of cerebrospinal fluid on antigen expression and cell percentages by flow cytometric analysis.\n \n \n \n \n\n\n \n Singh, G.; Van Laarhoven, A.; Adams, R.; Reid, T. D.; Combrinck, J.; Van Dorp, S.; Riou, C.; Thango, N.; Enslin, J.; Kruger, S.; Figaji, A. A.; and Rohlwink, U. K.\n\n\n \n\n\n\n Scientific Reports, 14(1): 2463. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{singh_influence_2024,\n\ttitle = {The influence of fixation and cryopreservation of cerebrospinal fluid on antigen expression and cell percentages by flow cytometric analysis},\n\tvolume = {14},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-024-52669-1},\n\tdoi = {10.1038/s41598-024-52669-1},\n\tabstract = {Abstract \n             \n              The pauci-cellular nature of cerebrospinal (CSF), particularly ventricular CSF, and the rapid cell death following sampling, incumbers the use of flow cytometric analysis of these samples in the investigation of central nervous system (CNS) pathologies. Developing a method that allows long-term storage and batched analysis of CSF samples without compromising cell integrity is highly desirable in clinical research, given that CSF is often sampled after hours creating logistical difficulties for fresh processing. We examined percentages and relative proportion of peripheral and brain-derived immune cells in cryopreserved and transfix-treated CSF, compared to freshly processed CSF. Cell proportions were more comparable between Fresh and Cryopreserved CSF (mean of differences = 3.19), than between fresh and transfix-treated CSF (mean of differences = 14.82). No significant differences in cell percentages were observed in fresh versus cryopreserved CSF; however significantly lower cell percentages were observed in transfix-treated CSF compared to Fresh CSF [(CD11b \n              ++ \n              ( \n              p \n               = 0.01), CD4 \n              + \n              ( \n              p \n               = 0.001), CD8 \n              + \n              ( \n              p \n               = 0.007), NK cells ( \n              p \n               = 0.04), as well as CD69 \n              + \n              activation marker ( \n              p \n               = 0.001)]. Furthermore, loss of marker expression of various lymphocyte sub-populations were observed in transfix-treated CSF. Cryopreservation is a feasible option for long-term storage of ventricular CSF and allows accurate immunophenotyping of peripheral and brain-derived cell populations by flow cytometry.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Scientific Reports},\n\tauthor = {Singh, Gabriela and Van Laarhoven, Arjan and Adams, Rozanne and Reid, Timothy Dawson and Combrinck, Jill and Van Dorp, Suzanne and Riou, Catherine and Thango, Nqobile and Enslin, Johannes and Kruger, Stefan and Figaji, Anthony Aaron and Rohlwink, Ursula Karin},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {2463},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Genomic Medicine in the Developing World: Cancer Spectrum, Cumulative Risk and Survival Outcomes for Lynch Syndrome Variant Heterozygotes with Germline Pathogenic Variants in the MLH1 and MSH2 Genes.\n \n \n \n \n\n\n \n Ndou, L.; Chambuso, R.; Algar, U.; Boutall, A.; Goldberg, P.; and Ramesar, R.\n\n\n \n\n\n\n Biomedicines, 12(12): 2906. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Genomic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{ndou_genomic_2024,\n\ttitle = {Genomic {Medicine} in the {Developing} {World}: {Cancer} {Spectrum}, {Cumulative} {Risk} and {Survival} {Outcomes} for {Lynch} {Syndrome} {Variant} {Heterozygotes} with {Germline} {Pathogenic} {Variants} in the {MLH1} and {MSH2} {Genes}},\n\tvolume = {12},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2227-9059},\n\tshorttitle = {Genomic {Medicine} in the {Developing} {World}},\n\turl = {https://www.mdpi.com/2227-9059/12/12/2906},\n\tdoi = {10.3390/biomedicines12122906},\n\tabstract = {Background: Although genetic testing has improved our ability to diagnose Lynch syndrome (LS), there is still limited information on the extent of variations in the clinical and genetic landscape among LS variant heterozygotes (LSVH) in Africa. We sought to investigate the cancer spectrum, cumulative risk, and survival outcomes of LSVH with pathogenic/likely pathogenic variants (P/LPVs) in the MLH1 and MSH2 genes using a LS registry in South Africa over the last 30 years. Methods: A retrospective study was conducted to retrieve demographic, clinical, and genetic data of all LSVH with P/LPVs in the MLH1 and MSH2 genes from our LS registry. Genetic data were analyzed according to cancer spectrum, cumulative risk, and crude survival. We used the Chi-squared and t-test to assess differences between groups, and Kaplan–Meier survival analyses were used to analyze the cumulative risk and crude survival outcomes. A p-value {\\textless} 0.05 at a 95\\% confidence interval was considered statistically significant. Results: We analyzed a total of 577 LSVH from 109 families. About 450 (78\\%) and 127 (22\\%) LSVH harbored a disease-causing mutation in MLH1 and MSH2, respectively. A South African founder PV (MLH1:c.1528C{\\textgreater}T) accounted for 74\\% (n = 426) of all LSVH. CRC was the most common diagnosed cancer in both MLH1 and MSH2 LSVH. MLH1 LSVH had a younger age at cancer diagnosis than MSH2 LSVH (43 vs. 47 years, respectively, p = 0.015). Extracolonic cancers were predominantly higher in female LSVH (n = 33, 35\\%) than in male LSVH (n = 8, 7\\%) with the MLH1:c.1528C{\\textgreater}T founder PV. The cumulative risk of any cancer and CRC at any age was higher in MLH1 LSVH than in MSH2 LSVH (p = 0.020 and p = 0.036, respectively). LSVH with the MLH1:c.1528C{\\textgreater}T PV had a better 10-year overall survival after the first cancer diagnosis, particularly for CRC. Conclusions: LSVH with P/LPVs in the MLH1 and MSH2 genes exhibited significant gene- and sex-specific differences in cancer spectrum, cumulative risk and survival outcomes. Cancer risk and survival estimates described in this study can be used to guide surveillance and genetic counselling for LSVH in our population.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {Biomedicines},\n\tauthor = {Ndou, Lutricia and Chambuso, Ramadhani and Algar, Ursula and Boutall, Adam and Goldberg, Paul and Ramesar, Raj},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {2906},\n}\n\n\n\n

\n

\n\n\n

\n Background: Although genetic testing has improved our ability to diagnose Lynch syndrome (LS), there is still limited information on the extent of variations in the clinical and genetic landscape among LS variant heterozygotes (LSVH) in Africa. We sought to investigate the cancer spectrum, cumulative risk, and survival outcomes of LSVH with pathogenic/likely pathogenic variants (P/LPVs) in the MLH1 and MSH2 genes using a LS registry in South Africa over the last 30 years. Methods: A retrospective study was conducted to retrieve demographic, clinical, and genetic data of all LSVH with P/LPVs in the MLH1 and MSH2 genes from our LS registry. Genetic data were analyzed according to cancer spectrum, cumulative risk, and crude survival. We used the Chi-squared and t-test to assess differences between groups, and Kaplan–Meier survival analyses were used to analyze the cumulative risk and crude survival outcomes. A p-value \\textless 0.05 at a 95% confidence interval was considered statistically significant. Results: We analyzed a total of 577 LSVH from 109 families. About 450 (78%) and 127 (22%) LSVH harbored a disease-causing mutation in MLH1 and MSH2, respectively. A South African founder PV (MLH1:c.1528C\\textgreaterT) accounted for 74% (n = 426) of all LSVH. CRC was the most common diagnosed cancer in both MLH1 and MSH2 LSVH. MLH1 LSVH had a younger age at cancer diagnosis than MSH2 LSVH (43 vs. 47 years, respectively, p = 0.015). Extracolonic cancers were predominantly higher in female LSVH (n = 33, 35%) than in male LSVH (n = 8, 7%) with the MLH1:c.1528C\\textgreaterT founder PV. The cumulative risk of any cancer and CRC at any age was higher in MLH1 LSVH than in MSH2 LSVH (p = 0.020 and p = 0.036, respectively). LSVH with the MLH1:c.1528C\\textgreaterT PV had a better 10-year overall survival after the first cancer diagnosis, particularly for CRC. Conclusions: LSVH with P/LPVs in the MLH1 and MSH2 genes exhibited significant gene- and sex-specific differences in cancer spectrum, cumulative risk and survival outcomes. Cancer risk and survival estimates described in this study can be used to guide surveillance and genetic counselling for LSVH in our population.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Identification of Small-Molecule Antagonists Targeting the Growth Hormone Releasing Hormone Receptor (GHRHR).\n \n \n \n \n\n\n \n Matsoukas, M.; Radomsky, T.; Panagiotopoulos, V.; Preez, R. D.; Papadourakis, M.; Tsianakas, K.; Millar, R. P; Anderson, R. C; Spyroulias, G. A; and Newton, C. L\n\n\n \n\n\n\n Journal of Chemical Information and Modeling, 64(18): 7056–7067. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Identification$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{matsoukas_identification_2024,\n\ttitle = {Identification of {Small}-{Molecule} {Antagonists} {Targeting} the {Growth} {Hormone} {Releasing} {Hormone} {Receptor} ({GHRHR})},\n\tvolume = {64},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1549-9596, 1549-960X},\n\turl = {https://pubs.acs.org/doi/10.1021/acs.jcim.4c00577},\n\tdoi = {10.1021/acs.jcim.4c00577},\n\tlanguage = {en},\n\tnumber = {18},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Chemical Information and Modeling},\n\tauthor = {Matsoukas, Minos-Timotheos and Radomsky, Tarryn and Panagiotopoulos, Vasilis and Preez, Robin Du and Papadourakis, Michail and Tsianakas, Konstantinos and Millar, Robert P and Anderson, Ross C and Spyroulias, Georgios A and Newton, Claire L},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {7056--7067},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Natural History of High-Risk Human Papillomavirus in Kenyan and South African Women: Implications for Vaccination Campaigns and Cervical Cancer Screening Programs.\n \n \n \n \n\n\n \n Happel, A.; Budiawan, E.; Onono, M.; Innes, S.; Palanee-Phillips, T.; Heuvel, J.; Rakiep, A.; Kellow-Webb, S.; Ongere, J.; Wakhungu, I.; Mkhize, Z.; Kapa, L.; Sigcu, N.; Dabee, S.; Nair, G.; Scoville, C.; Mugo, N. R; Williamson, A.; Passmore, J. S; Jaspan, H. B; and Heffron, R.\n\n\n \n\n\n\n Open Forum Infectious Diseases, 11(12): ofae690. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Natural$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{happel_natural_2024,\n\ttitle = {Natural {History} of {High}-{Risk} {Human} {Papillomavirus} in {Kenyan} and {South} {African} {Women}: {Implications} for {Vaccination} {Campaigns} and {Cervical} {Cancer} {Screening} {Programs}},\n\tvolume = {11},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2328-8957},\n\tshorttitle = {Natural {History} of {High}-{Risk} {Human} {Papillomavirus} in {Kenyan} and {South} {African} {Women}},\n\turl = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofae690/7907207},\n\tdoi = {10.1093/ofid/ofae690},\n\tabstract = {Abstract \n             \n              Objective \n              Human papillomavirus (HPV) vaccines and DNA testing roll out in resource-constrained settings. We evaluated the natural history of HPV infections in African women to contribute to normative guidance. \n             \n             \n              Methods \n              Women aged 16 to 35 years were enrolled from 3 sites in South Africa and Kenya and followed quarterly for 18 months. A subset was recalled 5 years postenrollment, when Papanicolaou smears were conducted. Endocervical swabs were tested for 36 HPV genotypes by HPV Direct Flow. Logistic regression models identified correlations between demographic, biological, or behavioral factors and baseline high-risk HPV (HR-HPV). \n             \n             \n              Results \n              At enrollment, 158 of 311 women (median age, 23 years; IQR, 20–27) had at least 1 HR-HPV genotype. HPV-52 (13.5\\%), HPV-16 (9.5\\%), HPV-58 (9.0\\%), HPV-18 (8.4\\%), and HPV-35 (8.4\\%) were most common. Coinfection with low-risk HPVs (odds ratio, 2.65; 95\\% CI, 1.59–4.45) were associated with HR-HPV positivity, while reported condom use (odds ratio, 0.57; 95\\% CI, .34–.98) and older age were protective. Of women with HR-HPV at enrollment, 87.3\\% cleared at least 1 HR-HPV infection over 18 months and 64.6\\% cleared all such infections. Few (1.9\\%) had evidence of high-grade cervical abnormalities, among which HPV-35 was the most prevalent during the study. \n             \n             \n              Conclusions \n              The high prevalence of HR-HPV emphasizes that HPV vaccination, screening, and testing campaigns in Africa are important. Nonvaccine HPV-35 was as common as HPV-18, suggesting the need to supplement current vaccines with this genotype. HR-HPV clearance was also common, highlighting that clear messaging is needed from health care providers to patients while discussing HPV DNA testing results.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {Open Forum Infectious Diseases},\n\tauthor = {Happel, Anna-Ursula and Budiawan, Elvira and Onono, Maricianah and Innes, Steve and Palanee-Phillips, Thesla and Heuvel, Janine and Rakiep, Adeebah and Kellow-Webb, Sarah and Ongere, Joan and Wakhungu, Imeldah and Mkhize, Zandile and Kapa, La-Donna and Sigcu, Nompumelelo and Dabee, Smritee and Nair, Gonasagrie and Scoville, Caitlin and Mugo, Nelly R and Williamson, Anna-Lise and Passmore, Jo-Ann S and Jaspan, Heather B and Heffron, Renee},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {ofae690},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Imaging in early tuberculosis.\n \n \n \n \n\n\n \n Wilkinson, R.\n\n\n \n\n\n\n Thorax, 79(12): 1114–1115. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Imaging$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{wilkinson_imaging_2024,\n\ttitle = {Imaging in early tuberculosis},\n\tvolume = {79},\n\tissn = {0040-6376, 1468-3296},\n\turl = {https://thorax.bmj.com/lookup/doi/10.1136/thorax-2024-221993},\n\tdoi = {10.1136/thorax-2024-221993},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {Thorax},\n\tauthor = {Wilkinson, Robert},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {1114--1115},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Cell-Specific Contribution of IL-4 Receptor α Signaling Shapes the Overall Manifestation of Allergic Airway Disease.\n \n \n \n \n\n\n \n Choudhary, I.; Lamichhane, R.; Singamsetty, D.; Vo, T.; Brombacher, F.; Patial, S.; and Saini, Y.\n\n\n \n\n\n\n American Journal of Respiratory Cell and Molecular Biology, 71(6): 702–717. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Cell-Specific$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{choudhary_cell-specific_2024,\n\ttitle = {Cell-{Specific} {Contribution} of {IL}-4 {Receptor} α {Signaling} {Shapes} the {Overall} {Manifestation} of {Allergic} {Airway} {Disease}},\n\tvolume = {71},\n\tissn = {1044-1549, 1535-4989},\n\turl = {https://www.atsjournals.org/doi/10.1165/rcmb.2024-0208OC},\n\tdoi = {10.1165/rcmb.2024-0208OC},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {American Journal of Respiratory Cell and Molecular Biology},\n\tauthor = {Choudhary, Ishita and Lamichhane, Richa and Singamsetty, Dhruthi and Vo, Thao and Brombacher, Frank and Patial, Sonika and Saini, Yogesh},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {702--717},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Movement of the A-strain maize streak virus in and out of Madagascar.\n \n \n \n \n\n\n \n Oyeniran, K. A.; Martin, D. P.; Lett, J.; Rakotomalala, M. R.; Azali, H. A.; and Varsani, A.\n\n\n \n\n\n\n Virology, 600: 110222. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Movement$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{oyeniran_movement_2024,\n\ttitle = {Movement of the {A}-strain maize streak virus in and out of {Madagascar}},\n\tvolume = {600},\n\tissn = {00426822},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0042682224002435},\n\tdoi = {10.1016/j.virol.2024.110222},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {Virology},\n\tauthor = {Oyeniran, Kehinde A. and Martin, Darren P. and Lett, Jean-Michel and Rakotomalala, Mbolarinosy Rasoafalimanana and Azali, Hamza A. and Varsani, Arvind},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {110222},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Neutralizing antibody correlate of protection against severe-critical COVID-19 in the ENSEMBLE single-dose Ad26.COV2.S vaccine efficacy trial.\n \n \n \n \n\n\n \n Carpp, L. N.; Hyrien, O.; Fong, Y.; Benkeser, D.; Roels, S.; Stieh, D. J.; Van Dromme, I.; Van Roey, G. A.; Kenny, A.; Huang, Y.; Carone, M.; McDermott, A. B.; Houchens, C. R.; Martins, K.; Jayashankar, L.; Castellino, F.; Amoa-Awua, O.; Basappa, M.; Flach, B.; Lin, B. C.; Moore, C.; Naisan, M.; Naqvi, M.; Narpala, S.; O’Connell, S.; Mueller, A.; Serebryannyy, L.; Castro, M.; Wang, J.; Petropoulos, C. J.; Luedtke, A.; Lu, Y.; Yu, C.; Juraska, M.; Hejazi, N. S.; Wolfe, D. N.; Sadoff, J.; Gray, G. E.; Grinsztejn, B.; Goepfert, P. A.; Bekker, L.; Gaur, A. H.; Veloso, V. G.; Randhawa, A. K.; Andrasik, M. P.; Hendriks, J.; Truyers, C.; Vandebosch, A.; Struyf, F.; Schuitemaker, H.; Douoguih, M.; Kublin, J. G.; Corey, L.; Neuzil, K. M.; Follmann, D.; Koup, R. A.; Donis, R. O.; Gilbert, P. B.; On behalf of the Immune Assays Team; the Coronavirus Vaccine Prevention Network (CoVPN)/ENSEMBLE Team; Van Dromme, I.; Van Roey, G. A.; and the United States Government (USG)/CoVPN Biostatistics Team\n\n\n \n\n\n\n Nature Communications, 15(1): 9785. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Neutralizing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{carpp_neutralizing_2024,\n\ttitle = {Neutralizing antibody correlate of protection against severe-critical {COVID}-19 in the {ENSEMBLE} single-dose {Ad26}.{COV2}.{S} vaccine efficacy trial},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-53727-y},\n\tdoi = {10.1038/s41467-024-53727-y},\n\tabstract = {Abstract \n             \n              Assessment of immune correlates of severe COVID-19 has been hampered by the low numbers of severe cases in COVID-19 vaccine efficacy (VE) trials. We assess neutralizing and binding antibody levels at 4 weeks post-Ad26.COV2.S vaccination as correlates of risk and of protection against severe-critical COVID-19 through 220 days post-vaccination in the ENSEMBLE trial (NCT04505722), constituting {\\textasciitilde}4.5 months longer follow-up than our previous correlates analysis and enabling inclusion of 42 severe-critical vaccine-breakthrough cases. Neutralizing antibody titer is a strong inverse correlate of severe-critical COVID-19, with estimated hazard ratio (HR) per 10-fold increase 0.35 (95\\% CI: 0.13, 0.90). In a multivariable model, HRs are 0.31 (0.11, 0.89) for neutralizing antibody titer and 1.22 (0.49, 3.02) for anti-Spike binding antibody concentration. VE against severe-critical COVID-19 rises with neutralizing antibody titer: 63.1\\% (95\\% CI: 40.0\\%, 77.3\\%) at unquantifiable [{\\textless}4.8975 International Units (IU)50/ml], 85.2\\% (47.2\\%, 95.3\\%) at just-quantifiable (5.2 IU50/ml), and 95.1\\% (81.1\\%, 96.9\\%) at 90 \n              th \n              percentile (30.2 IU50/ml). At the same titers, VE against moderate COVID-19 is 32.5\\% (11.8\\%, 48.4\\%), 33.9\\% (19.1\\%, 59.3\\%), and 60.7\\% (40.4\\%, 76.4\\%). Protection against moderate vs. severe disease may require higher antibody levels, and very low antibody levels and/or other immune responses may associate with protection against severe disease.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Carpp, Lindsay N. and Hyrien, Ollivier and Fong, Youyi and Benkeser, David and Roels, Sanne and Stieh, Daniel J. and Van Dromme, Ilse and Van Roey, Griet A. and Kenny, Avi and Huang, Ying and Carone, Marco and McDermott, Adrian B. and Houchens, Christopher R. and Martins, Karen and Jayashankar, Lakshmi and Castellino, Flora and Amoa-Awua, Obrimpong and Basappa, Manjula and Flach, Britta and Lin, Bob C. and Moore, Christopher and Naisan, Mursal and Naqvi, Muhammed and Narpala, Sandeep and O’Connell, Sarah and Mueller, Allen and Serebryannyy, Leo and Castro, Mike and Wang, Jennifer and Petropoulos, Christos J. and Luedtke, Alex and Lu, Yiwen and Yu, Chenchen and Juraska, Michal and Hejazi, Nima S. and Wolfe, Daniel N. and Sadoff, Jerald and Gray, Glenda E. and Grinsztejn, Beatriz and Goepfert, Paul A. and Bekker, Linda-Gail and Gaur, Aditya H. and Veloso, Valdilea G. and Randhawa, April K. and Andrasik, Michele P. and Hendriks, Jenny and Truyers, Carla and Vandebosch, An and Struyf, Frank and Schuitemaker, Hanneke and Douoguih, Macaya and Kublin, James G. and Corey, Lawrence and Neuzil, Kathleen M. and Follmann, Dean and Koup, Richard A. and Donis, Ruben O. and Gilbert, Peter B. and {On behalf of the Immune Assays Team} and {the Coronavirus Vaccine Prevention Network (CoVPN)/ENSEMBLE Team} and Van Dromme, Ilse and Van Roey, Griet A. and {the United States Government (USG)/CoVPN Biostatistics Team}},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {9785},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Determining Targets for Antiretroviral Drug Concentrations: A Causal Framework Illustrated With Pediatric Efavirenz Data From the \\textlessspan style=\"font-variant:small-caps;\"\\textgreaterCHAPAS\\textless/span\\textgreater ‐3 Trial.\n \n \n \n \n\n\n \n Schomaker, M.; Denti, P.; Bienczak, A.; Burger, D.; Díaz, I.; Gibb, D. M.; Walker, A. S.; and McIlleron, H.\n\n\n \n\n\n\n Pharmacoepidemiology and Drug Safety, 33(12): e70051. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Determining$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{schomaker_determining_2024,\n\ttitle = {Determining {Targets} for {Antiretroviral} {Drug} {Concentrations}: {A} {Causal} {Framework} {Illustrated} {With} {Pediatric} {Efavirenz} {Data} {From} the {\\textless}span style="font-variant:small-caps;"{\\textgreater}{CHAPAS}{\\textless}/span{\\textgreater} ‐3 {Trial}},\n\tvolume = {33},\n\tissn = {1053-8569, 1099-1557},\n\tshorttitle = {Determining {Targets} for {Antiretroviral} {Drug} {Concentrations}},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/pds.70051},\n\tdoi = {10.1002/pds.70051},\n\tabstract = {ABSTRACT \n             \n              Background \n              Determining a therapeutic window for maintaining antiretroviral drug concentrations within an appropriate range is required for identifying effective dosing regimens. The limits of this window are typically calculated using predictive models. We propose that target concentrations should instead be calculated based on counterfactual probabilities of relevant outcomes and describe a counterfactual framework for this. \n             \n             \n              Methods \n              The proposed framework is applied in an analysis including longitudinal observational data from 125 HIV‐positive children treated with efavirenz‐based regimens within the CHAPAS‐3 trial, which enrolled children {\\textless} 13 years in Zambia/Uganda. A directed acyclic graph was developed to visualize the mechanisms affecting antiretroviral concentrations. Causal concentration‐response curves, adjusted for measured time‐varying confounding of weight and adherence, are calculated using g‐computation. \n             \n             \n              Results \n              The estimated curves show that higher concentrations during follow‐up, 12/24 h after dose, lead to lower probabilities of viral failure ({\\textgreater} 100 c/mL) at 96 weeks of follow‐up. Estimated counterfactual failure probabilities under the current target range of 1–4 mg/L range from 24\\% to about 2\\%. The curves are almost identical for slow, intermediate and extensive metabolizers and show that a mid‐dose concentration level of ≥ 3.5 mg/L would be required to achieve a failure probability of {\\textless} 5\\%. \n             \n             \n              Conclusions \n              Our analyses demonstrate that a causal approach may lead to different minimum concentration limits than analyses that are based on purely predictive models. Moreover, the approach highlights that indirect causes of failure, such as patients' metabolizing status, may predict patients' failure risk, but do not alter the threshold at which antiviral activity of efavirenz is severely reduced.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2025-06-24},\n\tjournal = {Pharmacoepidemiology and Drug Safety},\n\tauthor = {Schomaker, Michael and Denti, Paolo and Bienczak, Andrzej and Burger, David and Díaz, Iván and Gibb, Diana M. and Walker, Ann Sarah and McIlleron, Helen},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {e70051},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Model‐Informed Approaches to Optimizing Therapeutics in the African Patient Populations.\n \n \n \n \n\n\n \n Mulubwa, M.; and Chibale, K.\n\n\n \n\n\n\n Clinical Pharmacology & Therapeutics, 116(6): 1391–1394. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Model‐Informed$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{mulubwa_modelinformed_2024,\n\ttitle = {Model‐{Informed} {Approaches} to {Optimizing} {Therapeutics} in the {African} {Patient} {Populations}},\n\tvolume = {116},\n\tissn = {0009-9236, 1532-6535},\n\turl = {https://ascpt.onlinelibrary.wiley.com/doi/10.1002/cpt.3425},\n\tdoi = {10.1002/cpt.3425},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2025-06-24},\n\tjournal = {Clinical Pharmacology \\& Therapeutics},\n\tauthor = {Mulubwa, Mwila and Chibale, Kelly},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {1391--1394},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Adolescent BCG revaccination induces a phenotypic shift in CD4+ T cell responses to Mycobacterium tuberculosis.\n \n \n \n \n\n\n \n Dintwe, O. B.; Ballweber Fleming, L.; Voillet, V.; McNevin, J.; Seese, A.; Naidoo, A.; Omarjee, S.; Bekker, L.; Kublin, J. G.; De Rosa, S. C.; Newell, E. W.; Fiore-Gartland, A.; Andersen-Nissen, E.; and McElrath, M. J.\n\n\n \n\n\n\n Nature Communications, 15(1): 5191. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Adolescent$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{dintwe_adolescent_2024,\n\ttitle = {Adolescent {BCG} revaccination induces a phenotypic shift in {CD4}+ {T} cell responses to {Mycobacterium} tuberculosis},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-49050-1},\n\tdoi = {10.1038/s41467-024-49050-1},\n\tabstract = {Abstract \n             \n              A recent clinical trial demonstrated that Bacille Calmette-Guérin (BCG) revaccination of adolescents reduced the risk of sustained infection with \n              Mycobacterium tuberculosis \n              ( \n              M.tb \n              ). In a companion phase 1b trial, HVTN 602/Aeras A-042, we characterize in-depth the cellular responses to BCG revaccination or to a H4:IC31 vaccine boost to identify T cell subsets that could be responsible for the protection observed. High-dimensional clustering analysis of cells profiled using a 26-color flow cytometric panel show marked increases in five effector memory CD4 \n              + \n              T cell subpopulations (T \n              EM \n              ) after BCG revaccination, two of which are highly polyfunctional. CITE-Seq single-cell analysis shows that the activated subsets include an abundant cluster of Th1 cells with migratory potential. Additionally, a small cluster of Th17 T \n              EM \n              cells induced by BCG revaccination expresses high levels of CD103; these may represent recirculating tissue-resident memory cells that could provide pulmonary immune protection. Together, these results identify unique populations of CD4 \n              + \n              T cells with potential to be immune correlates of protection conferred by BCG revaccination.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Dintwe, One B. and Ballweber Fleming, Lamar and Voillet, Valentin and McNevin, John and Seese, Aaron and Naidoo, Anneta and Omarjee, Saleha and Bekker, Linda-Gail and Kublin, James G. and De Rosa, Stephen C. and Newell, Evan W. and Fiore-Gartland, Andrew and Andersen-Nissen, Erica and McElrath, M. Juliana},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {5191},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Correction: Dihydroartemisinin inhibits prostate cancer via JARID2/miR-7/miR-34a-dependent downregulation of Axl.\n \n \n \n \n\n\n \n Paccez, J. D.; Duncan, K.; Sekar, D.; Correa, R. G.; Wang, Y.; Gu, X.; Bashin, M.; Chibale, K.; Libermann, T. A.; and Zerbini, L. F.\n\n\n \n\n\n\n Oncogenesis, 13(1): 32. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Correction:$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{paccez_correction_2024,\n\ttitle = {Correction: {Dihydroartemisinin} inhibits prostate cancer via {JARID2}/{miR}-7/{miR}-34a-dependent downregulation of {Axl}},\n\tvolume = {13},\n\tissn = {2157-9024},\n\tshorttitle = {Correction},\n\turl = {https://www.nature.com/articles/s41389-024-00533-2},\n\tdoi = {10.1038/s41389-024-00533-2},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Oncogenesis},\n\tauthor = {Paccez, Juliano D. and Duncan, Kristal and Sekar, Durairaj and Correa, Ricardo G. and Wang, Yihong and Gu, Xuesong and Bashin, Manoj and Chibale, Kelly and Libermann, Towia A. and Zerbini, Luiz F.},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {32},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n First-Line Antituberculosis Drug Challenge Reactions in Drug Reaction With Eosinophilia and Systemic Symptoms Syndrome in an HIV Endemic Setting.\n \n \n \n \n\n\n \n Porter, M.; Smith, R.; Teixeira, N.; Thwala, B.; Choshi, P.; Phillips, E. J.; Meintjes, G.; Dlamini, S.; Peter, J. G.; and Lehloenya, R. J.\n\n\n \n\n\n\n The Journal of Allergy and Clinical Immunology: In Practice, 12(10): 2798–2808.e12. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"First-Line$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{porter_first-line_2024,\n\ttitle = {First-{Line} {Antituberculosis} {Drug} {Challenge} {Reactions} in {Drug} {Reaction} {With} {Eosinophilia} and {Systemic} {Symptoms} {Syndrome} in an {HIV} {Endemic} {Setting}},\n\tvolume = {12},\n\tissn = {22132198},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2213219824005762},\n\tdoi = {10.1016/j.jaip.2024.05.045},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {The Journal of Allergy and Clinical Immunology: In Practice},\n\tauthor = {Porter, Mireille and Smith, Rhodine and Teixeira, Nadine and Thwala, Bukiwe and Choshi, Phuti and Phillips, Elizabeth J. and Meintjes, Graeme and Dlamini, Sipho and Peter, Jonathan Grant and Lehloenya, Rannakoe J.},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {2798--2808.e12},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Subtracting the background by reducing cell-free DNA’s confounding effects on Mycobacterium tuberculosis quantitation and the sputum microbiome.\n \n \n \n \n\n\n \n Naidoo, C. C.; Venter, R.; Codony, F.; Agustí, G.; Kitchin, N.; Naidoo, S.; Monaco, H.; Mishra, H.; Li, Y.; Clemente, J. C.; Warren, R. M.; Segal, L. N.; and Theron, G.\n\n\n \n\n\n\n Scientific Reports, 14(1): 22350. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Subtracting$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{naidoo_subtracting_2024,\n\ttitle = {Subtracting the background by reducing cell-free {DNA}’s confounding effects on {Mycobacterium} tuberculosis quantitation and the sputum microbiome},\n\tvolume = {14},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-024-73497-3},\n\tdoi = {10.1038/s41598-024-73497-3},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Scientific Reports},\n\tauthor = {Naidoo, Charissa C. and Venter, Rouxjeane and Codony, Francesc and Agustí, Gemma and Kitchin, Natasha and Naidoo, Selisha and Monaco, Hilary and Mishra, Hridesh and Li, Yonghua and Clemente, Jose C. and Warren, Robin M. and Segal, Leopoldo N. and Theron, Grant},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {22350},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n HOPE springs eternal: lack of HIV superinfection in HIV Organ Policy Equity Act kidney transplants.\n \n \n \n \n\n\n \n Durand, C. M.; and Redd, A. D.\n\n\n \n\n\n\n Journal of Clinical Investigation, 134(20): e184326. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"HOPE$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{durand_hope_2024,\n\ttitle = {{HOPE} springs eternal: lack of {HIV} superinfection in {HIV} {Organ} {Policy} {Equity} {Act} kidney transplants},\n\tvolume = {134},\n\tcopyright = {http://creativecommons.org/licenses/by/4.0/},\n\tissn = {1558-8238},\n\tshorttitle = {{HOPE} springs eternal},\n\turl = {https://www.jci.org/articles/view/184326},\n\tdoi = {10.1172/JCI184326},\n\tlanguage = {en},\n\tnumber = {20},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Clinical Investigation},\n\tauthor = {Durand, Christine M. and Redd, Andrew D.},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {e184326},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Monoclonal antibody applications in travel medicine.\n \n \n \n \n\n\n \n De Jong, H. K.; and Grobusch, M. P.\n\n\n \n\n\n\n Tropical Diseases, Travel Medicine and Vaccines, 10(1): 2. January 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Monoclonal$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{de_jong_monoclonal_2024,\n\ttitle = {Monoclonal antibody applications in travel medicine},\n\tvolume = {10},\n\tissn = {2055-0936},\n\turl = {https://tdtmvjournal.biomedcentral.com/articles/10.1186/s40794-023-00212-x},\n\tdoi = {10.1186/s40794-023-00212-x},\n\tabstract = {Abstract \n            For decades, immunoglobulin preparations have been used to prevent or treat infectious diseases. Since only a few years, monoclonal antibody applications (mAbs) are taking flight and are increasingly dominating this field. In 2014, only two mAbs were registered; end of October 2023, more than ten mAbs are registered or have been granted emergency use authorization, and many more are in (pre)clinical phases. Especially the COVID-19 pandemic has generated this surge in licensed monoclonal antibodies, although multiple phase 1 studies were already underway in 2019 for other infectious diseases such as malaria and yellow fever. Monoclonal antibodies could function as prophylaxis (i.e., for the prevention of malaria), or could be used to treat (tropical) infections (i.e., rabies, dengue fever, yellow fever). This review focuses on the discussion of the prospects of, and obstacles for, using mAbs in the prevention and treatment of (tropical) infectious diseases seen in the returning traveler; and provides an update on the mAbs currently being developed for infectious diseases, which could potentially be of interest for travelers.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Tropical Diseases, Travel Medicine and Vaccines},\n\tauthor = {De Jong, Hanna K. and Grobusch, Martin P.},\n\tmonth = jan,\n\tyear = {2024},\n\tpages = {2},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Comparing gene expression profiles of adults with isolated spinal tuberculosis to disseminated spinal tuberculosis identified by 18FDG-PET/CT at time of diagnosis, 6- and 12-months follow-up: classifying clinical stages of spinal tuberculosis and monitoring treatment response (Spinal TB X cohort study).\n \n \n \n \n\n\n \n Scherer, J.; Mukasa, S. L.; Wolmarans, K.; Guler, R.; Kotze, T.; Song, T.; Dunn, R.; Laubscher, M.; Pape, H.; Held, M.; and Thienemann, F.\n\n\n \n\n\n\n Journal of Orthopaedic Surgery and Research, 19(1): 376. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Comparing$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{scherer_comparing_2024,\n\ttitle = {Comparing gene expression profiles of adults with isolated spinal tuberculosis to disseminated spinal tuberculosis identified by {18FDG}-{PET}/{CT} at time of diagnosis, 6- and 12-months follow-up: classifying clinical stages of spinal tuberculosis and monitoring treatment response ({Spinal} {TB} {X} cohort study)},\n\tvolume = {19},\n\tissn = {1749-799X},\n\tshorttitle = {Comparing gene expression profiles of adults with isolated spinal tuberculosis to disseminated spinal tuberculosis identified by {18FDG}-{PET}/{CT} at time of diagnosis, 6- and 12-months follow-up},\n\turl = {https://josr-online.biomedcentral.com/articles/10.1186/s13018-024-04840-7},\n\tdoi = {10.1186/s13018-024-04840-7},\n\tabstract = {Abstract \n             \n              Background \n               \n                Tuberculosis (TB) is one of the top ten causes of death worldwide, with approximately 10 million cases annually. Focus has been on pulmonary TB, while extrapulmonary TB (EPTB) has received little attention. Diagnosis of EPTB remains challenging due to the invasive procedures required for sample collection. Spinal TB (STB) accounts for 10\\% of EPTB and often leads to lifelong debilitating disease due to devastating spinal deformation and compression of neural structures. Little is known about the extent of disease, although both isolated STB and a disseminated form of STB have been described. In our Spinal TB X cohort study, we aim to describe the clinical phenotype of STB using whole-body \n                18 \n                FDG-PET/CT, identify a specific gene expression profile for different stages of dissemination and compare findings to previously described gene expression signatures for latent and active pulmonary TB. \n               \n             \n             \n              Methods \n               \n                A single-centre, prospective cohort study will be established to describe the distributional pattern of STB detected by whole-body \n                18 \n                FDG-PET/CT and gene expression profile of patients with suspected STB on magnetic resonance imaging (MRI) at point of diagnosis, six months, and 12 months. Blood biobanking will be performed at these time points. Specimens for microbiology will be obtained from sputum/urine, from easily accessible sites of disease (e.g., lymph nodes, abscess) identified in the first \n                18 \n                FDG-PET/CT, from CT-guided biopsy and/or surgery. Clinical parameters and functional scores will be collected at every physical visit. Data will be entered into RedCap® database; data cleaning, validation and analysis will be performed by the study team. The University of Cape Town Ethics Committee approved the protocol (243/2022). \n               \n             \n             \n              Discussion \n               \n                The Spinal TB X cohort study is the first prospective cohort study using whole-body 18FDG-PET/CT scans in patients with microbiologically confirmed spinal tuberculosis. Dual imaging techniques of the spine using \n                18 \n                FDG-PET/CT and magnetic resonance imaging as well as tissue diagnosis (microbiology and histopathology) will allow us to develop a virtual biopsy model. If successful, a distinct gene-expression profile will aid in blood-based diagnosis (point of care testing) as well as treatment monitoring and would lead to earlier diagnosis of this devastating disease. \n               \n               \n                Trial registration \n                : The study has been registered on ClinicalTrials.gov (NCT05610098).},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Journal of Orthopaedic Surgery and Research},\n\tauthor = {Scherer, Julian and Mukasa, Sandra L. and Wolmarans, Karen and Guler, Reto and Kotze, Tessa and Song, Taeksun and Dunn, Robert and Laubscher, Maritz and Pape, Hans-Christoph and Held, Michael and Thienemann, Friedrich},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {376},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Background Tuberculosis (TB) is one of the top ten causes of death worldwide, with approximately 10 million cases annually. Focus has been on pulmonary TB, while extrapulmonary TB (EPTB) has received little attention. Diagnosis of EPTB remains challenging due to the invasive procedures required for sample collection. Spinal TB (STB) accounts for 10% of EPTB and often leads to lifelong debilitating disease due to devastating spinal deformation and compression of neural structures. Little is known about the extent of disease, although both isolated STB and a disseminated form of STB have been described. In our Spinal TB X cohort study, we aim to describe the clinical phenotype of STB using whole-body 18 FDG-PET/CT, identify a specific gene expression profile for different stages of dissemination and compare findings to previously described gene expression signatures for latent and active pulmonary TB. Methods A single-centre, prospective cohort study will be established to describe the distributional pattern of STB detected by whole-body 18 FDG-PET/CT and gene expression profile of patients with suspected STB on magnetic resonance imaging (MRI) at point of diagnosis, six months, and 12 months. Blood biobanking will be performed at these time points. Specimens for microbiology will be obtained from sputum/urine, from easily accessible sites of disease (e.g., lymph nodes, abscess) identified in the first 18 FDG-PET/CT, from CT-guided biopsy and/or surgery. Clinical parameters and functional scores will be collected at every physical visit. Data will be entered into RedCap® database; data cleaning, validation and analysis will be performed by the study team. The University of Cape Town Ethics Committee approved the protocol (243/2022). Discussion The Spinal TB X cohort study is the first prospective cohort study using whole-body 18FDG-PET/CT scans in patients with microbiologically confirmed spinal tuberculosis. Dual imaging techniques of the spine using 18 FDG-PET/CT and magnetic resonance imaging as well as tissue diagnosis (microbiology and histopathology) will allow us to develop a virtual biopsy model. If successful, a distinct gene-expression profile will aid in blood-based diagnosis (point of care testing) as well as treatment monitoring and would lead to earlier diagnosis of this devastating disease. Trial registration : The study has been registered on ClinicalTrials.gov (NCT05610098).\n

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\n \n\n \n \n \n \n \n \n Efficacy and safety of higher dose rifampicin in adults with presumed drug-susceptible tuberculosis: an updated systematic review and meta-analysis.\n \n \n \n \n\n\n \n Haigh, K. A.; Twabi, H. H.; Boloko, L.; Namale, P. E.; Lutje, V.; Nevitt, S.; and Davies, G.\n\n\n \n\n\n\n eClinicalMedicine, 77: 102857. November 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Efficacy$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{haigh_efficacy_2024,\n\ttitle = {Efficacy and safety of higher dose rifampicin in adults with presumed drug-susceptible tuberculosis: an updated systematic review and meta-analysis},\n\tvolume = {77},\n\tissn = {25895370},\n\tshorttitle = {Efficacy and safety of higher dose rifampicin in adults with presumed drug-susceptible tuberculosis},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S258953702400436X},\n\tdoi = {10.1016/j.eclinm.2024.102857},\n\tlanguage = {en},\n\turldate = {2025-06-24},\n\tjournal = {eClinicalMedicine},\n\tauthor = {Haigh, Kathryn A. and Twabi, Hussein H. and Boloko, Linda and Namale, Phiona E. and Lutje, Vittoria and Nevitt, Sarah and Davies, Geraint},\n\tmonth = nov,\n\tyear = {2024},\n\tpages = {102857},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Immunopathology in human tuberculosis.\n \n \n \n \n\n\n \n Scriba, T. J.; Maseeme, M.; Young, C.; Taylor, L.; and Leslie, A. J.\n\n\n \n\n\n\n Science Immunology, 9(102): eado5951. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Immunopathology$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{scriba_immunopathology_2024,\n\ttitle = {Immunopathology in human tuberculosis},\n\tvolume = {9},\n\tissn = {2470-9468},\n\turl = {https://www.science.org/doi/10.1126/sciimmunol.ado5951},\n\tdoi = {10.1126/sciimmunol.ado5951},\n\tabstract = {Mycobacterium tuberculosis \n              ( \n              M.tb \n              ) is a bacterial pathogen that has evolved in humans, and its interactions with the host are complex and best studied in humans. Myriad immune pathways are involved in infection control, granuloma formation, and progression to tuberculosis (TB) disease. Inflammatory cells, such as macrophages, neutrophils, conventional and unconventional T cells, B cells, NK cells, and innate lymphoid cells, interact via cytokines, cell-cell communication, and eicosanoid signaling to contain or eliminate infection but can alternatively mediate pathological changes required for pathogen transmission. Clinical manifestations include pulmonary and extrapulmonary TB, as well as post-TB lung disease. Risk factors for TB progression, in turn, largely relate to immune status and, apart from traditional chemotherapy, interventions primarily target immune mechanisms, highlighting the critical role of immunopathology in TB. Maintaining a balance between effector mechanisms to achieve protective immunity and avoid detrimental inflammation is central to the immunopathogenesis of TB. Many research gaps remain and deserve prioritization to improve our understanding of human TB immunopathogenesis. \n             \n          ,  \n             \n              The balance between protective and pathological immune responses shapes progression of \n              Mycobacterium tuberculosis \n              infection.},\n\tlanguage = {en},\n\tnumber = {102},\n\turldate = {2025-06-24},\n\tjournal = {Science Immunology},\n\tauthor = {Scriba, Thomas J. and Maseeme, Mahlatse and Young, Carly and Taylor, Laura and Leslie, Alasdair J.},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {eado5951},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Microbiome research in Africa must be based on equitable partnerships.\n \n \n \n \n\n\n \n Oduaran, O. H.; Foláyan, M. O.; Kamng’ona, A. W.; Nakimuli, A.; Mwapagha, L. M.; Setati, M. E.; Owusu, M.; Mulder, N.; Makhalanyane, T. P.; and Kouidhi, S.\n\n\n \n\n\n\n Nature Medicine, 30(10): 2715–2717. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Microbiome$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{oduaran_microbiome_2024,\n\ttitle = {Microbiome research in {Africa} must be based on equitable partnerships},\n\tvolume = {30},\n\tissn = {1078-8956, 1546-170X},\n\turl = {https://www.nature.com/articles/s41591-024-03026-2},\n\tdoi = {10.1038/s41591-024-03026-2},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {Nature Medicine},\n\tauthor = {Oduaran, Ovokeraye H. and Foláyan, Moréniké Oluwátóyìn and Kamng’ona, Arox W. and Nakimuli, Annettee and Mwapagha, Lamech M. and Setati, Mathabatha E. and Owusu, Michael and Mulder, Nicola and Makhalanyane, Thulani P. and Kouidhi, Soumaya},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {2715--2717},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Drug-resistant tuberculosis: a persistent global health concern.\n \n \n \n \n\n\n \n Farhat, M.; Cox, H.; Ghanem, M.; Denkinger, C. M.; Rodrigues, C.; Abd El Aziz, M. S.; Enkh-Amgalan, H.; Vambe, D.; Ugarte-Gil, C.; Furin, J.; and Pai, M.\n\n\n \n\n\n\n Nature Reviews Microbiology, 22(10): 617–635. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Drug-resistant$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{farhat_drug-resistant_2024,\n\ttitle = {Drug-resistant tuberculosis: a persistent global health concern},\n\tvolume = {22},\n\tissn = {1740-1526, 1740-1534},\n\tshorttitle = {Drug-resistant tuberculosis},\n\turl = {https://www.nature.com/articles/s41579-024-01025-1},\n\tdoi = {10.1038/s41579-024-01025-1},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {Nature Reviews Microbiology},\n\tauthor = {Farhat, Maha and Cox, Helen and Ghanem, Marwan and Denkinger, Claudia M. and Rodrigues, Camilla and Abd El Aziz, Mirna S. and Enkh-Amgalan, Handaa and Vambe, Debrah and Ugarte-Gil, Cesar and Furin, Jennifer and Pai, Madhukar},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {617--635},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Distributable, metabolic PET reporting of tuberculosis.\n \n \n \n \n\n\n \n Khan, R. M. N.; Ahn, Y.; Marriner, G. A.; Via, L. E.; D’Hooge, F.; Seo Lee, S.; Yang, N.; Basuli, F.; White, A. G.; Tomko, J. A.; Frye, L. J.; Scanga, C. A.; Weiner, D. M.; Sutphen, M. L.; Schimel, D. M.; Dayao, E.; Piazza, M. K.; Gomez, F.; Dieckmann, W.; Herscovitch, P.; Mason, N. S.; Swenson, R.; Kiesewetter, D. O.; Backus, K. M.; Geng, Y.; Raj, R.; Anthony, D. C.; Flynn, J. L.; Barry, C. E.; and Davis, B. G.\n\n\n \n\n\n\n Nature Communications, 15(1): 5239. June 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Distributable,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{khan_distributable_2024,\n\ttitle = {Distributable, metabolic {PET} reporting of tuberculosis},\n\tvolume = {15},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-024-48691-6},\n\tdoi = {10.1038/s41467-024-48691-6},\n\tabstract = {Abstract \n             \n              Tuberculosis remains a large global disease burden for which treatment regimens are protracted and monitoring of disease activity difficult. Existing detection methods rely almost exclusively on bacterial culture from sputum which limits sampling to organisms on the pulmonary surface. Advances in monitoring tuberculous lesions have utilized the common glucoside [ \n              18 \n              F]FDG, yet lack specificity to the causative pathogen \n              Mycobacterium tuberculosis \n              ( \n              Mtb \n              ) and so do not directly correlate with pathogen viability. Here we show that a close mimic that is also positron-emitting of the non-mammalian \n              Mtb \n              disaccharide trehalose – 2-[ \n              18 \n              F]fluoro-2-deoxytrehalose ([ \n              18 \n              F]FDT) – is a mechanism-based reporter of Mycobacteria-selective enzyme activity in vivo. Use of [ \n              18 \n              F]FDT in the imaging of \n              Mtb \n              in diverse models of disease, including non-human primates, successfully co-opts \n              Mtb \n              -mediated processing of trehalose to allow the specific imaging of TB-associated lesions and to monitor the effects of treatment. A pyrogen-free, direct enzyme-catalyzed process for its radiochemical synthesis allows the ready production of [ \n              18 \n              F]FDT from the most globally-abundant organic \n              18 \n              F-containing molecule, [ \n              18 \n              F]FDG. The full, pre-clinical validation of both production method and [ \n              18 \n              F]FDT now creates a new, bacterium-selective candidate for clinical evaluation. We anticipate that this distributable technology to generate clinical-grade [ \n              18 \n              F]FDT directly from the widely-available clinical reagent [ \n              18 \n              F]FDG, without need for either custom-made radioisotope generation or specialist chemical methods and/or facilities, could now usher in global, democratized access to a TB-specific PET tracer.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2025-06-24},\n\tjournal = {Nature Communications},\n\tauthor = {Khan, R. M. Naseer and Ahn, Yong-Mo and Marriner, Gwendolyn A. and Via, Laura E. and D’Hooge, Francois and Seo Lee, Seung and Yang, Nan and Basuli, Falguni and White, Alexander G. and Tomko, Jaime A. and Frye, L. James and Scanga, Charles A. and Weiner, Danielle M. and Sutphen, Michelle L. and Schimel, Daniel M. and Dayao, Emmanuel and Piazza, Michaela K. and Gomez, Felipe and Dieckmann, William and Herscovitch, Peter and Mason, N. Scott and Swenson, Rolf and Kiesewetter, Dale O. and Backus, Keriann M. and Geng, Yiqun and Raj, Ritu and Anthony, Daniel C. and Flynn, JoAnne L. and Barry, Clifton E. and Davis, Benjamin G.},\n\tmonth = jun,\n\tyear = {2024},\n\tpages = {5239},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Reply to “Inadequate representation of individuals of African ancestry in pharmacogenetics of tamoxifen research”.\n \n \n \n \n\n\n \n Kruger, B.; and Dandara, C.\n\n\n \n\n\n\n Clinical and Translational Science, 17(10): e70031. October 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Reply$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kruger_reply_2024,\n\ttitle = {Reply to “{Inadequate} representation of individuals of {African} ancestry in pharmacogenetics of tamoxifen research”},\n\tvolume = {17},\n\tissn = {1752-8054, 1752-8062},\n\turl = {https://ascpt.onlinelibrary.wiley.com/doi/10.1111/cts.70031},\n\tdoi = {10.1111/cts.70031},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2025-06-24},\n\tjournal = {Clinical and Translational Science},\n\tauthor = {Kruger, Bianca and Dandara, Collet},\n\tmonth = oct,\n\tyear = {2024},\n\tpages = {e70031},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The challenges of difficult-to-treat Acinetobacter infections.\n \n \n \n \n\n\n \n Richards, G. A.; Perovic, O.; and Brink, A. J.\n\n\n \n\n\n\n Clinical Microbiology Reviews, 37(4): e00093–24. December 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{richards_challenges_2024,\n\ttitle = {The challenges of difficult-to-treat \\textit{{Acinetobacter}} infections},\n\tvolume = {37},\n\tissn = {0893-8512, 1098-6618},\n\turl = {https://journals.asm.org/doi/10.1128/cmr.00093-24},\n\tdoi = {10.1128/cmr.00093-24},\n\tabstract = {SUMMARY \n             \n              Infections due to \n              Acinetobacter \n              spp. are among the most difficult to treat. Most are resistant to standard antibiotics, and there is difficulty in distinguishing colonizers from pathogens. This mini-review examines the available antibiotics that exhibit activity against these organisms and provides guidance as to which cultures are relevant and how to treat active infections. Antibiograms describing resistance mechanisms and the minimum inhibitory concentration (MIC) are essential to determine which agent or combination of agents should be used after confirmation of infection, utilizing clinical parameters and biomarkers such as procalcitonin. Directed therapy should be prompt as despite its reputation as a colonizer, the attributable mortality is high. However, although combination therapy is advised, no specific combination has definite evidence of superiority.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2025-06-24},\n\tjournal = {Clinical Microbiology Reviews},\n\tauthor = {Richards, Guy A. and Perovic, Olga and Brink, Adrian J.},\n\teditor = {Forrest, Graeme N.},\n\tcollaborator = {Nishida, Satoshi and Uppalapati, Siva},\n\tmonth = dec,\n\tyear = {2024},\n\tpages = {e00093--24},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Interpersonal trauma Dissociates borderline from other personality disorders in social orienting.\n \n \n \n \n\n\n \n Van Heusden, C.; Montagne, B.; Van Honk, J.; and Terburg, D.\n\n\n \n\n\n\n Psychiatry Research Communications, 4(3): 100189. September 2024.\n \n\n\n\n
\n\n\n\n \n \n $\"Interpersonal$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{van_heusden_interpersonal_2024,\n\ttitle = {Interpersonal trauma {Dissociates} borderline from other personality disorders in social orienting},\n\tvolume = {4},\n\tissn = {27725987},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2772598724000357},\n\tdoi = {10.1016/j.psycom.2024.100189},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2025-06-24},\n\tjournal = {Psychiatry Research Communications},\n\tauthor = {Van Heusden, Corine and Montagne, Barbara and Van Honk, Jack and Terburg, David},\n\tmonth = sep,\n\tyear = {2024},\n\tpages = {100189},\n}\n

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