\n \n\n \n \n \n \n \n \n Beyond MRS Broth: A Soytone Medium towards affordable culturing of South African vaginal Lactobacillaceae isolates.\n \n \n \n \n\n\n \n Jona, O. L.; Fagan-Endres, M. A; Happel, A.; Kullin, B.; Passmore, J. S; and Harrison, S. T L\n\n\n \n\n\n\n Journal of Industrial Microbiology and Biotechnology,kuaf021. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Beyond$ Paper\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{jona_beyond_2025,\n\ttitle = {Beyond {MRS} {Broth}: {A} {Soytone} {Medium} towards affordable culturing of {South} {African} vaginal \\textit{{Lactobacillaceae}} isolates},\n\tcopyright = {https://creativecommons.org/licenses/by-nc-nd/4.0/},\n\tissn = {1367-5435, 1476-5535},\n\tshorttitle = {Beyond {MRS} {Broth}},\n\turl = {https://academic.oup.com/jimb/advance-article/doi/10.1093/jimb/kuaf021/8199913},\n\tdoi = {10.1093/jimb/kuaf021},\n\tabstract = {Abstract \n            This study assesses a plant-based Soytone Medium as an alternative to the animal-derived standard MRS Broth for the cultivation of Lactobacillaceae. The application focuses on five isolates that have shown probiotic potential for bacterial vaginosis treatment. Cultivation was performed in 300 mL bench-scale bioreactors, monitored for cell density, pH, lactate production and glucose consumption. The media's carbon and nitrogen concentrations and costing were quantified. \n            Though the medium's carbon concentrations were identical, the Soytone Medium had a higher carbon-to-nitrogen ratio than MRS (8.1 vs 6.6). Four strains achieved higher cell densities and maximum specific growth rates in the Soytone Medium. The greatest benefit was shown for L. crispatus 70.6PA, which had a 45\\% higher final cell density. A cost analysis showed that the Soytone Medium was 44\\% cheaper than MRS Broth. It was thus confirmed that the proposed plant-based Soytone Medium is a viable and less expensive alternative for Lactobacillaceae cultures in which exposure to animal products was also avoided.},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Industrial Microbiology and Biotechnology},\n\tauthor = {Jona, Obakeng Luthando and Fagan-Endres, Marijke A and Happel, Anna-Ursula and Kullin, Brian and Passmore, Jo-Ann S and Harrison, Susan T L},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {kuaf021},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Dolutegravir regimens have transformed treatment, but ongoing drug resistance research is required to maintain success.\n \n \n \n \n\n\n \n Van Zyl, G. U.; Jennings, L.; Rabie, H.; and Orrell, C.\n\n\n \n\n\n\n AIDS, 39(4): 337–343. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Dolutegravir$ Paper\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_zyl_dolutegravir_2025,\n\ttitle = {Dolutegravir regimens have transformed treatment, but ongoing drug resistance research is required to maintain success},\n\tvolume = {39},\n\tissn = {0269-9370, 1473-5571},\n\turl = {https://journals.lww.com/10.1097/QAD.0000000000004099},\n\tdoi = {10.1097/QAD.0000000000004099},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-28},\n\tjournal = {AIDS},\n\tauthor = {Van Zyl, Gert U. and Jennings, Lauren and Rabie, Helena and Orrell, Catherine},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {337--343},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Impact of statins as immune-modulatory agents on inflammatory markers in adults with chronic diseases: A systematic review and meta-analysis.\n \n \n \n \n\n\n \n Sabeel, S.; Motaung, B.; Nguyen, K. A.; Ozturk, M.; Mukasa, S. L.; Wolmarans, K.; Blom, D. J.; Sliwa, K.; Nepolo, E.; Günther, G.; Wilkinson, R. J.; Schacht, C.; Kengne, A. P.; Thienemann, F.; and Guler, R.\n\n\n \n\n\n\n PLOS One, 20(5): e0323749. May 2025.\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{sabeel_impact_2025,\n\ttitle = {Impact of statins as immune-modulatory agents on inflammatory markers in adults with chronic diseases: {A} systematic review and meta-analysis},\n\tvolume = {20},\n\tissn = {1932-6203},\n\tshorttitle = {Impact of statins as immune-modulatory agents on inflammatory markers in adults with chronic diseases},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0323749},\n\tdoi = {10.1371/journal.pone.0323749},\n\tabstract = {While numerous studies have extensively documented the pleiotropic effects of statins, including their capacity to reduce inflammation, there is a lack of research estimating the anti-inflammatory effectiveness of statins among individuals with chronic diseases. This meta-analysis evaluates the effect of statin therapy on inflammatory markers and the lipid profile in patients with chronic diseases by analysing evidence from randomized controlled trials (RCTs). We conducted a systematic review and searched articles published between 1 \n              st \n              January 1999 and 31 \n              st \n              December 2023 in databases including PubMed, Web of Science, Scopus, and Cochrane. The meta-analysis was performed using random effects models and inverse variance. Effect measures were mean differences (MD) and 95\\% confidence intervals (CI). Collectively, statins significantly reduced IL-6 ( \n              MD = -0.24 \n              ng/dL \n              [95\\% CI, -0.36 to -0.13], I \n               \n                2 \n               \n                \n              = 98.3\\%, p {\\textless} 0.001 \n              ), TNF-α ( \n              MD = -0.74 \n              ng/dL \n              [95\\% CI, -1.08 to -0.40], I \n               \n                2 \n               \n                \n              = 98.8\\%, p {\\textless} 0.001 \n              ); and CRP ( \n              MD = -1.58 \n              mg/L \n              [95\\% CI, -2.22 to -0.94], I \n               \n                2 \n               \n                \n              = 86.5\\%, p {\\textless} 0.001 \n              ). Notably, atorvastatin demonstrated the most significant reduction in IL-6 and TNF-α levels, while fluvastatin and rosuvastatin displayed the greatest impact on decreasing CRP and LDL-C levels, respectively. Stratification by a longer treatment duration of more than four months revealed that atorvastatin achieved the most significant reduction in IL-6 and TNF-α. In conclusion, statin therapy not only regulates the lipid profile but also reduces systemic inflammatory biomarkers. Prolonged administration of statins led to a more substantial reduction in IL-6 and TNF-α, with atorvastatin exhibiting the greatest effect in our analysis.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {PLOS One},\n\tauthor = {Sabeel, Solima and Motaung, Bongani and Nguyen, Kim A. and Ozturk, Mumin and Mukasa, Sandra L. and Wolmarans, Karen and Blom, Dirk J. and Sliwa, Karen and Nepolo, Emmanuel and Günther, Gunar and Wilkinson, Robert J. and Schacht, Claudia and Kengne, Andre Pascal and Thienemann, Friedrich and Guler, Reto},\n\teditor = {Hariyanto, Timotius Ivan},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {e0323749},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The effect of smart pillboxes on TB stigma among adults in a cluster-randomised TB treatment trial.\n \n \n \n \n\n\n \n Jennings, L.; Maraba, N.; Mukora, R.; Hippner, P.; Velen, K.; Orrell, C.; Charalambous, S.; and Fielding, K.\n\n\n \n\n\n\n IJTLD Open, 2(10): 583–589. October 2025.\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{jennings_effect_2025,\n\ttitle = {The effect of smart pillboxes on {TB} stigma among adults in a cluster-randomised {TB} treatment trial},\n\tvolume = {2},\n\tissn = {3005-7590},\n\turl = {https://journals.theunion.org/lookup/doi/10.5588/ijtldopen.25.0113},\n\tdoi = {10.5588/ijtldopen.25.0113},\n\tabstract = {SUMMARY \n             \n              BACKGROUND \n              TB stigma has been shown to result in delayed health-seeking behaviours and treatment initiation. Few studies have quantitatively described stigma during treatment. As part of the TB Mate trial, we summarise TB stigma at treatment start and the effect of the intervention on stigma in follow-up. \n             \n             \n              METHODS \n              In the TB Mate trial, we conducted a cluster-randomised trial in 18 primary health care facilities from three provinces in South Africa to evaluate the use of alarmed electronic pillboxes in drug-sensitive TB on treatment adherence. We administered a questionnaire, measuring five TB stigma domains, at baseline, 6 months, and 18 months. We conducted a sub-analysis of these stigma data. \n             \n             \n              RESULTS \n              Overall, 2,469/2,657 adults with TB enrolled had a baseline stigma questionnaire. At baseline, reporting experience of stigma or internalised stigma was low (≤3\\%), whereas disclosure of TB status outside of the household was common (42.3\\%; 1,045/2,469). Prevalence of experiencing stigma remained low at the end of treatment. Disclosure increased at 6 months in the intervention (40\\%–64\\%) and standard of care arms (44.7\\%–56\\%), though was similar by arm (adjusted prevalence ratio 2.55 [95\\% confidence interval: 0.50–12.90]). \n             \n             \n              CONCLUSION \n              The overall prevalence of TB stigma, in domains other than disclosure, in our study population was low. There was no evidence that stigma increased with use of an alarmed smart pillbox.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-28},\n\tjournal = {IJTLD Open},\n\tauthor = {Jennings, L. and Maraba, N. and Mukora, R. and Hippner, P. and Velen, K. and Orrell, C. and Charalambous, S. and Fielding, K.},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {583--589},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Intersecting epidemics: immune dysregulation associated with HIV and tuberculosis syndemic contribute to increased risk of hypertensive disease in Sub-Saharan Africa.\n \n \n \n \n\n\n \n Letuka, P.; and Zulu, M. Z.\n\n\n \n\n\n\n Frontiers in Cardiovascular Medicine, 12: 1717609. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Intersecting$ Paper\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{letuka_intersecting_2025,\n\ttitle = {Intersecting epidemics: immune dysregulation associated with {HIV} and tuberculosis syndemic contribute to increased risk of hypertensive disease in {Sub}-{Saharan} {Africa}},\n\tvolume = {12},\n\tissn = {2297-055X},\n\tshorttitle = {Intersecting epidemics},\n\turl = {https://www.frontiersin.org/articles/10.3389/fcvm.2025.1717609/full},\n\tdoi = {10.3389/fcvm.2025.1717609},\n\tabstract = {Hypertension (HTN) is a chronic medical condition characterized by systolic blood pressure of ≥140 mmHg and diastolic blood pressure \\&gt;80 mmHg upon repeated measurements. It is one of the most common non-communicable diseases affecting 30\\% of the global population. Sub-Saharan Africa (SSA) has a high burden of infectious diseases, which contribute to the increased prevalence of hypertension. Furthermore, SSA has the highest number of people living with chronic infectious diseases, such as human immunodeficiency virus (HIV) and tuberculosis (TB). The pathogenesis of these conditions is associated with chronic, low-grade inflammation and immune activation that complicates various homeostatic functions, leading to increased risk of non-communicable diseases among this population. Furthermore, persistent immune activation leads to endothelial dysfunction, arterial stiffness, and altered vascular tone, which contribute to elevated and treatment-refractory blood pressure. However, immunological factors that contribute to the development and pathogenesis of hypertension remain poorly understood. Antiretroviral therapy and anti-TB medications further complicate this landscape by inducing metabolic disturbances and modulating drug metabolism, which affects the efficacy of anti-hypertensive medications. There is a paucity of data and studies reporting on immune dysregulation associated with HTN amongst people living with chronic infections such as HIV and TB. This review aims to highlight this gap in knowledge and the need for more translational research studies to improve health outcomes in hypertensive individuals living with HIV and TB in SSA. Understanding these intertwined immunological and pathophysiological mechanisms is crucial to developing targeted interventions for managing HTN, especially in this vulnerable population.},\n\turldate = {2026-05-28},\n\tjournal = {Frontiers in Cardiovascular Medicine},\n\tauthor = {Letuka, Pheletso and Zulu, Michael Z.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {1717609},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Comprehensive analysis of human dendritic spine morphology and density.\n \n \n \n \n\n\n \n Schünemann, K. D.; Hattingh, R. M.; Verhoog, M. B.; Yang, D.; Bak, A. V.; Peter, S.; Van Loo, K. M. J.; Wolking, S.; Kronenberg-Versteeg, D.; Weber, Y.; Schwarz, N.; Raimondo, J. V.; Melvill, R.; Tromp, S. A.; Butler, J. T.; Höllig, A.; Delev, D.; Wuttke, T. V.; Kampa, B. M.; and Koch, H.\n\n\n \n\n\n\n Journal of Neurophysiology, 133(4): 1086–1102. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Comprehensive$ Paper\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{schunemann_comprehensive_2025,\n\ttitle = {Comprehensive analysis of human dendritic spine morphology and density},\n\tvolume = {133},\n\tissn = {0022-3077, 1522-1598},\n\turl = {https://journals.physiology.org/doi/10.1152/jn.00622.2024},\n\tdoi = {10.1152/jn.00622.2024},\n\tabstract = {This study presents a dataset of nearly 4,000 morphologically reconstructed human dendritic spines across different ages, gender, and tissue conditions. The dataset was further used to evaluate a deep learning algorithm for three-dimensional spine reconstruction, offering a scalable method for semiautomated spine analysis across various tissues and microscopy setups. The findings enhance understanding of human neurology, indicating potential connections between spine morphology, brain function, and the mechanisms of neurological and psychiatric diseases. \n , \n Dendritic spines, small protrusions on neuronal dendrites, play a crucial role in brain function by changing shape and size in response to neural activity. So far, in-depth analysis of dendritic spines in human brain tissue is lacking. This study presents a comprehensive analysis of human dendritic spine morphology and density using a unique dataset from human brain tissue from 27 patients (8 females, 19 males, aged 18–71 yr) undergoing tumor or epilepsy surgery at three neurosurgery sites. We used acute slices and organotypic brain slice cultures to examine dendritic spines, classifying them into the three main morphological subtypes: mushroom, thin, and stubby, via three-dimensional (3-D) reconstruction using ZEISS arivis Pro software. A deep learning model, trained on 39 diverse datasets, automated spine segmentation and 3-D reconstruction, achieving a 74\\% F1-score and reducing processing time by over 50\\%. We show significant differences in spine density by sex, dendrite type, and tissue condition. Females had higher spine densities than males, and apical dendrites were denser in spines than basal ones. Acute tissue showed higher spine densities compared with cultured human brain tissue. With time in culture, mushroom spines decreased, whereas stubby and thin spine percentages increased, particularly from 7–9 to 14 days in vitro, reflecting potential synaptic plasticity changes. Our study underscores the importance of using human brain tissue to understand unique synaptic properties and shows that integrating deep learning with traditional methods enables efficient large-scale analysis, revealing key insights into sex- and tissue-specific dendritic spine dynamics relevant to neurological diseases. \n NEW \\& NOTEWORTHY This study presents a dataset of nearly 4,000 morphologically reconstructed human dendritic spines across different ages, gender, and tissue conditions. The dataset was further used to evaluate a deep learning algorithm for three-dimensional spine reconstruction, offering a scalable method for semiautomated spine analysis across various tissues and microscopy setups. The findings enhance understanding of human neurology, indicating potential connections between spine morphology, brain function, and the mechanisms of neurological and psychiatric diseases.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Neurophysiology},\n\tauthor = {Schünemann, Kerstin D. and Hattingh, Roxanne M. and Verhoog, Matthijs B. and Yang, Danqing and Bak, Aniella V. and Peter, Sabrina and Van Loo, Karen M. J. and Wolking, Stefan and Kronenberg-Versteeg, Deborah and Weber, Yvonne and Schwarz, Niklas and Raimondo, Joseph V. and Melvill, Roger and Tromp, Sean A. and Butler, James T. and Höllig, Anke and Delev, Daniel and Wuttke, Thomas V. and Kampa, Björn M. and Koch, Henner},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {1086--1102},\n}\n\n\n\n

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\n This study presents a dataset of nearly 4,000 morphologically reconstructed human dendritic spines across different ages, gender, and tissue conditions. The dataset was further used to evaluate a deep learning algorithm for three-dimensional spine reconstruction, offering a scalable method for semiautomated spine analysis across various tissues and microscopy setups. The findings enhance understanding of human neurology, indicating potential connections between spine morphology, brain function, and the mechanisms of neurological and psychiatric diseases. , Dendritic spines, small protrusions on neuronal dendrites, play a crucial role in brain function by changing shape and size in response to neural activity. So far, in-depth analysis of dendritic spines in human brain tissue is lacking. This study presents a comprehensive analysis of human dendritic spine morphology and density using a unique dataset from human brain tissue from 27 patients (8 females, 19 males, aged 18–71 yr) undergoing tumor or epilepsy surgery at three neurosurgery sites. We used acute slices and organotypic brain slice cultures to examine dendritic spines, classifying them into the three main morphological subtypes: mushroom, thin, and stubby, via three-dimensional (3-D) reconstruction using ZEISS arivis Pro software. A deep learning model, trained on 39 diverse datasets, automated spine segmentation and 3-D reconstruction, achieving a 74% F1-score and reducing processing time by over 50%. We show significant differences in spine density by sex, dendrite type, and tissue condition. Females had higher spine densities than males, and apical dendrites were denser in spines than basal ones. Acute tissue showed higher spine densities compared with cultured human brain tissue. With time in culture, mushroom spines decreased, whereas stubby and thin spine percentages increased, particularly from 7–9 to 14 days in vitro, reflecting potential synaptic plasticity changes. Our study underscores the importance of using human brain tissue to understand unique synaptic properties and shows that integrating deep learning with traditional methods enables efficient large-scale analysis, revealing key insights into sex- and tissue-specific dendritic spine dynamics relevant to neurological diseases. NEW & NOTEWORTHY This study presents a dataset of nearly 4,000 morphologically reconstructed human dendritic spines across different ages, gender, and tissue conditions. The dataset was further used to evaluate a deep learning algorithm for three-dimensional spine reconstruction, offering a scalable method for semiautomated spine analysis across various tissues and microscopy setups. The findings enhance understanding of human neurology, indicating potential connections between spine morphology, brain function, and the mechanisms of neurological and psychiatric diseases.\n

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\n \n\n \n \n \n \n \n \n Immunogenicity, safety, and efficacy of the vaccine H56:IC31 in reducing the rate of tuberculosis disease recurrence in HIV-negative adults successfully treated for drug-susceptible pulmonary tuberculosis: a double-blind, randomised, placebo-controlled, phase 2b trial.\n \n \n \n \n\n\n \n Borges, Á. H; Russell, M.; Tait, D.; Scriba, T. J; Nemes, E.; Skallerup, P.; Van Brakel, E.; Cabibbe, A. M; Cirillo, D. M; Leuvennink-Steyn, M.; Rutkowski, K. T; Wood, G. K; Thierry-Carstensen, B.; Tingskov, P. N; Meldgaard, E. C; Kristiansen, M. P; Søndergaard, R. E; Hansen, C. H; Follmann, F.; Jensen, C. G; Gela, A.; Ntinginya, N. E; Ruhwald, M.; Shenje, J.; White, L.; Innes, C.; Selepe, P.; Ngaraguza, B.; Holmgren, C.; Collings, T.; Andersen, P.; Dawson, R.; Churchyard, G.; Sabi, I.; Diacon, A. H; Mortensen, R.; Hatherill, M.; Shenje, J.; Van As, D.; Luabeya-Kanykany, A.; Tameris, M.; Mendelsohn, S.; Tredoux, N.; Geldenhuys, H.; Companie, A.; Buhlungu, S.; Stryers, S.; Moses, M.; Baartman, V.; Gwintsa, C.; Arendsen, D.; Valley, H.; Africa, H.; Steyn, M.; Mabwe, S.; Van Rooyen, J.; Mouton, A.; Opperman, F.; Noble, J.; Leopeng, T.; Mulenga, H.; Segelaar, C.; Beyers, E.; Van Der Westhuizen, D.; Esterhuizen, T.; Toefy, A.; Erasmus, M.; Cloete, Y.; Jaxa, L.; Schreuder, C.; Nombida, O.; Raphela, R.; Bilek, N.; Ontong, C.; Davids, I.; Erasmus, M.; Petersen, C.; Ockhius, R.; Vasana, B.; Moleleki-Mabala, M.; Mangali, S.; Nkambule, H.; Carstens, A.; Visagie, S.; Langafa, P.; Verster, E.; Oelofse, R.; Dawson, R.; White, L.; Di Marco, F.; Sabi, I.; Ntinginya, N. E.; Ngaraguza, B.; Lalashowi, J.; Chimbe, O.; Mtafya, B.; Chaula, G.; Sichone, E.; Sudi, L.; Kisinda, A.; Kunambi, R.; Myombe, B.; Mwanyonga, S.; Mtweve, C.; Tait, D.; Van Brakel, E.; Lambrick, M.; Swanson, F.; Rutkowski, K.; Hunt, D.; Van Der Westhuizen, A.; Siefers, H.; Coetzee, L.; Leuvennink-Steyn, M.; Albertyn, D.; Russell, M.; Raubenheimer, V.; Van Der Merwe, A.; Gangat, A.; Kock, A.; Van Aswegen, A.; Nyathi, A. D.; Lakhi, A.; Dlamini, A.; Pei, B.; Makhubalo, B.; Eyre, C.; Innes, C.; Serake, M. G.; Selepe, P.; Malefo-Grootboom, S.; Van Rensburg, E. B. J.; Ledwaba, H.; Mabasa, I.; Market, J.; Clarke, K.; Ntoahae, L.; Tswaile, L. I.; Seabela, L.; Erasmus, L.; Nhlangulela, L.; Makhetha, M.; Collignon, M.; Zietsman, M.; Nel, M.; Tlhapi, M. M.; Majola, M.; Fikizolo, M.; Motsiri, M. J.; Makoanyane, M.; Kunene, N. I.; Ndlovu, N.; Arjun, N.; Mabuza, N.; Langa, N.; Mbipha, N.; Mosweu, P.; Sanyaka, P. N.; Nteleki, R.; Mompati, S.; Modipa, S. S.; Ntshauba, T.; Goliath, T.; Mugwena, T.; Mabe, T.; Rameetse, V.; Tshikovhi, V.; Galaive, W. P.; Borges, Á. H; Mortensen, R.; Skallerup, P.; Thierry-Carstensen, B.; Follmann, F.; Jensen, C. G; Tingskov, P. N; Meldgaard, E. C; Kristiansen, M. P; Dohn, R. B.; Bartholomæussen, R. D.; Van Deventer, A.; Van Huyssteen, H.; Kleinhans, C.; Sims, J.; Patientia, M.; Govender, T.; and Samaai, P.\n\n\n \n\n\n\n The Lancet Infectious Diseases, 25(7): 751–763. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Immunogenicity,$ Paper\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{borges_immunogenicity_2025,\n\ttitle = {Immunogenicity, safety, and efficacy of the vaccine {H56}:{IC31} in reducing the rate of tuberculosis disease recurrence in {HIV}-negative adults successfully treated for drug-susceptible pulmonary tuberculosis: a double-blind, randomised, placebo-controlled, phase 2b trial},\n\tvolume = {25},\n\tissn = {14733099},\n\tshorttitle = {Immunogenicity, safety, and efficacy of the vaccine {H56}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1473309924008144},\n\tdoi = {10.1016/S1473-3099(24)00814-4},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Infectious Diseases},\n\tauthor = {Borges, Álvaro H and Russell, Marisa and Tait, Dereck and Scriba, Thomas J and Nemes, Elisa and Skallerup, Per and Van Brakel, Elana and Cabibbe, Andrea M and Cirillo, Daniela M and Leuvennink-Steyn, Mildie and Rutkowski, Kathryn T and Wood, Grith K and Thierry-Carstensen, Birgit and Tingskov, Pernille N and Meldgaard, Emilie C and Kristiansen, Max P and Søndergaard, Rie E and Hansen, Christian H and Follmann, Frank and Jensen, Charlotte G and Gela, Anele and Ntinginya, Nyanda E and Ruhwald, Morten and Shenje, Justin and White, Lisa and Innes, Craig and Selepe, Pearl and Ngaraguza, Beatrice and Holmgren, Chantelle and Collings, Tarryn and Andersen, Peter and Dawson, Rodney and Churchyard, Gavin and Sabi, Issa and Diacon, Andreas H and Mortensen, Rasmus and Hatherill, Mark and Shenje, Justin and Van As, Danelle and Luabeya-Kanykany, Angelique and Tameris, Michele and Mendelsohn, Simon and Tredoux, Nicolette and Geldenhuys, Hennie and Companie, Alessandro and Buhlungu, Sivuyile and Stryers, Sonia and Moses, Miriam and Baartman, Veronica and Gwintsa, Cynthia and Arendsen, Denis and Valley, Habibullah and Africa, Haydn and Steyn, Marcia and Mabwe, Simbarashe and Van Rooyen, Johanna and Mouton, Angelique and Opperman, Fajwa and Noble, Julia and Leopeng, Thelma and Mulenga, Humphrey and Segelaar, Carmen and Beyers, Elizabeth and Van Der Westhuizen, Denise and Esterhuizen, Terence and Toefy, Asma and Erasmus, Mzwandile and Cloete, Yolundi and Jaxa, Lungisa and Schreuder, Constance and Nombida, Onke and Raphela, Rodney and Bilek, Nicole and Ontong, Cynthia and Davids, Ilse and Erasmus, Margareth and Petersen, Christel and Ockhius, Rose and Vasana, Bongiwe and Moleleki-Mabala, Mamosa and Mangali, Sandisiwe and Nkambule, Hlengiwe and Carstens, Alida and Visagie, Suzette and Langafa, Phumzile and Verster, Elmien and Oelofse, Rachel and Dawson, Rodney and White, Linda and Di Marco, Frederico and Sabi, Issa and Ntinginya, Nyanda Elias and Ngaraguza, Beatrice and Lalashowi, Julieth and Chimbe, Ombeni and Mtafya, Bariki and Chaula, Godlove and Sichone, Emmanuel and Sudi, Lwitiho and Kisinda, Abisai and Kunambi, Revocatus and Myombe, Bahati and Mwanyonga, Simeon and Mtweve, Cyprian and Tait, Dereck and Van Brakel, Elana and Lambrick, Maureen and Swanson, Fay and Rutkowski, Kathryn and Hunt, Devin and Van Der Westhuizen, Anja and Siefers, Heather and Coetzee, Leonie and Leuvennink-Steyn, Mildie and Albertyn, Deidre and Russell, Marisa and Raubenheimer, Viola-Marie and Van Der Merwe, Arrie and Gangat, Aaliya and Kock, Adriane and Van Aswegen, Amanda and Nyathi, Amukelani Dolly and Lakhi, Aneesa and Dlamini, Audrey and Pei, Bertha and Makhubalo, Blossom and Eyre, Candice and Innes, Craig and Serake, Moeti Godfrey and Selepe, Pearl and Malefo-Grootboom, Shirley and Van Rensburg, Elizabeth Barbara Janse and Ledwaba, Hildah and Mabasa, Immaculate and Market, Juanita and Clarke, Ken and Ntoahae, Lawrence and Tswaile, Lebogang Isaac and Seabela, Letlhogonolo and Erasmus, Lezaan-Marie and Nhlangulela, Lindiwe and Makhetha, Mantai and Collignon, Marelize and Zietsman, Marietjie and Nel, Maryna and Tlhapi, Mmanare Maria and Majola, Molly and Fikizolo, Moogo and Motsiri, Morongoenyane Josephine and Makoanyane, Mpho and Kunene, Ndlela Israel and Ndlovu, Nhlamulo and Arjun, Nishanee and Mabuza, Nkosinathi and Langa, Nondumiso and Mbipha, Nontsikelelo and Mosweu, Palesa and Sanyaka, Pearl Nomsa and Nteleki, Richard and Mompati, Samuel and Modipa, Serame Sylvester and Ntshauba, Tedrius and Goliath, Thelma and Mugwena, Thompho and Mabe, Tshegofatso and Rameetse, Victor and Tshikovhi, Vincent and Galaive, Welseh Phindile and Borges, Álvaro H and Mortensen, Rasmus and Skallerup, Per and Thierry-Carstensen, Birgit and Follmann, Frank and Jensen, Charlotte G and Tingskov, Pernille N and Meldgaard, Emilie C and Kristiansen, Max P and Dohn, Rebecca Bach and Bartholomæussen, Rikke Dahl and Van Deventer, Alida and Van Huyssteen, Hesti-Mari and Kleinhans, Carmen and Sims, Julia and Patientia, Monde and Govender, Thirumani and Samaai, Priscilla},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {751--763},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n HIV Superinfection in Kidney Transplant Recipients With HIV Who Received Organs From Donors With HIV.\n \n \n \n \n\n\n \n Rozek, G. M; Yang, P.; Eby, Y.; Benner, S. E; Martens, C.; Habtehyimer, F.; Chahoud, M.; Brown, D.; Desai, N. M; Florman, S.; Rana, M. M; Pereira, M. R; Hand, J.; Mehta, S. A; Schaenman, J.; Santos, C. A Q; Aslam, S.; Elias, N.; Odim, J.; Morsheimer, M.; Segev, D. L; Durand, C. M; Tobian, A. A R; and Redd, A. D\n\n\n \n\n\n\n The Journal of Infectious Diseases, 232(2): 359–363. August 2025.\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{rozek_hiv_2025,\n\ttitle = {{HIV} {Superinfection} in {Kidney} {Transplant} {Recipients} {With} {HIV} {Who} {Received} {Organs} {From} {Donors} {With} {HIV}},\n\tvolume = {232},\n\tcopyright = {https://academic.oup.com/pages/standard-publication-reuse-rights},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/232/2/359/8152684},\n\tdoi = {10.1093/infdis/jiaf284},\n\tabstract = {Abstract \n            Transplantation of kidneys from donors with HIV to recipients with HIV (HIV D+/R+) has been shown to be safe and effective, but there is a unique risk of donor-derived HIV superinfection (HIV-SI) in these recipients. Recipients from a multicenter observational HIV D+/R+ study were examined for HIV-SI by site-directed next-generation sequencing (Illumina). Eighteen recipients of HIV D+/R+ kidney transplants had baseline and follow-up samples that successfully amplified. One recipient was confirmed to have experienced donor-derived HIV-SI at week 26 but did not experience any clinically significant changes. HIV-SI in recipients of HIV D+/R+ transplants is rare, and the clinical ramifications appear negligible.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Rozek, Gracie M and Yang, Ping and Eby, Yolanda and Benner, Sarah E and Martens, Craig and Habtehyimer, Feben and Chahoud, Maggie and Brown, Diane and Desai, Niraj M and Florman, Sander and Rana, Meenakshi M and Pereira, Marcus R and Hand, Jonathan and Mehta, Sapna A and Schaenman, Joanna and Santos, Carlos A Q and Aslam, Saima and Elias, Nahel and Odim, Jonah and Morsheimer, Megan and Segev, Dorry L and Durand, Christine M and Tobian, Aaron A R and Redd, Andrew D},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {359--363},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Identifying Key Questions and Challenges in Microchimerism Biology.\n \n \n \n \n\n\n \n Chua, K. J.; Quilang, R. C.; Sallinger, K.; Aktipis, C. A.; Arck, P.; Bianchi, D. W.; Chang, H.; Cleaves, H. J.; Eikmans, M.; Fjeldstad, H. E. S.; Haig, D.; Harrington, W. E.; Horsnell, W.; Jacobsen, D. P.; Kamper‐Jørgensen, M.; Kanaan, S. B.; Khosrotehrani, K.; Lambert, N. C.; Nelson, J. L.; Olsen, M. B.; Pan, T. D.; Prins, J. R.; Schildberg, F. A.; Staff, A. C.; Ståhlberg, A.; Stelzer, I. A.; Urbschat, C.; Way, S. S.; Wilson, M. A.; Ye, J.; Kroneis, T.; and Boddy, A. M.\n\n\n \n\n\n\n Advanced Science, 12(48): e14969. December 2025.\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 abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{chua_identifying_2025,\n\ttitle = {Identifying {Key} {Questions} and {Challenges} in {Microchimerism} {Biology}},\n\tvolume = {12},\n\tissn = {2198-3844, 2198-3844},\n\turl = {https://advanced.onlinelibrary.wiley.com/doi/10.1002/advs.202514969},\n\tdoi = {10.1002/advs.202514969},\n\tabstract = {Abstract \n            Microchimerism research has recently gained renewed attention despite known existence of these rare cells for decades. Fetal and maternal microchimeric‐derived cells may have functional capabilities, and are increasingly associated with both beneficial and adverse health outcomes. Yet, establishing the role of microchimerism in health has been largely constrained methodologically and theoretically. The Microchimerism, Human Health, and Evolution Project address these challenges by calling on 29 leading microchimerism experts to put forth key research questions that can substantially advance the field. Seven major categories are identified: function and mechanism; microchimerism in interventions, treatment, and transplant; mapping “generational microchimerism”; evolution; microchimerism detection; appropriate experimental model systems; and definition of microchimerism. Identifying these questions ‐ and continuing to find answers ‐ will be crucial for advancing the knowledge of microchimerism in health and disease.},\n\tlanguage = {en},\n\tnumber = {48},\n\turldate = {2026-05-28},\n\tjournal = {Advanced Science},\n\tauthor = {Chua, Kristine J. and Quilang, Rachel C. and Sallinger, Katja and Aktipis, Christina Athena and Arck, Petra and Bianchi, Diana W. and Chang, Hyun‐Dong and Cleaves, Henderson J. and Eikmans, Michael and Fjeldstad, Heidi E. S. and Haig, David and Harrington, Whitney E. and Horsnell, William and Jacobsen, Daniel P. and Kamper‐Jørgensen, Mads and Kanaan, Sami B. and Khosrotehrani, Kiarash and Lambert, Nathalie C. and Nelson, J. Lee and Olsen, Maria B. and Pan, Tiffany D. and Prins, Jelmer R. and Schildberg, Frank A. and Staff, Anne Cathrine and Ståhlberg, Anders and Stelzer, Ina A. and Urbschat, Christopher and Way, Sing Sing and Wilson, Melissa A. and Ye, Jody and Kroneis, Thomas and Boddy, Amy M.},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e14969},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Single-gene transcripts for subclinical tuberculosis: an individual participant data meta-analysis.\n \n \n \n \n\n\n \n Greenan-Barrett, J.; Mendelsohn, S. C; Scriba, T. J; Noursadeghi, M.; and Gupta, R. K\n\n\n \n\n\n\n The Lancet Microbe, 6(11): 101186. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Single-gene$ Paper\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{greenan-barrett_single-gene_2025,\n\ttitle = {Single-gene transcripts for subclinical tuberculosis: an individual participant data meta-analysis},\n\tvolume = {6},\n\tissn = {26665247},\n\tshorttitle = {Single-gene transcripts for subclinical tuberculosis},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524725001144},\n\tdoi = {10.1016/j.lanmic.2025.101186},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Greenan-Barrett, James and Mendelsohn, Simon C and Scriba, Thomas J and Noursadeghi, Mahdad and Gupta, Rishi K},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {101186},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Treatment outcomes of bedaquiline-resistant tuberculosis: a retrospective and matched cohort study.\n \n \n \n \n\n\n \n Mdlenyani, L.; Mohamed, Z.; Stadler, J. A M; Mtwa, N.; Meintjes, G.; Warren, R.; Saunders, M. J; Kuhlin, J.; and Wasserman, S.\n\n\n \n\n\n\n The Lancet Infectious Diseases, 25(10): 1149–1158. October 2025.\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

\n

@article{mdlenyani_treatment_2025,\n\ttitle = {Treatment outcomes of bedaquiline-resistant tuberculosis: a retrospective and matched cohort study},\n\tvolume = {25},\n\tissn = {14733099},\n\tshorttitle = {Treatment outcomes of bedaquiline-resistant tuberculosis},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S147330992500218X},\n\tdoi = {10.1016/S1473-3099(25)00218-X},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Infectious Diseases},\n\tauthor = {Mdlenyani, Lindokuhle and Mohamed, Zahraa and Stadler, Jacob A M and Mtwa, Nomfuneko and Meintjes, Graeme and Warren, Robin and Saunders, Matthew J and Kuhlin, Johanna and Wasserman, Sean},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {1149--1158},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Development and validation of a time-varying correction factor for QT interval assessment in drug-resistant tuberculosis patients.\n \n \n \n \n\n\n \n Vongjarudech, T.; Dosne, A.; Remmerie, B.; Dooley, K. E.; Brust, J. C.; Maartens, G.; Meintjes, G.; Karlsson, M. O.; and Svensson, E. M.\n\n\n \n\n\n\n International Journal of Antimicrobial Agents, 65(4): 107460. April 2025.\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

\n

@article{vongjarudech_development_2025,\n\ttitle = {Development and validation of a time-varying correction factor for {QT} interval assessment in drug-resistant tuberculosis patients},\n\tvolume = {65},\n\tissn = {09248579},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0924857925000184},\n\tdoi = {10.1016/j.ijantimicag.2025.107460},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-28},\n\tjournal = {International Journal of Antimicrobial Agents},\n\tauthor = {Vongjarudech, Thanakorn and Dosne, Anne-Gaëlle and Remmerie, Bart and Dooley, Kelly E. and Brust, James C.M. and Maartens, Gary and Meintjes, Graeme and Karlsson, Mats O. and Svensson, Elin M.},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {107460},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Life‐years lost associated with mental disorders in people with HIV: a cohort study in South Africa, Canada and the United States.\n \n \n \n \n\n\n \n Ruffieux, Y.; Joska, J. A.; Lang, R.; Zheng, C.; Folb, N.; Kirk, G. D.; Parcesepe, A. M.; Silverberg, M. J.; Napravnik, S.; Gebo, K.; Jr, J. J. E.; Hogan, B. C.; Althoff, K. N.; Tlali, M.; Grelotti, D. J.; Loutfy, M.; Rebeiro, P. F.; Davies, M.; Egger, M.; Maartens, G.; and Haas, A. D.\n\n\n \n\n\n\n Journal of the International AIDS Society, 28(8): e70023. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Life‐years$ Paper\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{ruffieux_lifeyears_2025,\n\ttitle = {Life‐years lost associated with mental disorders in people with {HIV}: a cohort study in {South} {Africa}, {Canada} and the {United} {States}},\n\tvolume = {28},\n\tissn = {1758-2652, 1758-2652},\n\tshorttitle = {Life‐years lost associated with mental disorders in people with {HIV}},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.70023},\n\tdoi = {10.1002/jia2.70023},\n\tabstract = {Abstract \n             \n              Introduction \n              People with HIV (PWH) have a high burden of mental health disorders, which contribute to increased mortality due to elevated rates of physical illness, suicide or fatal accidents. Additionally, mental health disorders can adversely affect antiretroviral therapy (ART) adherence, leading to increased HIV‐related mortality. This study aims to quantify the difference in mortality between PWH who have a mental health disorder and PWH without mental health disorders in South Africa (SA) and North America (NA). \n             \n             \n              Methods \n              This cohort study includes PWH aged 18 years or older who initiated ART between 2000 and 2021 at a national private‐sector HIV programme in SA and 13 programmes in the United States and Canada. Mental health disorders were diagnosed according to ICD‐10 codes F10‐F99, which include psychotic disorders, bipolar disorders, depression, anxiety and substance use disorders. We estimated life‐years lost (LYL) associated with mental health disorders, quantifying the average difference in remaining life expectancy between individuals diagnosed with a mental health disorder and those without such diagnoses. \n             \n             \n              Results \n              The study included 119,785 participants from SA (57.4\\% female, median age 39 years) and 142,044 from NA (85.0\\% male, median age 43 years). In SA, 57,999 (48.4\\%) were diagnosed with a mental health disorder, compared with 93,518 (65.8\\%) in NA. In SA, the LYL associated with any mental health disorder were 3.42 years (95\\% CI 2.42−4.28) in males and 2.95 years (0.67−5.95) in females. Corresponding figures for NA were 4.16 years (3.71−4.59) in males and 4.64 years (2.93−6.05) in females. In both regions, LYL were higher for psychotic and substance use disorders than for depression and anxiety. Losses were primarily due to natural deaths at CD4 counts ≥200 cells/µl, with considerable contributions at CD4 counts {\\textless}200 cells/µl. Unnatural causes also contributed to the loss of life‐years in males from SA and males and females from NA. \n             \n             \n              Conclusions \n              PWH affected by mental health disorders experience higher mortality, primarily from natural causes. LYL were associated with both immunosuppression and higher CD4 levels. Improved management of HIV and physical comorbidities among PWH affected by mental health disorders may enhance their prognosis.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-28},\n\tjournal = {Journal of the International AIDS Society},\n\tauthor = {Ruffieux, Yann and Joska, John A. and Lang, Raynell and Zheng, Chunyan and Folb, Naomi and Kirk, Gregory D. and Parcesepe, Angela M. and Silverberg, Michael J. and Napravnik, Sonia and Gebo, Kelly and Jr, Joseph J. Eron and Hogan, Brenna C. and Althoff, Keri N. and Tlali, Mpho and Grelotti, David J. and Loutfy, Mona and Rebeiro, Peter F. and Davies, Mary‐Ann and Egger, Matthias and Maartens, Gary and Haas, Andreas D.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {e70023},\n}\n\n\n\n

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\n\n\n

\n Abstract Introduction People with HIV (PWH) have a high burden of mental health disorders, which contribute to increased mortality due to elevated rates of physical illness, suicide or fatal accidents. Additionally, mental health disorders can adversely affect antiretroviral therapy (ART) adherence, leading to increased HIV‐related mortality. This study aims to quantify the difference in mortality between PWH who have a mental health disorder and PWH without mental health disorders in South Africa (SA) and North America (NA). Methods This cohort study includes PWH aged 18 years or older who initiated ART between 2000 and 2021 at a national private‐sector HIV programme in SA and 13 programmes in the United States and Canada. Mental health disorders were diagnosed according to ICD‐10 codes F10‐F99, which include psychotic disorders, bipolar disorders, depression, anxiety and substance use disorders. We estimated life‐years lost (LYL) associated with mental health disorders, quantifying the average difference in remaining life expectancy between individuals diagnosed with a mental health disorder and those without such diagnoses. Results The study included 119,785 participants from SA (57.4% female, median age 39 years) and 142,044 from NA (85.0% male, median age 43 years). In SA, 57,999 (48.4%) were diagnosed with a mental health disorder, compared with 93,518 (65.8%) in NA. In SA, the LYL associated with any mental health disorder were 3.42 years (95% CI 2.42−4.28) in males and 2.95 years (0.67−5.95) in females. Corresponding figures for NA were 4.16 years (3.71−4.59) in males and 4.64 years (2.93−6.05) in females. In both regions, LYL were higher for psychotic and substance use disorders than for depression and anxiety. Losses were primarily due to natural deaths at CD4 counts ≥200 cells/µl, with considerable contributions at CD4 counts \\textless200 cells/µl. Unnatural causes also contributed to the loss of life‐years in males from SA and males and females from NA. Conclusions PWH affected by mental health disorders experience higher mortality, primarily from natural causes. LYL were associated with both immunosuppression and higher CD4 levels. Improved management of HIV and physical comorbidities among PWH affected by mental health disorders may enhance their prognosis.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Hepatitis A breakthrough infections despite vaccination: A systematic review and meta-analysis.\n \n \n \n \n\n\n \n Schnyder, J. L.; Hutten, D.; Bache, B. E.; Spijker, R.; Welkers, M. R.; De Jong, H. K.; Grobusch, M. P.; and Goorhuis, A.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 161: 108113. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Hepatitis$ Paper\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{schnyder_hepatitis_2025,\n\ttitle = {Hepatitis {A} breakthrough infections despite vaccination: {A} systematic review and meta-analysis},\n\tvolume = {161},\n\tissn = {12019712},\n\tshorttitle = {Hepatitis {A} breakthrough infections despite vaccination},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971225003352},\n\tdoi = {10.1016/j.ijid.2025.108113},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Schnyder, Jenny L. and Hutten, David and Bache, Bache E. and Spijker, René and Welkers, Matthijs R.A. and De Jong, Hanna K. and Grobusch, Martin P. and Goorhuis, Abraham},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {108113},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Growing through the cracks: Navigating global research funding cuts as an early career researcher.\n \n \n \n \n\n\n \n Young, C.; Mbangiwa, T.; and Mbano, I.\n\n\n \n\n\n\n South African Journal of Science, 121(5/6). May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Growing$ Paper\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{young_growing_2025,\n\ttitle = {Growing through the cracks: {Navigating} global research funding cuts as an early career researcher},\n\tvolume = {121},\n\tissn = {1996-7489},\n\tshorttitle = {Growing through the cracks},\n\turl = {https://sajs.co.za/article/view/21941},\n\tdoi = {10.17159/sajs.2025/21941},\n\tlanguage = {en},\n\tnumber = {5/6},\n\turldate = {2026-05-28},\n\tjournal = {South African Journal of Science},\n\tauthor = {Young, Carly and Mbangiwa, Tshepiso and Mbano, Ian},\n\tmonth = may,\n\tyear = {2025},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Advancing the chemotherapy of tuberculous meningitis: a consensus view.\n \n \n \n \n\n\n \n Wasserman, S.; Donovan, J.; Kestelyn, E.; Watson, J. A; Aarnoutse, R. E; Barnacle, J. R; Boulware, D. R; Chow, F. C; Cresswell, F. V; Davis, A. G; Dooley, K. E; Figaji, A. A; Gibb, D. M; Huynh, J.; Imran, D.; Marais, S.; Meya, D. B; Misra, U. K; Modi, M.; Raberahona, M.; Ganiem, A. R.; Rohlwink, U. K; Ruslami, R.; Seddon, J. A; Skolimowska, K. H; Solomons, R. S; Stek, C. J; Thuong, N. T. T.; Van Crevel, R.; Whitaker, C.; Thwaites, G. E; and Wilkinson, R. J\n\n\n \n\n\n\n The Lancet Infectious Diseases, 25(1): e47–e58. January 2025.\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

\n

@article{wasserman_advancing_2025,\n\ttitle = {Advancing the chemotherapy of tuberculous meningitis: a consensus view},\n\tvolume = {25},\n\tissn = {14733099},\n\tshorttitle = {Advancing the chemotherapy of tuberculous meningitis},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1473309924005127},\n\tdoi = {10.1016/S1473-3099(24)00512-7},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Infectious Diseases},\n\tauthor = {Wasserman, Sean and Donovan, Joseph and Kestelyn, Evelyne and Watson, James A and Aarnoutse, Robert E and Barnacle, James R and Boulware, David R and Chow, Felicia C and Cresswell, Fiona V and Davis, Angharad G and Dooley, Kelly E and Figaji, Anthony A and Gibb, Diana M and Huynh, Julie and Imran, Darma and Marais, Suzaan and Meya, David B and Misra, Usha K and Modi, Manish and Raberahona, Mihaja and Ganiem, Ahmad Rizal and Rohlwink, Ursula K and Ruslami, Rovina and Seddon, James A and Skolimowska, Keira H and Solomons, Regan S and Stek, Cari J and Thuong, Nguyen Thuy Thuong and Van Crevel, Reinout and Whitaker, Claire and Thwaites, Guy E and Wilkinson, Robert J},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {e47--e58},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Benzothiazole and 2,3-dihydro-1,5-benzoxazepine Derivatives Demonstrate Antimicrobial Activity: An Antimicrobial and ADMET Study.\n \n \n \n \n\n\n \n Odame, F.; Neglo, D.; Warner, D.; Amengor, C.; and Arthur, R.\n\n\n \n\n\n\n Pharmaceutical Fronts, 07(04): e363–e378. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Benzothiazole$ Paper\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{odame_benzothiazole_2025,\n\ttitle = {Benzothiazole and 2,3-dihydro-1,5-benzoxazepine {Derivatives} {Demonstrate} {Antimicrobial} {Activity}: {An} {Antimicrobial} and {ADMET} {Study}},\n\tvolume = {07},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2628-5088, 2628-5096},\n\tshorttitle = {Benzothiazole and 2,3-dihydro-1,5-benzoxazepine {Derivatives} {Demonstrate} {Antimicrobial} {Activity}},\n\turl = {http://www.thieme-connect.de/DOI/DOI?10.1055/a-2712-4936},\n\tdoi = {10.1055/a-2712-4936},\n\tabstract = {Antimicrobial resistance continues to be a serious public health threat globally, hence the continuous design of new clinical candidates with novel mechanisms of action. Heterocyclic drugs have been a hotspot in antibiotic research. Benzothiazole and 2,3-dihydro-1,5-benzoxazepine are anticancer derivatives. To follow up on their antimicrobial activity, the current work resynthesized 13 benzothiazole, benzimidazole, benzothiazepine, and 2,3-dihydro-1,5-benzoxazepine derivatives, followed by the evaluation of their antimicrobial and antitubercular activity against methicillin-resistant Staphylococcus aureus (MRSA), Escherichia coli, Klebsiella pneumonia, Bacillus subtilis, Streptococcus mutans, Salmonella typhi, and Mycobacterium tuberculosis. In addition, in silico ADMET studies were performed on the compounds using the ADMET Laboratory 2.0 platform. The compounds were found to be active against all the bacterial strains except against S. mutans and S. typhi. 4-[(E)-2-(2-chlorophenyl)ethenyl]-2,2-dimethyl-2,3-dihydro-1,5-benzoxazepine (3) was found to be the most active against E. coli, 2,2,4-trimethyl-2,3-dihydrobenzoxazepine (12) the most active against MRSA, and 4-[(E)-2-(4-methoxyphenyl)ethenyl]-2,2-dimethyl-2,3-dihydro-1,5-benzoxazepine (6) the most active against Klebsiella pneumoniae. The compounds also showed moderate activity against M. tuberculosis. The ADMET analysis predicted largely drug-like properties of the compounds and their suitability as potential drugs. The synthesized compounds showed good activity against some of the selected organisms and, therefore, could be modified to improve their action as antimicrobial agents.},\n\tlanguage = {en},\n\tnumber = {04},\n\turldate = {2026-05-28},\n\tjournal = {Pharmaceutical Fronts},\n\tauthor = {Odame, Felix and Neglo, David and Warner, Digby and Amengor, Cedric and Arthur, Richmond},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e363--e378},\n}\n\n\n\n

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

\n \n\n \n \n \n \n \n \n Safety, reactogenicity, and immunogenicity of MTBVAC in infants: a phase 2a randomised, double-blind, dose-defining trial in a TB endemic setting.\n \n \n \n \n\n\n \n Tameris, M.; Rozot, V.; Imbratta, C.; Geldenhuys, H.; Mendelsohn, S. C.; Kany Luabeya, A. K.; Shenje, J.; Tredoux, N.; Fisher, M.; Mulenga, H.; Bilek, N.; Young, C.; Veldsman, A.; Botes, N.; Thole, J.; Fritzell, B.; Mukherjee, R.; Jelsbak, I. M.; Rodriguez, E.; Puentes, E.; Doce, J.; Marinova, D.; Gonzalo-Asensio, J.; Aguilo, N.; Martin, C.; Scriba, T. J.; Hatherill, M.; Abrahams, C.; Africa, H.; Arendsen, D.; Barnard, L.; Cloete, Y.; Davids, I.; Erasmus, M.; Filander, E.; Gregg, Y.; Herling, R.; Jansen, R.; Jack, L.; Kelepu, X.; Kyepa, H.; Leopeng, T.; Mabwe, S.; Mactavie, L.; Makhete, L.; Mangali, S.; Mouton, A.; Nkambule, H.; Noble, J.; Nombida, O.; Nqakala, N.; Opperman, F.; Raphela, R.; Rossouw, S.; Schoeman, E.; Schreuder, C.; Steyn, M.; Swanepoel, L.; Toefy, A.; Tromp, A.; Tyambethu, P.; Valley, H.; and Van Rooyes, J.\n\n\n \n\n\n\n eBioMedicine, 114: 105628. April 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{tameris_safety_2025,\n\ttitle = {Safety, reactogenicity, and immunogenicity of {MTBVAC} in infants: a phase 2a randomised, double-blind, dose-defining trial in a {TB} endemic setting},\n\tvolume = {114},\n\tissn = {23523964},\n\tshorttitle = {Safety, reactogenicity, and immunogenicity of {MTBVAC} in infants},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352396425000726},\n\tdoi = {10.1016/j.ebiom.2025.105628},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {eBioMedicine},\n\tauthor = {Tameris, Michele and Rozot, Virginie and Imbratta, Claire and Geldenhuys, Hennie and Mendelsohn, Simon C. and Kany Luabeya, Angelique Kany and Shenje, Justin and Tredoux, Nicolette and Fisher, Michelle and Mulenga, Humphrey and Bilek, Nicole and Young, Carly and Veldsman, Ashley and Botes, Natasja and Thole, Jelle and Fritzell, Bernard and Mukherjee, Rajat and Jelsbak, Ingrid Murillo and Rodriguez, Esteban and Puentes, Eugenia and Doce, Juana and Marinova, Dessislava and Gonzalo-Asensio, Jesús and Aguilo, Nacho and Martin, Carlos and Scriba, Thomas J. and Hatherill, Mark and Abrahams, Charmaine and Africa, Hadn and Arendsen, Denis and Barnard, Liezl and Cloete, Yolundi and Davids, Ilse and Erasmus, Mzwandile and Filander, Elizabeth and Gregg, Yolande and Herling, Roxane and Jansen, Ruwiyda and Jack, Lungisa and Kelepu, Xoliswe and Kyepa, Henriette and Leopeng, Thelma and Mabwe, Simbarahse and Mactavie, Lauren and Makhete, Lebohang and Mangali, Sandisiwe and Mouton, Angelique and Nkambule, Hlengiwe and Noble, Julia and Nombida, Onke and Nqakala, Nambitha and Opperman, Fajwa and Raphela, Rodney and Rossouw, Susan and Schoeman, Elisma and Schreuder, Constance and Steyn, Marcia and Swanepoel, Liticia and Toefy, Asma and Tromp, Anele and Tyambethu, Petrus and Valley, Habibullah and Van Rooyes, Johanna},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {105628},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Reduced Metformin Concentrations in Obese Women With Human Immunodeficiency Virus Treated With Dolutegravir.\n \n \n \n \n\n\n \n Van Rensburg, R.; Kellermann, T.; Pillay-Fuentes Lorente, V.; Du Plessis, C.; Orrell, C.; Maposa, I.; Schreuder, C.; Jennings, L.; Van Zyl, G.; Schifitto, G.; and Decloedt, E.\n\n\n \n\n\n\n The Journal of Infectious Diseases, 232(6): e1012–e1021. December 2025.\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 abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{van_rensburg_reduced_2025,\n\ttitle = {Reduced {Metformin} {Concentrations} in {Obese} {Women} {With} {Human} {Immunodeficiency} {Virus} {Treated} {With} {Dolutegravir}},\n\tvolume = {232},\n\tcopyright = {https://creativecommons.org/licenses/by-nc-nd/4.0/},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/232/6/e1012/8157047},\n\tdoi = {10.1093/infdis/jiaf305},\n\tabstract = {Abstract \n             \n              Background \n              Obesity among women with human immunodeficiency virus (WWH) is nearly 2-fold higher than in men. Obesity is closely associated with dysglycemia, and frequently necessitates the coadministration of dolutegravir and metformin. A pharmacokinetic study in 15 nonobese healthy volunteers determined that dolutegravir increased metformin plasma exposure by 79\\%, prompting regulatory and guideline recommendations to limit metformin to 1000 mg/day when coadministered with dolutegravir. Obesity has been linked to lower metformin exposures, and our study aimed to verify the metformin pharmacokinetic exposure in the increasing population of obese WWH. \n             \n             \n              Methods \n              We conducted intensive plasma sampling in virally suppressed WWH receiving metformin extended-release 1000 mg once daily with concomitant dolutegravir 50 mg once daily. Dual-energy X-ray absorptiometry was performed to quantify body fat composition. Noncompartmental analysis of metformin and dolutegravir concentrations was performed, and our findings were compared to the reference study. \n             \n             \n              Results \n              We enrolled 15 participants with a mean body mass index of 45.6 kg/m2. Metformin area under the concentration-time curve over the 24-hour dosing interval (AUC0–24) was 40.9\\% lower and dolutegravir AUC0–24 was 54.4\\% lower in obese WWH compared to the reference study. Metformin and dolutegravir clearance were 1.7- and 2.2-fold higher, respectively. Linear regression did not show associations between body fat composition and metformin or dolutegravir exposures. \n             \n             \n              Conclusions \n              Limiting metformin to 1000 mg daily is likely to lead to underdosing in obese WWH on dolutegravir. Lower metformin exposure appears to be due to the reduced inhibitory effect of lower dolutegravir concentrations on metformin clearance and increased volume of distribution due to obesity. Our data support the revision of the current maximum dose restriction of metformin in the target population of obese WWH.},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Van Rensburg, Roland and Kellermann, Tracy and Pillay-Fuentes Lorente, Veshni and Du Plessis, Christiena and Orrell, Catherine and Maposa, Innocent and Schreuder, Chantel and Jennings, Lauren and Van Zyl, Gert and Schifitto, Giovanni and Decloedt, Eric},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e1012--e1021},\n}\n\n\n\n

\n

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

\n \n\n \n \n \n \n \n \n Exploring pharmacogenetic factors influencing hydroxyurea response in tanzanian sickle cell disease patients: a genomic medicine approach.\n \n \n \n \n\n\n \n Nkya, S.; Nzunda, C.; Saukiwa, E.; Kaywanga, F.; Buchard, E.; Solomon, D.; Christopher, H.; Ngowi, D.; Johansen, J.; Urio, F.; Mgaya, J.; Kindole, C.; Yonazi, M.; Karim, S.; Alimohamed, M. Z.; Sangeda, R. Z.; Chamba, C.; Dandara, C.; Novelli, E.; Chimusa, E. R.; and Makani, J.\n\n\n \n\n\n\n The Pharmacogenomics Journal, 25(3): 11. June 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{nkya_exploring_2025,\n\ttitle = {Exploring pharmacogenetic factors influencing hydroxyurea response in tanzanian sickle cell disease patients: a genomic medicine approach},\n\tvolume = {25},\n\tissn = {1470-269X, 1473-1150},\n\tshorttitle = {Exploring pharmacogenetic factors influencing hydroxyurea response in tanzanian sickle cell disease patients},\n\turl = {https://www.nature.com/articles/s41397-025-00372-3},\n\tdoi = {10.1038/s41397-025-00372-3},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {The Pharmacogenomics Journal},\n\tauthor = {Nkya, Siana and Nzunda, Collin and Saukiwa, Emmanuel and Kaywanga, Frida and Buchard, Eliud and Solomon, David and Christopher, Heavenlight and Ngowi, Doreen and Johansen, Julieth and Urio, Florence and Mgaya, Josephine and Kindole, Christina and Yonazi, Mbonea and Karim, Salman and Alimohamed, Mohamed Zahir and Sangeda, Raphael Z. and Chamba, Clara and Dandara, Collet and Novelli, Enrico and Chimusa, Emile R. and Makani, Julie},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {11},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Motivations for Starting and Stopping PrEP: Experiences of Adolescent Girls and Young Women in the HPTN 082 Trial.\n \n \n \n \n\n\n \n Mills, L.; Ndimande-Khoza, M. N.; Velloza, J.; Atujuna, M.; Chitukuta, M.; Hosek, S.; Chauke, H.; Musara, P.; Mangxilana, N.; Mutero, P.; Makhale, L. M.; Tauya, T.; Celum, C.; Delany-Moretlwe, S.; and the HPTN 082 study team\n\n\n \n\n\n\n AIDS and Behavior, 29(8): 2408–2419. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Motivations$ Paper\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{mills_motivations_2025,\n\ttitle = {Motivations for {Starting} and {Stopping} {PrEP}: {Experiences} of {Adolescent} {Girls} and {Young} {Women} in the {HPTN} 082 {Trial}},\n\tvolume = {29},\n\tissn = {1090-7165, 1573-3254},\n\tshorttitle = {Motivations for {Starting} and {Stopping} {PrEP}},\n\turl = {https://link.springer.com/10.1007/s10461-025-04703-0},\n\tdoi = {10.1007/s10461-025-04703-0},\n\tabstract = {Abstract \n            Oral PrEP effectiveness depends on consistent use during periods of potential HIV exposure, but adolescent girls and young women (AGYW) find this challenging. Data on PrEP use decision-making and alignment with risk among AGYW are limited. From 2016 to 2018, we conducted in-depth interviews with participants in HPTN 082, an open-label PrEP study in South Africa and Zimbabwe, to explore reasons for PrEP starts, stops, and restarts. Of 60 PrEP acceptors, 12 delayed acceptance, 15 used PrEP intermittently, 18 paused and restarted PrEP, and 13 permanently discontinued PrEP during 12-month follow-up. Perceived HIV vulnerability motivated PrEP start, but there was little evidence that fluctuating risk perception motivated prevention-effective use. PrEP stops were motivated by stigma, misconceptions and side effects; PrEP restarts were prompted by support from family, peers and clinic staff. Decision-making was related to social, gendered and normative influences, highlighting opportunities for psycho-educational support and multimedia campaigns to normalise HIV prevention.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-28},\n\tjournal = {AIDS and Behavior},\n\tauthor = {Mills, Lisa and Ndimande-Khoza, Makhosazane Nomhle and Velloza, Jennifer and Atujuna, Millicent and Chitukuta, Miria and Hosek, Sybil and Chauke, Hlukelo and Musara, Petina and Mangxilana, Nomvuyo and Mutero, Prisca and Makhale, Lerato Michelle and Tauya, Thelma and Celum, Connie and Delany-Moretlwe, Sinead and {the HPTN 082 study team}},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {2408--2419},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Strategies for shortening tuberculosis therapy.\n \n \n \n \n\n\n \n Dartois, V. A.; Mizrahi, V.; Savic, R. M.; Silverman, J. A.; Hermann, D.; and Barry, C. E.\n\n\n \n\n\n\n Nature Medicine, 31(6): 1765–1775. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Strategies$ Paper\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{dartois_strategies_2025,\n\ttitle = {Strategies for shortening tuberculosis therapy},\n\tvolume = {31},\n\tissn = {1078-8956, 1546-170X},\n\turl = {https://www.nature.com/articles/s41591-025-03742-3},\n\tdoi = {10.1038/s41591-025-03742-3},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {Nature Medicine},\n\tauthor = {Dartois, Véronique A. and Mizrahi, Valerie and Savic, Radojka M. and Silverman, Jared A. and Hermann, David and Barry, Clifton E.},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {1765--1775},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Discrete and conserved inflammatory signatures drive thrombosis in different organs after Salmonella infection.\n \n \n \n \n\n\n \n Perez-Toledo, M.; Beristain-Covarrubias, N.; Pillaye, J.; Persaud, R. R.; Marcial-Juarez, E.; Jossi, S. E.; Hitchcock, J. R.; Alshayea, A.; Channell, W. M.; Wiersma, N. T. J.; Lamerton, R. E.; Kavanagh, D. P.; Carestia, A.; Horsnell, W. G.; Henderson, I. R.; Mackman, N.; Clark, A. R.; Jenne, C. N.; Rayes, J.; Watson, S. P.; and Cunningham, A. F.\n\n\n \n\n\n\n Nature Communications, 16(1): 2356. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Discrete$ Paper\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{perez-toledo_discrete_2025,\n\ttitle = {Discrete and conserved inflammatory signatures drive thrombosis in different organs after {Salmonella} infection},\n\tvolume = {16},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-025-57466-6},\n\tdoi = {10.1038/s41467-025-57466-6},\n\tabstract = {Abstract \n             \n              Inflammation-induced thrombosis is a common consequence of bacterial infections, such as those caused by \n              Salmonella \n              Typhimurium (STm). The presentation of multi-organ thrombosis post-infection that develops and resolves with organ-specific kinetics raises significant challenges for its therapeutic control. Here, we identify specific inflammatory events driving thrombosis in the spleens and livers of STm-infected mice. IFN-γ or platelet expression of C-type lectin-like receptor CLEC-2, key drivers of thrombosis in liver, are dispensable for thrombosis in the spleen. Platelets, monocytes, and neutrophils are identified as core constituents of thrombi in both organs. Depleting either neutrophils or monocytic cells abrogates thrombus formation. Neutrophils and monocytes secrete TNF and blocking TNF diminishes both thrombosis and inflammation, which correlates with reduced endothelial expression of E-selectin and leukocyte infiltration. Moreover, inhibiting tissue factor and P-selectin glycoprotein ligand-1 pathways impairs thrombosis in both spleen and liver. Therefore, we identify organ-specific, and shared mechanisms driving thrombosis within a single infection. This may inform on tailoring treatments towards infection-induced inflammation, and single- or multi-organ thrombosis, based on the clinical need.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Nature Communications},\n\tauthor = {Perez-Toledo, Marisol and Beristain-Covarrubias, Nonantzin and Pillaye, Jamie and Persaud, Ruby R. and Marcial-Juarez, Edith and Jossi, Sian E. and Hitchcock, Jessica R. and Alshayea, Areej and Channell, William M. and Wiersma, Niek T. J. and Lamerton, Rachel E. and Kavanagh, Dean P. and Carestia, Agostina and Horsnell, William G. and Henderson, Ian R. and Mackman, Nigel and Clark, Andrew R. and Jenne, Craig N. and Rayes, Julie and Watson, Steve P. and Cunningham, Adam F.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {2356},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n To be or not to be a virus: A novel chimeric circular Rep-encoding single stranded DNA virus with interfamilial gene exchange illustrates the considerable evolutionary capacity of ssDNA viruses.\n \n \n \n \n\n\n \n Ben Chéhida, S.; Lacroix, S.; Hoareau, M.; Fenelon, B.; Varsani, A.; Martin, D. P.; Teycheney, P.; Lefeuvre, P.; and Lett, J.\n\n\n \n\n\n\n PLOS One, 20(8): e0309278. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"To$ Paper\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_be_2025,\n\ttitle = {To be or not to be a virus: {A} novel chimeric circular {Rep}-encoding single stranded {DNA} virus with interfamilial gene exchange illustrates the considerable evolutionary capacity of {ssDNA} viruses},\n\tvolume = {20},\n\tissn = {1932-6203},\n\tshorttitle = {To be or not to be a virus},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0309278},\n\tdoi = {10.1371/journal.pone.0309278},\n\tabstract = {Viruses in the family \n              Geminiviridae \n              cause significant economic losses in numerous crops worldwide. Some geminiviruses are often associated with satellite DNA molecules, such as alphasatellites (familly \n              Alphasatellitidae \n              ), that require the assistance of a helper virus for their transmission. Here, we report the discovery of a chimeric virus, tentatively named Cenchrus purpureus associated virus (CPAV), in \n              Cenchrus purpureus \n              plants in La Réunion. The genome of CPAV consists of a single component that is primarily geminivirus-like. It contains a \n              rep \n              gene phylogenetically most closely related alphasatellites. This \n              rep \n              gene is positioned upstream of, and in the same orientation as, the movement and capsid protein genes. Both of these genes are phylogenetically most related to members of the genus \n              Mastrevirus \n              (family \n              Geminiviridae \n              ). We found that CPAV is associated in the field with Cenchrus purpureus mild streak virus (CPMSV). Using agroinfectious clones and insect transmission assays, we demonstrated that CPAV is able to initiate infections in \n              C. purpureus \n              but its ability to establish long-term infection and be insect transmitted is apparently facilitated by CPMSV. This raises the question of whether CPAV qualifies as an autonomous virus or rather a satellite-like element with partial autonomy. The chimeric nature of CPAV illustrates the interfamily gene exchange between circular ssDNA viruses and satellites and how such recombination events can blur the boundaries between viruses and subviral agents. These findings highlight the evolutionary plasticity of circular ssDNA viruses and suggest that chimerism may be a key mechanism driving the emergence of novel viral forms with modified pathogenicity and host range.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-28},\n\tjournal = {PLOS One},\n\tauthor = {Ben Chéhida, Sélim and Lacroix, Sylvain and Hoareau, Murielle and Fenelon, Babbitha and Varsani, Arvind and Martin, Darren P. and Teycheney, Pierre-Yves and Lefeuvre, Pierre and Lett, Jean-Michel},\n\teditor = {Ghorbani, Abozar},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {e0309278},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The dubious case of Urbanorum: a call to strengthen global pathogen verification mechanisms.\n \n \n \n \n\n\n \n Van Der Ende, J.; Dávila Campos, V.; Grobusch, M. P.; and Hanscheid, T.\n\n\n \n\n\n\n The Lancet Microbe, 6(7): 101043. July 2025.\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{van_der_ende_dubious_2025,\n\ttitle = {The dubious case of {Urbanorum}: a call to strengthen global pathogen verification mechanisms},\n\tvolume = {6},\n\tissn = {26665247},\n\tshorttitle = {The dubious case of {Urbanorum}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524724003112},\n\tdoi = {10.1016/j.lanmic.2024.101043},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Van Der Ende, Jacob and Dávila Campos, Vanessa and Grobusch, Martin Peter and Hanscheid, Thomas},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {101043},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Molecular basis of human angiotensin‐1 converting enzyme inhibition by a series of diprolyl‐derived compounds.\n \n \n \n \n\n\n \n Gregory, K. S.; Cozier, G. E.; Fienberg, S.; Chibale, K.; Sturrock, E. D.; and Acharya, K. R.\n\n\n \n\n\n\n The FEBS Journal, 292(5): 1141–1158. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Molecular$ Paper\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{gregory_molecular_2025,\n\ttitle = {Molecular basis of human angiotensin‐1 converting enzyme inhibition by a series of diprolyl‐derived compounds},\n\tvolume = {292},\n\tissn = {1742-464X, 1742-4658},\n\turl = {https://febs.onlinelibrary.wiley.com/doi/10.1111/febs.17384},\n\tdoi = {10.1111/febs.17384},\n\tabstract = {Angiotensin‐1‐converting enzyme (ACE) is a zinc‐dependent carboxypeptidase of therapeutic interest for the treatment of hypertension, inflammation and fibrosis. It consists of two homologous N and C catalytic domains, nACE and cACE, respectively. Unfortunately, the current clinically available ACE inhibitors produce undesirable side effects due to the nonselective inhibition of these domains. Through structure‐based drug design, we previously identified a series of diprolyl‐derived inhibitors (SG3, SG15, SG16, SG17 and SG18) in an attempt to specifically target nACE. Only one compound, SG16, possessed significant nACEselectivity. The previously determined \n              16 \n              ‐nACE crystal structure (nACE:SG16) suggested interactions with Tyr369 (Phe381 in cACE) are responsible for this selectivity. To better understand the molecular basis for the lack of selectivity in the remaining compounds, we have cocrystallised nACE in complex with SG3, SG15, SG17 and SG18 and cACE in complex with SG3, SG15, SG16 and SG18 and determined their structures at high resolution. Apart from the catalytic residues, these structures further highlight the importance of residues distal to the active site that may play an important role in the design of domain‐selective inhibitors of ACE.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {The FEBS Journal},\n\tauthor = {Gregory, Kyle S. and Cozier, Gyles E. and Fienberg, Stephen and Chibale, Kelly and Sturrock, Edward D. and Acharya, K. Ravi},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {1141--1158},\n}\n\n\n\n

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

\n \n\n \n \n \n \n \n \n Synthesis and SAR Studies of Acyl-Thiourea Platinum(II) Complexes Yield Analogs with Dual-Stage Antiplasmodium Activity.\n \n \n \n \n\n\n \n Ishmail, F.; Coertzen, D.; Tshabalala, S.; Leshabane, M.; Da Rocha, S.; Njoroge, M.; Gibhard, L.; Birkholtz, L.; Woodland, J. G.; Egan, T. J.; Wicht, K. J.; and Chibale, K.\n\n\n \n\n\n\n ACS Medicinal Chemistry Letters, 16(3): 428–435. March 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{ishmail_synthesis_2025,\n\ttitle = {Synthesis and {SAR} {Studies} of {Acyl}-{Thiourea} {Platinum}({II}) {Complexes} {Yield} {Analogs} with {Dual}-{Stage} {Antiplasmodium} {Activity}},\n\tvolume = {16},\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.4c00545},\n\tdoi = {10.1021/acsmedchemlett.4c00545},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {ACS Medicinal Chemistry Letters},\n\tauthor = {Ishmail, Fatima-Zahra and Coertzen, Dina and Tshabalala, Sizwe and Leshabane, Meta and Da Rocha, Shante and Njoroge, Mathew and Gibhard, Liezl and Birkholtz, Lyn-Marie and Woodland, John G. and Egan, Timothy J. and Wicht, Kathryn J. and Chibale, Kelly},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {428--435},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Infection prevention and control measures during the COVID-19 pandemic and airborne tuberculosis transmission during primary care visits in South Africa.\n \n \n \n \n\n\n \n Banholzer, N.; Middelkoop, K.; Schmutz, R.; Leukes, J.; Zürcher, K.; Egger, M.; Wood, R.; and Fenner, L.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 156: 107921. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Infection$ Paper\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{banholzer_infection_2025,\n\ttitle = {Infection prevention and control measures during the {COVID}-19 pandemic and airborne tuberculosis transmission during primary care visits in {South} {Africa}},\n\tvolume = {156},\n\tissn = {12019712},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971225001444},\n\tdoi = {10.1016/j.ijid.2025.107921},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Banholzer, Nicolas and Middelkoop, Keren and Schmutz, Remo and Leukes, Juane and Zürcher, Kathrin and Egger, Matthias and Wood, Robin and Fenner, Lukas},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {107921},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The association of class II HLA alleles with tuberculosis-associated immune reconstitution inflammatory syndrome.\n \n \n \n \n\n\n \n Choshi, P.; Pedretti, S.; Chimbetete, T.; Gangula, R.; Shey, M.; Stek, C.; Lai, R. P. J.; Wilkinson, R.; Meintjes, G.; Phillips, E.; and Peter, J.\n\n\n \n\n\n\n PLOS Pathogens, 21(9): e1013497. September 2025.\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{choshi_association_2025,\n\ttitle = {The association of class {II} {HLA} alleles with tuberculosis-associated immune reconstitution inflammatory syndrome},\n\tvolume = {21},\n\tissn = {1553-7374},\n\turl = {https://dx.plos.org/10.1371/journal.ppat.1013497},\n\tdoi = {10.1371/journal.ppat.1013497},\n\tabstract = {Genetic associations within the human leukocyte antigen (HLA) gene complex and linked genes in TB-IRIS outcomes remains population specific and not well understood. Here, we conducted a study including well characterised HIV-TB coinfected patients with (n = 86) and without (n = 124) TB-IRIS from the randomized, double-blind, prophylactic prednisone trial (PredART study) with HLA, ERAP and KIR genotyping data. We confirmed the association of TB-IRIS with lower CD4 counts pre-ART initiation. We identified nine classical class I and II HLA alleles protective against TB-IRIS, while four alleles were linked to increased risk. Associations ranged from strongly protective (HLA-DQB1*05:01, OR: 0.07, 95\\%CI: 0.02-0.28, Pc {\\textless} 0.001) to strongly risk associated (notably DRB1*01:02, OR: 5.92, 95\\%CI: 1.36-26.7, Pc = 0.028), with conflicting signals at the HLA-DRB1 locus. Conditional regression analysis revealed that residue E71 at the polymorphic position 71 within the HLA-DRB1 peptide-binding groove was critical, and grouping of HLA-DRB1 alleles by the residue at position 71 corresponded with differential TB-IRIS association. In conclusion, this study identifies population-specific genetic factors influencing TB-IRIS susceptibility and highlights a potential mechanistic role for specific HLA-DRB1 residues in modulating immune responses during ART.},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-28},\n\tjournal = {PLOS Pathogens},\n\tauthor = {Choshi, Phuti and Pedretti, Sarah and Chimbetete, Tafadzwa and Gangula, Rama and Shey, Muki and Stek, Cari and Lai, Rachel P. J. and Wilkinson, Robert and Meintjes, Graeme and Phillips, Elizabeth and Peter, Jonny},\n\teditor = {Koup, Richard A.},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {e1013497},\n}\n\n\n\n

\n

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

\n \n\n \n \n \n \n \n \n Addressing infectious diseases in Africa by accelerating drug discovery through data science.\n \n \n \n \n\n\n \n Turon, G.; Hlozek, J.; Duran-Frigola, M.; Chibale, K.; and Woodland, J. G.\n\n\n \n\n\n\n Communications Medicine, 5(1): 498. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Addressing$ Paper\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{turon_addressing_2025,\n\ttitle = {Addressing infectious diseases in {Africa} by accelerating drug discovery through data science},\n\tvolume = {5},\n\tissn = {2730-664X},\n\turl = {https://www.nature.com/articles/s43856-025-01211-z},\n\tdoi = {10.1038/s43856-025-01211-z},\n\tabstract = {Abstract \n            Despite being rich in natural resources and scientific talent, Africa continues to bear a staggering infectious disease burden. Historically, health innovation on the continent has relied on international funding and has been constrained by limited infrastructure and the emigration of skilled professionals. Data science tools offer a promising alternative, typically requiring fewer costly resources than traditional empirical research, with the potential to empower African scientists to generate tangible and impactful health solutions for the continent. Rapid progress in data science is expected to transform infectious disease research; thus, it is encouraging that numerous African initiatives are already applying data science tools to tackling pressing unmet medical needs, particularly in drug discovery. These efforts include identifying novel therapeutic targets, predicting drug-like molecules and their synthesis, enhancing clinical trial success rates and preparing for future disease threats. This review examines the current landscape of data science in infectious disease drug discovery across Africa.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Communications Medicine},\n\tauthor = {Turon, Gemma and Hlozek, Jason and Duran-Frigola, Miquel and Chibale, Kelly and Woodland, John G.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {498},\n}\n\n\n\n

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

\n \n\n \n \n \n \n \n \n Patient and provider preferences for long-acting TB preventive therapy.\n \n \n \n \n\n\n \n Vermeulen, M.; Scarsi, K.; Furl, R.; Sayles, H.; Anderson, M.; Valawalkar, S.; Kadam, A.; Cox, S.; Mave, V.; Barthwal, M.; Schutz, C.; Ward, A.; Dountio Ofimboudem, J.; Meintjes, G.; Rannard, S.; Owen, A.; and Swindells, S.\n\n\n \n\n\n\n IJTLD Open, 2(5): 276–283. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Patient$ Paper\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{vermeulen_patient_2025,\n\ttitle = {Patient and provider preferences for long-acting {TB} preventive therapy},\n\tvolume = {2},\n\tissn = {3005-7590},\n\turl = {https://journals.theunion.org/lookup/doi/10.5588/ijtldopen.24.0670},\n\tdoi = {10.5588/ijtldopen.24.0670},\n\tabstract = {SUMMARY \n             \n              BACKGROUND \n              Tuberculosis preventive therapy (TPT) is critical for TB elimination but is underutilised. Long-acting (LA) TPT can potentially improve linkage to care, treatment adherence and outcomes. \n             \n             \n              METHODS \n              We conducted a cross-sectional in-person survey in two high TB burden countries to evaluate preferences and concerns about LA formulations for TPT. The survey compared oral pills to LA injections, implants, and microarray patches (MAPs). A parallel online survey of healthcare providers (HCPs) in low- and middle-income countries (LMICs) assessed the perceived feasibility of implementation. Data were summarised by descriptive statistics. \n             \n             \n              RESULTS \n               \n                We recruited 409 patients (India, \n                n \n                = 209; South Africa, \n                n \n                = 200) and 94 HCP participants. The mean age of patients was 40 years; 65\\% were female, and 26\\% reported a history of TPT. Injectable LA-TPT was the most preferred modality, followed by pills, implants, and then MAPs. The majority (75\\%) expressed a strong willingness to try injectable LA-TPT. Among providers, 43\\% favoured injectable LA-TPT, 26\\% preferred oral pills, 18\\% implants, and 13\\% MAPs. Cost was a significant factor influencing HCPs’ willingness to adopt LA-TPT, while potential inefficacy and prolonged side effects were the highest concerns of patient respondents. \n               \n             \n             \n              CONCLUSION \n              Injectable LA-TPT may be highly acceptable and feasible if concerns surrounding cost, effectiveness, and safety are addressed.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {IJTLD Open},\n\tauthor = {Vermeulen, M. and Scarsi, K.K. and Furl, R. and Sayles, H. and Anderson, M.J. and Valawalkar, S. and Kadam, A. and Cox, S.R. and Mave, V. and Barthwal, M. and Schutz, C. and Ward, A. and Dountio Ofimboudem, J. and Meintjes, G. and Rannard, S. and Owen, A. and Swindells, S.},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {276--283},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Characterization of Early Viral Populations in Infants Acquiring HIV Through Perinatal and Breastmilk Transmission: A Review of what is Currently Known and the Gaps that Need to be Addressed to Guide Passive HIV Immunization of Breastfeeding Infants.\n \n \n \n \n\n\n \n Giorgi, E. E.; Abrahams, M.; Fouda, G.; John-Stewart, G.; Goga, A.; Mullins, J. I.; Permar, S. R.; Janes, H.; and Martin, T. M.\n\n\n \n\n\n\n Current HIV Research, 23(6): 363–379. November 2025.\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{giorgi_characterization_2025,\n\ttitle = {Characterization of {Early} {Viral} {Populations} in {Infants} {Acquiring} {HIV} {Through} {Perinatal} and {Breastmilk} {Transmission}: {A} {Review} of what is {Currently} {Known} and the {Gaps} that {Need} to be {Addressed} to {Guide} {Passive} {HIV} {Immunization} of {Breastfeeding} {Infants}},\n\tvolume = {23},\n\tissn = {1570162X},\n\tshorttitle = {Characterization of {Early} {Viral} {Populations} in {Infants} {Acquiring} {HIV} {Through} {Perinatal} and {Breastmilk} {Transmission}},\n\turl = {https://www.eurekaselect.com/245021/article},\n\tdoi = {10.2174/011570162X357975250902104402},\n\tabstract = {Newborns represent only 1\\% of the population. Yet, HIV vertical transmissions represent \n10\\% of all new infections globally, even though antiretroviral therapy (ART) has been shown \nto reduce the risk of vertical transmission to less than 2\\%. While vaccines still represent the most \nefficient and cost-effective intervention to eradicate new infections, HIV immunogens that can \neffectively elicit broad-spectrum protection are still at least a decade away. In contrast, passive \nimmunization with broadly neutralizing antibody (bnAb) combinations has the potential to provide \na more immediate pathway to HIV prophylaxis. Early-phase infant trials are underway to \nestablish the safety and pharmacokinetics of bnAb combinations selected for their potency against \nviruses acquired via adult transmissions. However, the specific characteristics and phenotypic \ndifferences of vertically transmitted viruses in infants compared to those in adults remain uncertain, \nincluding their susceptibility to known broadly neutralizing antibodies (bnAbs). We review \nthe current knowledge of vertically transmitted HIV viruses, including their genetics and phenotypic \nfeatures. Differences in immunity between adults and infants lead us to hypothesize that \ndistinct selection and evolutionary pressures act on the virus at the time of transmission and during \nthe early phases of infection, and these may in turn affect the choice of bnAb combinations needed \nfor protection against vertical transmission of HIV.},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {Current HIV Research},\n\tauthor = {Giorgi, Elena E. and Abrahams, Melissa-Rose and Fouda, Genevieve and John-Stewart, Grace and Goga, Ameena and Mullins, James I. and Permar, Sallie R. and Janes, Holly and Martin, Troy M.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {363--379},\n}\n\n\n\n

\n

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

\n \n\n \n \n \n \n \n \n Comparative pangenomics of Streptococcus pneumoniae from Malawi: uncovering genetic variability and pathogenicity.\n \n \n \n \n\n\n \n Iranzadeh, A.; Alisoltani, A.; Kiran, A. M.; Breiman, R. F.; Chaguza, C.; Peno, C.; Cornick, J. E.; Everett, D. B.; and Mulder, N.\n\n\n \n\n\n\n Microbial Genomics, 11(4). April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Comparative$ Paper\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{iranzadeh_comparative_2025,\n\ttitle = {Comparative pangenomics of {Streptococcus} pneumoniae from {Malawi}: uncovering genetic variability and pathogenicity},\n\tvolume = {11},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2057-5858},\n\tshorttitle = {Comparative pangenomics of {Streptococcus} pneumoniae from {Malawi}},\n\turl = {https://www.microbiologyresearch.org/content/journal/mgen/10.1099/mgen.0.001370},\n\tdoi = {10.1099/mgen.0.001370},\n\tabstract = {Streptococcus pneumoniae \n              is a significant cause of bacterial infections, including pneumonia, meningitis and septicemia, primarily affecting children, the elderly and immunocompromised individuals. This study aimed to elucidate the serotype and lineage distribution and molecular mechanisms underlying pneumococcal invasiveness through a comprehensive pangenomic analysis of 1416 isolates from Malawi. Our analysis comprised 810 isolates from asymptomatic carriers and 606 isolates from patients with bacteraemia or meningitis. We identified 58 serotypes, with serotypes 1, 5 and 12F exhibiting significantly higher prevalence among patients. These serotypes likely exhibit reduced nasopharyngeal colonization and demonstrate rapid dissemination to sterile sites. Notably, these serotypes form a distinct lineage with distinct genomic characteristics, including the absence of V-type ATP synthase. The pangenome analysis revealed two highly conserved surface protein complexes, F-type ATP synthase and SecA1-SecY, which deserve further investigation as potential targets for novel therapeutic interventions.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-28},\n\tjournal = {Microbial Genomics},\n\tauthor = {Iranzadeh, Arash and Alisoltani, Arghavan and Kiran, Anmol M. and Breiman, Robert F. and Chaguza, Chrispin and Peno, Chikondi and Cornick, Jennifer E. and Everett, Dean B. and Mulder, Nicola},\n\tmonth = apr,\n\tyear = {2025},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The effect of treatment with a non-ionic surfactant vesicular formulation of sodium stibogluconate on host immune responses and serum metabolites in a murine model of Leishmania donovani.\n \n \n \n \n\n\n \n Aruleba, R. T.; Osero, B. O.; Loots, D. T.; Luies, L.; Cele, Z.; Opare, P. A. A.; Van Reenen, M.; Brombacher, F.; Carter, K. C.; and Hurdayal, R.\n\n\n \n\n\n\n Frontiers in Immunology, 16: 1499513. October 2025.\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{aruleba_effect_2025,\n\ttitle = {The effect of treatment with a non-ionic surfactant vesicular formulation of sodium stibogluconate on host immune responses and serum metabolites in a murine model of {Leishmania} donovani},\n\tvolume = {16},\n\tissn = {1664-3224},\n\turl = {https://www.frontiersin.org/articles/10.3389/fimmu.2025.1499513/full},\n\tdoi = {10.3389/fimmu.2025.1499513},\n\tabstract = {Introduction \n               \n                Visceral leishmaniasis (VL), caused by \n                Leishmania donovani \n                , is associated with parasite-induced immunological and physiological changes that ensure the survival of amastigotes within the host. Both the parasite and the host have nutritional requirements, and for auxotrophic \n                Leishmania \n                , dependence on the host to supply specific growth requirements is essential. This highlights an intricate link between host immunity and metabolism during VL. This study explores the interplay between the host metabolome and immune responses pre- and post-infection and treatment, aiming to identify early metabolite markers of therapeutic success against \n                Leishmania \n                . \n               \n             \n             \n              Methods \n               \n                BALB/c mice infected with \n                L. donovani \n                were divided into cured and non-cured groups based on treatment with a non-ionic surfactant vesicle formulation of sodium stibogluconate (300 mg Sb \n                v \n                /kg, SSG-NIV) or PBS vehicle control. Specific immune responses were determined at day 21 and day 60 post-infection, and serum metabolite levels was measured using untargeted GC×GC-TOFMS metabolomics. \n               \n             \n             \n              Results and discussions \n              Treatment effectively reduced parasite loads, triggering heightened CD4+ and CD8+ T-cell responses at day 21, with increased IFN-γ, IL-12, and IL-4, and decreased IL-10 and TGF-β. Pre-treatment metabolomics analysis identified changes in glycolysis, fatty acid and amino acid metabolism 1-week PI, suggesting an increased Warburg effect to supplement parasite survival and initiation of immune responses. Valine, lactic acid, and glycerol-1-oleate were identified as markers of early infection. Treatment with SSG-NIV altered metabolism of major macromolecules and the TCA cycle relative to non-cured groups. Additionally, glycine and ribitol show promise as immune correlates for antiparasitic therapies. These findings highlight the diagnostic and prognostic potential of serum-derived metabolites in monitoring host immune responses to VL and treatment.},\n\turldate = {2026-05-28},\n\tjournal = {Frontiers in Immunology},\n\tauthor = {Aruleba, Raphael Taiwo and Osero, Bernard Ong’ondo and Loots, Du Toit and Luies, Laneke and Cele, Zama and Opare, Priscilla Abena Ankamaa and Van Reenen, Mari and Brombacher, Frank and Carter, Katharine C. and Hurdayal, Ramona},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {1499513},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Effectiveness and uptake of WhatsApp-based HIV microlearning for healthcare workers in remote South African clinics: A pragmatic, mixed-methods, cluster-randomised trial.\n \n \n \n \n\n\n \n Chisholm, B. S.; Mapahla, L.; Lombard, C.; Blockman, M.; and Orrell, C.\n\n\n \n\n\n\n Nurse Education in Practice, 86: 104326. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Effectiveness$ Paper\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{chisholm_effectiveness_2025,\n\ttitle = {Effectiveness and uptake of {WhatsApp}-based {HIV} microlearning for healthcare workers in remote {South} {African} clinics: {A} pragmatic, mixed-methods, cluster-randomised trial},\n\tvolume = {86},\n\tissn = {14715953},\n\tshorttitle = {Effectiveness and uptake of {WhatsApp}-based {HIV} microlearning for healthcare workers in remote {South} {African} clinics},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1471595325000824},\n\tdoi = {10.1016/j.nepr.2025.104326},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Nurse Education in Practice},\n\tauthor = {Chisholm, Briony Sue and Mapahla, Lovemore and Lombard, Carl and Blockman, Marc and Orrell, Catherine},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {104326},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Quantification of tuberculosis exposure in a high-burdened setting.\n \n \n \n \n\n\n \n Patterson, B.; Hermans, S.; Wood, R.; and Cobelens, F.\n\n\n \n\n\n\n Scientific Reports, 15(1): 22687. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Quantification$ Paper\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{patterson_quantification_2025,\n\ttitle = {Quantification of tuberculosis exposure in a high-burdened setting},\n\tvolume = {15},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-024-81558-w},\n\tdoi = {10.1038/s41598-024-81558-w},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Scientific Reports},\n\tauthor = {Patterson, Benjamin and Hermans, Sabine and Wood, Robin and Cobelens, Frank},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {22687},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n T cell monocyte complexes exhibit distinct immune signatures during infection.\n \n \n \n \n\n\n \n Kang, N.; Chawla, A.; Hillman, H.; Tippalagama, R.; Kim, C.; Mikulski, Z.; McArdle, S.; Seumois, G.; Vijayanand, P.; Scriba, T. J.; De Silva, A. D.; Balmaseda, A.; Harris, E.; Weiskopf, D.; Sette, A.; Arlehamn, C. L.; Peters, B.; and Burel, J. G.\n\n\n \n\n\n\n iScience, 28(9): 113432. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"T$ Paper\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{kang_t_2025,\n\ttitle = {T cell monocyte complexes exhibit distinct immune signatures during infection},\n\tvolume = {28},\n\tissn = {25890042},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2589004225016931},\n\tdoi = {10.1016/j.isci.2025.113432},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-28},\n\tjournal = {iScience},\n\tauthor = {Kang, Ningxin and Chawla, Ashu and Hillman, Hannah and Tippalagama, Rashmi and Kim, Cheryl and Mikulski, Zbigniew and McArdle, Sara and Seumois, Grégory and Vijayanand, Pandurangan and Scriba, Thomas J. and De Silva, Aruna D. and Balmaseda, Angel and Harris, Eva and Weiskopf, Daniela and Sette, Alessandro and Arlehamn, Cecilia Lindestam and Peters, Bjoern and Burel, Julie G.},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {113432},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Virology Africa 2024: a short report.\n \n \n \n \n\n\n \n Rybicki, E. P; Williamson, A.; and Venter, M.\n\n\n \n\n\n\n The Lancet Microbe, 6(6): 101093. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Virology$ Paper\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{rybicki_virology_2025,\n\ttitle = {Virology {Africa} 2024: a short report},\n\tvolume = {6},\n\tissn = {26665247},\n\tshorttitle = {Virology {Africa} 2024},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524725000217},\n\tdoi = {10.1016/j.lanmic.2025.101093},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Rybicki, Edward P and Williamson, Anna-Lise and Venter, Marietjie},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {101093},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Oral Regimens for Rifampin-Resistant, Fluoroquinolone-Susceptible Tuberculosis.\n \n \n \n \n\n\n \n Guglielmetti, L.; Khan, U.; Velásquez, G. E.; Gouillou, M.; Abubakirov, A.; Baudin, E.; Berikova, E.; Berry, C.; Bonnet, M.; Cellamare, M.; Chavan, V.; Cox, V.; Dakenova, Z.; De Jong, B. C.; Ferlazzo, G.; Karabayev, A.; Kirakosyan, O.; Kiria, N.; Kunda, M.; Lachenal, N.; Lecca, L.; McIlleron, H.; Motta, I.; Toscano, S. M.; Mushtaque, H.; Nahid, P.; Oyewusi, L.; Panda, S.; Patil, S.; Phillips, P. P. J.; Ruiz, J.; Salahuddin, N.; Garavito, E. S.; Seung, K. J.; Ticona, E.; Trippa, L.; Vasquez, D. E. V.; Wasserman, S.; Rich, M. L.; Varaine, F.; and Mitnick, C. D.\n\n\n \n\n\n\n New England Journal of Medicine, 392(5): 468–482. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Oral$ Paper\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{guglielmetti_oral_2025,\n\ttitle = {Oral {Regimens} for {Rifampin}-{Resistant}, {Fluoroquinolone}-{Susceptible} {Tuberculosis}},\n\tvolume = {392},\n\tcopyright = {http://www.nejmgroup.org/legal/terms-of-use.htm},\n\tissn = {0028-4793, 1533-4406},\n\turl = {http://www.nejm.org/doi/10.1056/NEJMoa2400327},\n\tdoi = {10.1056/NEJMoa2400327},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {New England Journal of Medicine},\n\tauthor = {Guglielmetti, Lorenzo and Khan, Uzma and Velásquez, Gustavo E. and Gouillou, Maelenn and Abubakirov, Amanzhan and Baudin, Elisabeth and Berikova, Elmira and Berry, Catherine and Bonnet, Maryline and Cellamare, Matteo and Chavan, Vijay and Cox, Vivian and Dakenova, Zhanna and De Jong, Bouke Catherine and Ferlazzo, Gabriella and Karabayev, Aydarkhan and Kirakosyan, Ohanna and Kiria, Nana and Kunda, Mikanda and Lachenal, Nathalie and Lecca, Leonid and McIlleron, Helen and Motta, Ilaria and Toscano, Sergio Mucching and Mushtaque, Hebah and Nahid, Payam and Oyewusi, Lawrence and Panda, Samiran and Patil, Sandip and Phillips, Patrick P. J. and Ruiz, Jimena and Salahuddin, Naseem and Garavito, Epifanio Sanchez and Seung, Kwonjune J. and Ticona, Eduardo and Trippa, Lorenzo and Vasquez, Dante E. Vargas and Wasserman, Sean and Rich, Michael L. and Varaine, Francis and Mitnick, Carole D.},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {468--482},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Sample size efficiency of restricting participation in tuberculosis vaccine trials to interferon-gamma release assay-positive participants.\n \n \n \n \n\n\n \n Cobelens, F.; Pelzer, P. T.; Churchyard, G. J.; Garcia-Basteiro, A.; Hatherill, M.; Hill, P. C.; Martinez, L.; and White, R. G.\n\n\n \n\n\n\n Vaccine, 61: 127301. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Sample$ Paper\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{cobelens_sample_2025,\n\ttitle = {Sample size efficiency of restricting participation in tuberculosis vaccine trials to interferon-gamma release assay-positive participants},\n\tvolume = {61},\n\tissn = {0264410X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0264410X25005985},\n\tdoi = {10.1016/j.vaccine.2025.127301},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Vaccine},\n\tauthor = {Cobelens, Frank and Pelzer, Puck T. and Churchyard, Gavin J. and Garcia-Basteiro, Alberto and Hatherill, Mark and Hill, Philip C. and Martinez, Leonardo and White, Richard G.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {127301},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n A One Health approach to bovine coronavirus vaccine development, using LSDV as a live virus vector.\n \n \n \n \n\n\n \n Chineka, N.; Whittle, L.; Douglass, N.; Williamson, A.; and Chapman, R.\n\n\n \n\n\n\n Human Vaccines & Immunotherapeutics, 21(1): 2480891. December 2025.\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{chineka_one_2025,\n\ttitle = {A {One} {Health} approach to bovine coronavirus vaccine development, using {LSDV} as a live virus vector},\n\tvolume = {21},\n\tissn = {2164-5515, 2164-554X},\n\turl = {https://www.tandfonline.com/doi/full/10.1080/21645515.2025.2480891},\n\tdoi = {10.1080/21645515.2025.2480891},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Human Vaccines \\& Immunotherapeutics},\n\tauthor = {Chineka, Nicole and Whittle, Leah and Douglass, Nicola and Williamson, Anna-Lise and Chapman, Ros},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {2480891},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Strategic positioning of immunization at the heart of Africa’s health and development agenda.\n \n \n \n \n\n\n \n Wiysonge, C. S.; Ndwandwe, D.; Iwu-Jaja, C.; Nnaji, C. A.; Machingaidze, S.; Adamu, A. A.; Bita Fouda, A. A.; and Hussey, G. D.\n\n\n \n\n\n\n Human Vaccines & Immunotherapeutics, 21(1): 2599628. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Strategic$ Paper\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{wiysonge_strategic_2025,\n\ttitle = {Strategic positioning of immunization at the heart of {Africa}’s health and development agenda},\n\tvolume = {21},\n\tissn = {2164-5515, 2164-554X},\n\turl = {https://www.tandfonline.com/doi/full/10.1080/21645515.2025.2599628},\n\tdoi = {10.1080/21645515.2025.2599628},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Human Vaccines \\& Immunotherapeutics},\n\tauthor = {Wiysonge, Charles S. and Ndwandwe, Duduzile and Iwu-Jaja, Chinwe and Nnaji, Chukwudi A. and Machingaidze, Shingai and Adamu, Abdu A. and Bita Fouda, Andre Arsene and Hussey, Gregory D.},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {2599628},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Novel Inhibitors of Plasmodium Phosphatidylinositol 4-kinase IIIβ with Low Propensity for Resistance: Life Cycle Stage Activity and In Vivo Efficacy in a Humanized Mouse Malaria Infection Model.\n \n \n \n \n\n\n \n Dziwornu, G. A.; Mmonwa, M. M.; Coertzen, D.; Krugmann, L.; Salomane, N.; Leshabane, M.; Thomas, J.; Da Rocha, S.; Reader, J.; Masike, K.; Njoroge, M.; Sevilleno, N.; Coyle, R.; Boonyalai, N.; Mayville, E.; Lee, M. C. S.; Fidock, D. A.; Coulson, L. B.; Woodland, J. G.; Wicht, K. J.; Ghorpade, S. R.; Birkholtz, L.; and Chibale, K.\n\n\n \n\n\n\n Journal of Medicinal Chemistry, 68(16): 17736–17751. August 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{dziwornu_novel_2025,\n\ttitle = {Novel {Inhibitors} of \\textit{{Plasmodium}} {Phosphatidylinositol} 4-kinase {IIIβ} with {Low} {Propensity} for {Resistance}: {Life} {Cycle} {Stage} {Activity} and \\textit{{In} {Vivo}} {Efficacy} in a {Humanized} {Mouse} {Malaria} {Infection} {Model}},\n\tvolume = {68},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0022-2623, 1520-4804},\n\tshorttitle = {Novel {Inhibitors} of \\textit{{Plasmodium}} {Phosphatidylinositol} 4-kinase {IIIβ} with {Low} {Propensity} for {Resistance}},\n\turl = {https://pubs.acs.org/doi/10.1021/acs.jmedchem.5c01417},\n\tdoi = {10.1021/acs.jmedchem.5c01417},\n\tlanguage = {en},\n\tnumber = {16},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Medicinal Chemistry},\n\tauthor = {Dziwornu, Godwin A. and Mmonwa, Mmakwena M. and Coertzen, Dina and Krugmann, Liezl and Salomane, Nicolaas and Leshabane, Meta and Thomas, Jean and Da Rocha, Shante and Reader, Janette and Masike, Keabetswe and Njoroge, Mathew and Sevilleno, Nicole and Coyle, Rachael and Boonyalai, Nonlawat and Mayville, Emily and Lee, Marcus C. S. and Fidock, David A. and Coulson, Lauren B. and Woodland, John G. and Wicht, Kathryn J. and Ghorpade, Sandeep R. and Birkholtz, Lyn-Marié and Chibale, Kelly},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {17736--17751},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n The Kinetics of Bedaquiline Diffusion in Tuberculous Cavities Open a Window for the Emergence of Resistance.\n \n \n \n \n\n\n \n Bustion, A. E; Ernest, J. P; Kaya, F.; Silva, C.; Sarathy, J.; Blanc, L.; Imperial, M.; Gengenbacher, M.; Xie, M.; Zimmerman, M. D; Robertson, G. T; Weiner, D.; Via, L. E; Barry, C. E; Savic, R. M; and Dartois, V.\n\n\n \n\n\n\n The Journal of Infectious Diseases, 232(3): e431–e441. September 2025.\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{bustion_kinetics_2025,\n\ttitle = {The {Kinetics} of {Bedaquiline} {Diffusion} in {Tuberculous} {Cavities} {Open} a {Window} for the {Emergence} of {Resistance}},\n\tvolume = {232},\n\tcopyright = {https://creativecommons.org/licenses/by-nc-nd/4.0/},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/232/3/e431/8156692},\n\tdoi = {10.1093/infdis/jiaf303},\n\tabstract = {Abstract \n             \n              Background \n              Cavitary tuberculosis is difficult to cure and constitutes a site of relapse. Bedaquiline has been a wonder drug in the treatment of multidrug-resistant tuberculosis, but emergence of resistance threatens the sustainability of its success. We designed site-of-disease pharmacokinetic studies to spatially resolve the penetration of bedaquiline, and 2 next-generation diarylquinolines, TBAJ876 and TBAJ587, in cavities. \n             \n             \n              Methods \n              Rabbits with established cavitary tuberculosis received the study drugs. A laser-capture microdissections scheme was developed to measure drug concentrations as a function of distance from blood supply in caseum. To simulate drug coverage in patient cavities, the data were modeled, and parameter estimates were linked to clinical plasma pharmacokinetic models. \n             \n             \n              Results \n              Pharmacokinetic-pharmacodynamic simulations in caseum revealed that bedaquiline reaches steady state and efficacious concentrations in deep caseum after several weeks to months and lingers at subtherapeutic concentrations up to 3 years after therapy ends. TBAJ876 and TBAJ587, achieve bactericidal concentrations in caseum layers more rapidly and shorten the window of suboptimal concentrations post treatment compared to bedaquiline. \n             \n             \n              Conclusions \n              The slow kinetics of diffusion of bedaquiline into and out of caseum creates spatiotemporal windows of subtherapeutic concentrations. Site-of-disease simulations of TBAJ587 and TBAJ876 predict reduced opportunities for resistance development.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Bustion, Annamarie E and Ernest, Jacqueline P and Kaya, Firat and Silva, Connie and Sarathy, Jansy and Blanc, Landry and Imperial, Marjorie and Gengenbacher, Martin and Xie, Min and Zimmerman, Matthew D and Robertson, Gregory T and Weiner, Danielle and Via, Laura E and Barry, Clifton E and Savic, Radojka M and Dartois, Véronique},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {e431--e441},\n}\n\n\n\n

\n

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

\n \n\n \n \n \n \n \n \n Distinct dysregulated pathways in sporadic and Lynch syndrome‐associated colorectal cancer offer insights for targeted treatment.\n \n \n \n \n\n\n \n Krause, M. J.; Sinkala, M.; and Ramesar, R.\n\n\n \n\n\n\n FEBS Letters, 599(7): 1006–1028. April 2025.\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 abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{krause_distinct_2025,\n\ttitle = {Distinct dysregulated pathways in sporadic and {Lynch} syndrome‐associated colorectal cancer offer insights for targeted treatment},\n\tvolume = {599},\n\tissn = {0014-5793, 1873-3468},\n\turl = {https://febs.onlinelibrary.wiley.com/doi/10.1002/1873-3468.70010},\n\tdoi = {10.1002/1873-3468.70010},\n\tabstract = {Lynch syndrome (LS) is a hereditary disorder that increases the risk of colorectal cancer (CRC) due to constitutional pathogenic variants in mismatch repair (MMR) genes. When coupled with somatic mutations in the same gene, MMR deficiency occurs. However, the mechanisms driving cancer development remain unclear. This study aimed to identify distinct molecular drivers in LS‐associated and sporadic CRC. We found that PI3K–Akt signalling is dysregulated in LS‐associated CRC, while Wnt signalling predominates in sporadic CRC. Moreover, our findings highlight the therapeutic potential of PI3K–Akt pathway inhibitors, such as taselisib, for LS‐associated CRC patients with high pathway dependency. Similarly, Wnt signalling pathway inhibitors, such as XAV939, offer a promising therapeutic approach for sporadic CRC. These findings underscore the importance of understanding the biological basis of disease for developing targeted therapies tailored to CRC subtype‐specific oncogenic pathways.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-28},\n\tjournal = {FEBS Letters},\n\tauthor = {Krause, May J. and Sinkala, Musalula and Ramesar, Raj},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {1006--1028},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Proceedings from the Third International Post-Tuberculosis Symposium: expanding the circle.\n \n \n \n \n\n\n \n Allwood, B.; Auld, S.; Beko, B.; Bisson, G.; Borges De Almeida, C.; Byrne, A.; Chow, F.; Davis, A.; Defres, S.; Drage, M.; Evans, D.; Gai, X.; Günther, G.; Gupte, A.; Hoddinott, G.; Huaman, M.; Huddart, S.; Huynh, J.; Kalyatanda, G.; Khosa, C.; Kutadza, T.; Makanda, G.; Marais, S.; Meghji, J.; Navuluri, N.; Nkereuwem, E.; Rajaratnam, A.; Romanowski, K.; Schoeman, I.; Seddon, J.; Sohn, H.; Thienemann, F.; Wademan, D.; Walker, N.; Van Der Zalm, M.; and Nightingale, R.\n\n\n \n\n\n\n IJTLD Open, 2(12): 727–738. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Proceedings$ Paper\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{allwood_proceedings_2025,\n\ttitle = {Proceedings from the {Third} {International} {Post}-{Tuberculosis} {Symposium}: expanding the circle},\n\tvolume = {2},\n\tissn = {3005-7590},\n\tshorttitle = {Proceedings from the {Third} {International} {Post}-{Tuberculosis} {Symposium}},\n\turl = {https://journals.theunion.org/lookup/doi/10.5588/ijtldopen.25.0637},\n\tdoi = {10.5588/ijtldopen.25.0637},\n\tabstract = {SUMMARY \n            In light of the recent growth in interest and knowledge of post-TB sequelae, there were high levels of engagement during the 3rd International Post-Tuberculosis Symposium held in Stellenbosch, South Africa. This multi-disciplinary symposium aimed to: 1) Advocate for greater global awareness of post-TB sequelae and empower TB-affected communities; 2) Advance knowledge by sharing current evidence and identifying key priorities; 3) Foster collaborations by strengthening research networks and developing concrete plans for research driven advocacy; and 4) Advance the field by establishing areas of consensus around diagnosis, care, and management. Guided by a 14-member Steering Committee, 9 academic working groups came together to develop key content for plenary sessions and facilitated workshops related to: Patient Engagement, Epidemiology and Modelling, Pathogenesis, Post-TB Lung Disease; Cardiovascular and Pulmonary Vascular Disease; Central Nervous System and Musculoskeletal Disease; Paediatrics Economic; Social and Psychological Sequelae; and Advocacy, Policy, and Stakeholder Engagement. Each group outlined progress within their respective fields and defined key priorities to focus discussion. The Symposium further catalysed coordinated action for the post-TB community of patients, advocates, clinicians, and researchers to define a clear path towards improving outcomes, reducing inequities, and ensuring TB survivors receive the care and support they deserve.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2026-05-28},\n\tjournal = {IJTLD Open},\n\tauthor = {Allwood, B.W. and Auld, S.C. and Beko, B. and Bisson, G.P. and Borges De Almeida, C.P. and Byrne, A. and Chow, F.C. and Davis, A. and Defres, S. and Drage, M. and Evans, D. and Gai, X. and Günther, G. and Gupte, A.N. and Hoddinott, G. and Huaman, M.A. and Huddart, S. and Huynh, J. and Kalyatanda, G. and Khosa, C. and Kutadza, T. and Makanda, G. and Marais, S. and Meghji, J. and Navuluri, N. and Nkereuwem, E. and Rajaratnam, A. and Romanowski, K. and Schoeman, I. and Seddon, J.A. and Sohn, H. and Thienemann, F. and Wademan, D.T. and Walker, N.F. and Van Der Zalm, M.M. and Nightingale, R.},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {727--738},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Scaling-up symptom-agnostic, community-wide screening toward global tuberculosis elimination: opportunities, challenges, and lessons from history.\n \n \n \n \n\n\n \n Esmail, H.; Miller, C.; Falzon, D.; De Vries, G.; Chijioke-Akaniro, O.; Horton, K. C.; Kohli, M.; Dharmapuri Vachaspathi, T.; Vo, L. N.; Zaidi, S. M.; Squire, S. B.; Coussens, A. K.; and Houben, R. M.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 155: 107875. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Scaling-up$ Paper\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{esmail_scaling-up_2025,\n\ttitle = {Scaling-up symptom-agnostic, community-wide screening toward global tuberculosis elimination: opportunities, challenges, and lessons from history},\n\tvolume = {155},\n\tissn = {12019712},\n\tshorttitle = {Scaling-up symptom-agnostic, community-wide screening toward global tuberculosis elimination},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971225000980},\n\tdoi = {10.1016/j.ijid.2025.107875},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Esmail, Hanif and Miller, Cecily and Falzon, Dennis and De Vries, Gerard and Chijioke-Akaniro, Obioma and Horton, Katherine C. and Kohli, Mikashmi and Dharmapuri Vachaspathi, Tejaswini and Vo, Luan N.Q. and Zaidi, Syed M.A. and Squire, S. Bertel and Coussens, Anna K. and Houben, Rein M.G.J.},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {107875},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Hyperspectral Imaging for the Diagnosis of Latent Tuberculosis Infection.\n \n \n \n \n\n\n \n Oladokun, A. S.; Malila, B.; Shey, M.; and Mutsvangwa, T.\n\n\n \n\n\n\n In Bajaj, A.; and Abraham, A., editor(s), Computational Intelligence Based Hyperspectral Image Analysis and Applications, volume 269, pages 1–48. Springer Nature Switzerland, Cham, 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Hyperspectral$ Paper\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{bajaj_hyperspectral_2025,\n\taddress = {Cham},\n\ttitle = {Hyperspectral {Imaging} for the {Diagnosis} of {Latent} {Tuberculosis} {Infection}},\n\tvolume = {269},\n\tisbn = {9783031831263 9783031831270},\n\turl = {https://link.springer.com/10.1007/978-3-031-83127-0_1},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tbooktitle = {Computational {Intelligence} {Based} {Hyperspectral} {Image} {Analysis} and {Applications}},\n\tpublisher = {Springer Nature Switzerland},\n\tauthor = {Oladokun, Ajibola S. and Malila, Bessie and Shey, Muki and Mutsvangwa, Tinashe},\n\teditor = {Bajaj, Anu and Abraham, Ajith},\n\tyear = {2025},\n\tdoi = {10.1007/978-3-031-83127-0_1},\n\tpages = {1--48},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n CYP1A2 contributes to the metabolism of mefloquine: Exploration using in vitro metabolism and physiologically-based pharmacokinetic modelling.\n \n \n \n \n\n\n \n Cloete, C. K.; Govender, P.; Njuguna, N.; Parrott, N. J.; Umehara, K.; Chibale, K.; and Njoroge, M.\n\n\n \n\n\n\n Drug Metabolism and Disposition, 53(4): 100060. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"CYP1A2$ Paper\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{cloete_cyp1a2_2025,\n\ttitle = {{CYP1A2} contributes to the metabolism of mefloquine: {Exploration} using in vitro metabolism and physiologically-based pharmacokinetic modelling},\n\tvolume = {53},\n\tissn = {00909556},\n\tshorttitle = {{CYP1A2} contributes to the metabolism of mefloquine},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0090955625090695},\n\tdoi = {10.1016/j.dmd.2025.100060},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-28},\n\tjournal = {Drug Metabolism and Disposition},\n\tauthor = {Cloete, Cleavon K. and Govender, Preshendren and Njuguna, Nicholas and Parrott, Neil J. and Umehara, Kenichi and Chibale, Kelly and Njoroge, Mathew},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {100060},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n In vitro anti-tumor activities of a novel recombinant immunotoxin targeting differentially overexpressed Leucine-rich repeat-containing G-protein-coupled receptor 5 in cervical cancer.\n \n \n \n \n\n\n \n Henry, M.; Ngwegya, T.; Lekena, N.; and Barth, S.\n\n\n \n\n\n\n Immunopharmacology and Immunotoxicology, 47(4): 450–459. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"<i>In$ 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{henry_vitro_2025,\n\ttitle = {\\textit{{In} vitro} anti-tumor activities of a novel recombinant immunotoxin targeting differentially overexpressed {Leucine}-rich repeat-containing {G}-protein-coupled receptor 5 in cervical cancer},\n\tvolume = {47},\n\tissn = {0892-3973, 1532-2513},\n\turl = {https://www.tandfonline.com/doi/full/10.1080/08923973.2025.2504904},\n\tdoi = {10.1080/08923973.2025.2504904},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-28},\n\tjournal = {Immunopharmacology and Immunotoxicology},\n\tauthor = {Henry, Marc and Ngwegya, Takunda and Lekena, Nkhasi and Barth, Stefan},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {450--459},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Association between HIV-1 Nef-mediated MHC-I downregulation and the maintenance of the replication-competent latent viral reservoir in individuals with virally suppressed HIV-1 in Uganda: an exploratory cohort study.\n \n \n \n \n\n\n \n Mumby, M. J; Prodger, J. L; Hackman, J.; Saraf, S.; Zhu, X.; Ferreira, R.; Tomusange, S.; Jamiru, S.; Anok, A.; Kityamuweesi, T.; Buule, P.; Fink, C.; Edgar, C. R; Trothen, S. M; Dekaban, G. A; Brown, E. E; Capoferri, A. A; Baker, O. R; Klock, E.; Miller, J. C; Kirby, C.; Lynch, B.; Tobian, A. A R; Poon, A. F Y; Quinn, T. C; Galiwango, R. M; Reynolds, S. J; Redd, A. D; and Dikeakos, J. D\n\n\n \n\n\n\n The Lancet Microbe, 6(5): 101018. May 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{mumby_association_2025,\n\ttitle = {Association between {HIV}-1 {Nef}-mediated {MHC}-{I} downregulation and the maintenance of the replication-competent latent viral reservoir in individuals with virally suppressed {HIV}-1 in {Uganda}: an exploratory cohort study},\n\tvolume = {6},\n\tissn = {26665247},\n\tshorttitle = {Association between {HIV}-1 {Nef}-mediated {MHC}-{I} downregulation and the maintenance of the replication-competent latent viral reservoir in individuals with virally suppressed {HIV}-1 in {Uganda}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524724002866},\n\tdoi = {10.1016/j.lanmic.2024.101018},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Mumby, Mitchell J and Prodger, Jessica L and Hackman, Jada and Saraf, Sharada and Zhu, Xianming and Ferreira, Roux-Cil and Tomusange, Stephen and Jamiru, Samiri and Anok, Aggrey and Kityamuweesi, Taddeo and Buule, Paul and Fink, Corby and Edgar, Cassandra R and Trothen, Steven M and Dekaban, Gregory A and Brown, Erin E and Capoferri, Adam A and Baker, Owen R and Klock, Ethan and Miller, Jernelle C and Kirby, Charles and Lynch, Briana and Tobian, Aaron A R and Poon, Art F Y and Quinn, Thomas C and Galiwango, Ronald M and Reynolds, Steven J and Redd, Andrew D and Dikeakos, Jimmy D},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {101018},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Chemistry as a Catalyst for Transforming the Health and Wealth of South Africa.\n \n \n \n \n\n\n \n Veale, C. G. L.; Woodland, J. G.; Wicht, K. J.; and Chibale, K.\n\n\n \n\n\n\n Angewandte Chemie International Edition, 64(12): e202419681. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Chemistry$ Paper\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{veale_chemistry_2025,\n\ttitle = {Chemistry as a {Catalyst} for {Transforming} the {Health} and {Wealth} of {South} {Africa}},\n\tvolume = {64},\n\tissn = {1433-7851, 1521-3773},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/anie.202419681},\n\tdoi = {10.1002/anie.202419681},\n\tabstract = {Abstract \n            South Africa's rich natural resources remain a key driver of its chemical industrialisation but are tainted and constrained by its complex colonial history. Thirty years since the advent of democracy in South Africa, deep sociopolitical inequalities are amplified by an intolerable infectious disease burden amongst disadvantaged communities. In that respect, South Africa shares challenges with many other nations in the Global South; there are limited opportunities for the economic development and growth needed to uplift all strata of society. This Viewpoint examines the role of the chemical sciences in South Africa's unique history and the current state of its academic and industrial sectors, with a focus on the intersection of chemistry, healthcare and biomedical research. We argue that the opportunities offered through chemistry research and development, including local manufacturing, should be exploited and that scientific advancements should be tailored to and integrated with the socioeconomic realities of South Africa for an effective and multidisciplinary approach to improving healthcare outcomes. This Viewpoint aims to inspire a renewed focus on the pivotal role of chemical scientists and their broader societal contributions to combating the country's infectious disease burden and shaping a healthier future for South Africa.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2026-05-28},\n\tjournal = {Angewandte Chemie International Edition},\n\tauthor = {Veale, Clinton G. L. and Woodland, John G. and Wicht, Kathryn J. and Chibale, Kelly},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {e202419681},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Clinical epidemiology, genetic diversity, and drug susceptibility patterns by whole genome sequencing of Mycobacterium tuberculosis complex isolates in Gabon from 2012 to 2022.\n \n \n \n \n\n\n \n Adegbite, B. R.; Dreyer, V.; Agbo, J. B.; Mevyann, R. C.; Mfoumbi, G. A.; Ndanga, M. E.; Biyogho, C. M.; Edoa, J. R.; M'Baidiguim, F. B.; Ndong, A. R. O.; Alabi, A. S.; Kremsner, P. G.; Adegnika, A. A.; Niemann, S.; and Grobusch, M. P.\n\n\n \n\n\n\n IJID Regions, 14: 100501. March 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{adegbite_clinical_2025,\n\ttitle = {Clinical epidemiology, genetic diversity, and drug susceptibility patterns by whole genome sequencing of {Mycobacterium} tuberculosis complex isolates in {Gabon} from 2012 to 2022},\n\tvolume = {14},\n\tissn = {27727076},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S277270762400170X},\n\tdoi = {10.1016/j.ijregi.2024.100501},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {IJID Regions},\n\tauthor = {Adegbite, Bayode R. and Dreyer, Viola and Agbo, Jabar B.P.A.A. and Mevyann, Rhett C. and Mfoumbi, Guy A.R.I. and Ndanga, Micheska E.D. and Biyogho, Christopher M. and Edoa, Jean R. and M'Baidiguim, Fabrice Beral and Ndong, Andréa R.O. Obele and Alabi, Abraham S. and Kremsner, Peter G. and Adegnika, Ayola A. and Niemann, Stefan and Grobusch, Martin P.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {100501},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Authors’ reply “Lessons from tuberculosis history”.\n \n \n \n \n\n\n \n De Vries, G.; Houben, R. M.; and Esmail, H.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 158: 107977. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Authors’$ Paper\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{de_vries_authors_2025,\n\ttitle = {Authors’ reply “{Lessons} from tuberculosis history”},\n\tvolume = {158},\n\tissn = {12019712},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971225002012},\n\tdoi = {10.1016/j.ijid.2025.107977},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {De Vries, Gerard and Houben, Rein M.G.J. and Esmail, Hanif},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {107977},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Household economic impact of HIV‐associated cryptococcal meningitis in five countries in Southern and Eastern Africa.\n \n \n \n \n\n\n \n Lawrence, D. S.; Muthoga, C.; Adams, J.; Ndweni, A. B.; Boulware, D. R.; Chawinga, C.; Comins, K.; Dziwani, E. N.; Hlupeni, A.; Hosseinipour, M. C.; Jjunju, S.; Kanyama, C.; Leeme, T. B.; Meintjes, G.; Meya, D. B.; Mosepele, M.; Moyo, M.; Mwandumba, H. C.; Muzoora, C.; Ndhlovu, C. E.; Nuwagira, E.; Schutz, C.; Tugume, L.; Williams, D.; Molloy, S. F.; Boyer‐Chammard, T.; Youssouf, N.; Jaffar, S.; Niessen, L. W.; Harrison, T. S.; Cunnama, L.; Jarvis, J. N.; and the AMBITION Study Group\n\n\n \n\n\n\n Journal of the International AIDS Society, 28(6): e26441. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Household$ Paper\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{lawrence_household_2025,\n\ttitle = {Household economic impact of {HIV}‐associated cryptococcal meningitis in five countries in {Southern} and {Eastern} {Africa}},\n\tvolume = {28},\n\tissn = {1758-2652, 1758-2652},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.26441},\n\tdoi = {10.1002/jia2.26441},\n\tabstract = {Abstract \n             \n              Introduction \n              HIV‐associated cryptococcal meningitis is the second leading cause of AIDS‐related mortality. Cryptococcal meningitis is a poverty‐related disease and the majority of cases occur in settings where resources are limited and access to quality care is often linked to an individual's ability to pay for services. We have previously demonstrated the efficacy, safety and cost‐effectiveness of a single, high‐dose liposomal amphotericin‐based treatment regimen within the AMBITION‐cm trial. Here, we present a five‐country, within‐trial analysis exploring the household economic impact of cryptococcal meningitis. \n             \n             \n              Methods \n              Eight hundred and ten participants were recruited into this sub‐study in Botswana, Malawi, South Africa, Uganda and Zimbabwe between January 2018 and February 2021. We collected data on annual household expenditure, direct costs and indirect costs incurred prior to enrolment and during the 10‐week trial period. Costs were inflated and converted to 2022 USD. We calculated out‐of‐pocket expenditure, lost income and catastrophic healthcare expenditure, defined as costs exceeding 20\\% of annual household expenditure. \n             \n             \n              Results \n              The average total out‐of‐pocket expenditure plus lost income prior to enrolment was \\$132 and 17.9\\% (145/810, 95\\% CI 15.3–20.5) of participant households had already experienced catastrophic healthcare expenditure. Among the 592 surviving participants, when combining out‐of‐pocket expenditure and lost income, the average cost was \\$516 and 29.1\\% of annual household expenditure across all countries, ranging from \\$230 (7.6\\%) in South Africa to \\$592 (64.2\\%) in Zimbabwe. More than half (296/581, 51.0\\%, 95\\% CI 46.9–55.0) of households experienced catastrophic healthcare expenditure by the end of the trial, ranging from 16.0\\% (13/81, 95\\% CI 7.9–24.2) in South Africa to 68.1\\% (156/229, 95\\% CI 62.0–74.2) in Uganda. \n             \n             \n              Conclusions \n              This is the first study exploring the household economic impact experienced by those diagnosed with cryptococcal meningitis. The household economic impact of cryptococcal meningitis is high and more than half of households of individuals who survive experience catastrophic healthcare expenditure. It is likely these figures are higher outside of the research setting. This highlights the profound financial impact of this devastating infection and provides a rationale to offer financial and social protection to those affected. \n             \n             \n              Trial Registration Number \n              ISRCTN72509687},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {Journal of the International AIDS Society},\n\tauthor = {Lawrence, David S. and Muthoga, Charles and Adams, Jack and Ndweni, Antoinette Buhle and Boulware, David R. and Chawinga, Chimwemwe and Comins, Kyla and Dziwani, Eltas N. and Hlupeni, Admire and Hosseinipour, Mina C. and Jjunju, Samuel and Kanyama, Cecilia and Leeme, Tshepo B. and Meintjes, Graeme and Meya, David B. and Mosepele, Mosepele and Moyo, Melanie and Mwandumba, Henry C. and Muzoora, Conrad and Ndhlovu, Chiratidzo E. and Nuwagira, Edwin and Schutz, Charlotte and Tugume, Lillian and Williams, Darlisha and Molloy, Síle F. and Boyer‐Chammard, Timothée and Youssouf, Nabila and Jaffar, Shabbar and Niessen, Louis W. and Harrison, Thomas S. and Cunnama, Lucy and Jarvis, Joseph N. and {the AMBITION Study Group}},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {e26441},\n}\n\n\n\n

\n

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\n Abstract Introduction HIV‐associated cryptococcal meningitis is the second leading cause of AIDS‐related mortality. Cryptococcal meningitis is a poverty‐related disease and the majority of cases occur in settings where resources are limited and access to quality care is often linked to an individual's ability to pay for services. We have previously demonstrated the efficacy, safety and cost‐effectiveness of a single, high‐dose liposomal amphotericin‐based treatment regimen within the AMBITION‐cm trial. Here, we present a five‐country, within‐trial analysis exploring the household economic impact of cryptococcal meningitis. Methods Eight hundred and ten participants were recruited into this sub‐study in Botswana, Malawi, South Africa, Uganda and Zimbabwe between January 2018 and February 2021. We collected data on annual household expenditure, direct costs and indirect costs incurred prior to enrolment and during the 10‐week trial period. Costs were inflated and converted to 2022 USD. We calculated out‐of‐pocket expenditure, lost income and catastrophic healthcare expenditure, defined as costs exceeding 20% of annual household expenditure. Results The average total out‐of‐pocket expenditure plus lost income prior to enrolment was $132 and 17.9% (145/810, 95% CI 15.3–20.5) of participant households had already experienced catastrophic healthcare expenditure. Among the 592 surviving participants, when combining out‐of‐pocket expenditure and lost income, the average cost was $516 and 29.1% of annual household expenditure across all countries, ranging from $230 (7.6%) in South Africa to $592 (64.2%) in Zimbabwe. More than half (296/581, 51.0%, 95% CI 46.9–55.0) of households experienced catastrophic healthcare expenditure by the end of the trial, ranging from 16.0% (13/81, 95% CI 7.9–24.2) in South Africa to 68.1% (156/229, 95% CI 62.0–74.2) in Uganda. Conclusions This is the first study exploring the household economic impact experienced by those diagnosed with cryptococcal meningitis. The household economic impact of cryptococcal meningitis is high and more than half of households of individuals who survive experience catastrophic healthcare expenditure. It is likely these figures are higher outside of the research setting. This highlights the profound financial impact of this devastating infection and provides a rationale to offer financial and social protection to those affected. Trial Registration Number ISRCTN72509687\n

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\n \n\n \n \n \n \n \n \n Maximizing Potential: Academic–Industry Collaborations in Drug Discovery.\n \n \n \n \n\n\n \n Winks, S.; Reinhard-Rupp, J.; and Chibale, K.\n\n\n \n\n\n\n ACS Medicinal Chemistry Letters, 16(8): 1452–1455. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Maximizing$ Paper\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{winks_maximizing_2025,\n\ttitle = {Maximizing {Potential}: {Academic}–{Industry} {Collaborations} in {Drug} {Discovery}},\n\tvolume = {16},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1948-5875, 1948-5875},\n\tshorttitle = {Maximizing {Potential}},\n\turl = {https://pubs.acs.org/doi/10.1021/acsmedchemlett.5c00331},\n\tdoi = {10.1021/acsmedchemlett.5c00331},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-28},\n\tjournal = {ACS Medicinal Chemistry Letters},\n\tauthor = {Winks, Susan and Reinhard-Rupp, Jutta and Chibale, Kelly},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {1452--1455},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Taxes for tuberculosis: could tobacco and sugar tax revenue fund tuberculosis control interventions?.\n \n \n \n \n\n\n \n Coleman, M.; Coussens, A. K; Calderwood, C. J.; Schoeman, I.; Bhargava, M.; Sinha, P.; Marais, B. J; and Kranzer, K.\n\n\n \n\n\n\n BMJ Global Health, 10(9): e019770. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Taxes$ Paper\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{coleman_taxes_2025,\n\ttitle = {Taxes for tuberculosis: could tobacco and sugar tax revenue fund tuberculosis control interventions?},\n\tvolume = {10},\n\tissn = {2059-7908},\n\tshorttitle = {Taxes for tuberculosis},\n\turl = {https://gh.bmj.com/lookup/doi/10.1136/bmjgh-2025-019770},\n\tdoi = {10.1136/bmjgh-2025-019770},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-28},\n\tjournal = {BMJ Global Health},\n\tauthor = {Coleman, Mikaela and Coussens, Anna K and Calderwood, Claire Jacqueline and Schoeman, Ingrid and Bhargava, Madhavi and Sinha, Pranay and Marais, Ben J and Kranzer, Katharina},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {e019770},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The burden of dengue fever in travellers: a systematic literature review.\n \n \n \n \n\n\n \n Grobusch, M. P.; Díaz-Menéndez, M.; De Gomensoro, E. B.; Mächler, C.; and Milovanović, B.\n\n\n \n\n\n\n New Microbes and New Infections, 67: 101631. October 2025.\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{grobusch_burden_2025,\n\ttitle = {The burden of dengue fever in travellers: a systematic literature review},\n\tvolume = {67},\n\tissn = {20522975},\n\tshorttitle = {The burden of dengue fever in travellers},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2052297525000708},\n\tdoi = {10.1016/j.nmni.2025.101631},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {New Microbes and New Infections},\n\tauthor = {Grobusch, Martin P. and Díaz-Menéndez, Marta and De Gomensoro, Eduardo Bittencourt and Mächler, Caroline and Milovanović, Bojana},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {101631},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Molecular surveillance of influenza A and B in namibia: seasonal patterns and clinical correlates (2021–2023).\n \n \n \n \n\n\n \n !Garus-oas, N.; Dunaiski, C. M.; Naupu, P. N.; Frans, N.; Onywera, H.; Shiningavamwe, A.; Tjombonde, K.; and Konstantinus, I. N.\n\n\n \n\n\n\n BMC Infectious Diseases, 25(1): 1315. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Molecular$ Paper\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{garus-oas_molecular_2025,\n\ttitle = {Molecular surveillance of influenza {A} and {B} in namibia: seasonal patterns and clinical correlates (2021–2023)},\n\tvolume = {25},\n\tissn = {1471-2334},\n\tshorttitle = {Molecular surveillance of influenza {A} and {B} in namibia},\n\turl = {https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-025-11554-6},\n\tdoi = {10.1186/s12879-025-11554-6},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {BMC Infectious Diseases},\n\tauthor = {!Garus-oas, Nathalia and Dunaiski, Cara Mia and Naupu, Paulina N. and Frans, Ndahafa and Onywera, Harris and Shiningavamwe, Andreas and Tjombonde, Kapena and Konstantinus, Iyaloo N.},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {1315},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Herpesviruses Reactivation and Systemic Inflammation Before and After Initiating Antiretroviral Therapy Among Women with HIV in Rakai, Uganda.\n \n \n \n \n\n\n \n Ssempijja, V.; Callier, V.; Nason, M.; Anok, A.; Lisco, A.; Redd, A. D; Quinn, T. C; Rupert, A.; Towlerton, A.; Das, S.; Walker, L.; Tomusange, S.; Kityamuweesi, T.; Bbuule, P.; Sereti, I.; and Reynolds, S. J\n\n\n \n\n\n\n Open Forum Infectious Diseases, 12(10): ofaf603. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Herpesviruses$ Paper\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{ssempijja_herpesviruses_2025,\n\ttitle = {Herpesviruses {Reactivation} and {Systemic} {Inflammation} {Before} and {After} {Initiating} {Antiretroviral} {Therapy} {Among} {Women} with {HIV} in {Rakai}, {Uganda}},\n\tvolume = {12},\n\tissn = {2328-8957},\n\turl = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofaf603/8277447},\n\tdoi = {10.1093/ofid/ofaf603},\n\tabstract = {Abstract \n             \n              Introduction \n              The association of mucosal shedding of human simplex virus (HSV)-2, Kaposi’s sarcoma-associated herpesvirus (KSHV) and cytomegalovirus (CMV) after antiretroviral therapy (ART) initiation in women-living-with-HIV (WLWH) with systemic inflammation is unclear. \n             \n             \n              Methods \n              We recruited 187 ART-naive adult WLWH in south-central Uganda. HSV-1, HSV-2, CMV, and Varicella Zoster Virus (VZV) in vaginal secretions and Kaposi’s sarcoma-associated herpesvirus (KSHV) in oral swabs were quantified by PCR. Plasma biomarkers of systemic inflammation were measured by ELISA or electrochemiluminescence before and after ART initiation (weeks 8, 12, and 24). \n             \n             \n              Results \n              Participants had a baseline median age of 28 years and CD4 count of 413 cells/μL. Viral shedding rates were similar for all tested viruses between baseline and post-ART timepoints in the overall study population. CMV shedding significantly increased from a baseline rate of 53\\% to 77\\% at week 4 visit (P-value = .016), and 73\\% at week 8 visit (P-value = .027) in participants with a baseline CD4 count ≤200 cells/µL. CRP, TNFα, and TNFR1 levels associated with CMV shedding at week 8, IL-6 associated with HSV-2 shedding at week 4, while sCD14 and TNFR1 associated with HSV-2 shedding at week 8. Also, CRP and IL-27 were associated with KSHV shedding at week 4 and week 8, respectively. \n             \n             \n              Conclusions \n              Although ART initiation was not associated with increased herpesvirus shedding overall, CMV shedding increased in women with advanced HIV-1. The association of mucosal shedding of CMV, HSV-2, and KSHV in post-ART timepoints with different baseline biomarkers of systemic inflammation suggest that distinct immunological functions are implicated in the control of their viral replication.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-28},\n\tjournal = {Open Forum Infectious Diseases},\n\tauthor = {Ssempijja, Victor and Callier, Viviane and Nason, Martha and Anok, Aggrey and Lisco, Andrea and Redd, Andrew D and Quinn, Thomas C and Rupert, Adam and Towlerton, Andrea and Das, Sanchita and Walker, Lorenzo and Tomusange, Stephen and Kityamuweesi, Taddeo and Bbuule, Paul and Sereti, Irini and Reynolds, Steven J},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {ofaf603},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Exploring the relationship between established HIV risk factors and depressive symptoms amongst young women without HIV in two sites in South Africa.\n \n \n \n \n\n\n \n Gumbi, Z.; Mehou-Loko, C.; Masson, L.; Mdladla, M.; Maphumulo, N.; Passmore, J.; Mbeje, S.; Bekker, L. G.; Potloane, D.; Jaspan, H.; Radzey, N.; Abrahams, A.; Harryparsad, R.; Mkhize, P.; and Humphries, H.\n\n\n \n\n\n\n PLOS ONE, 20(1): e0317732. January 2025.\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{gumbi_exploring_2025,\n\ttitle = {Exploring the relationship between established {HIV} risk factors and depressive symptoms amongst young women without {HIV} in two sites in {South} {Africa}},\n\tvolume = {20},\n\tissn = {1932-6203},\n\turl = {https://dx.plos.org/10.1371/journal.pone.0317732},\n\tdoi = {10.1371/journal.pone.0317732},\n\tabstract = {Purpose \n              Adolescent girls are at high risk for depression and human immunodeficiency virus (HIV) acquisition. Poor mental health can increase vulnerability to risky sexual behaviours. Therefore, this study aims to determine the prevalence of depressive symptomology and explore the convergence of HIV risk factors with depressive symptoms amongst cis-gender adolescent girls and young women (AGYW) in rural KwaZulu-Natal (KZN) and peri-urban Western Cape (WC) communities in South Africa. \n             \n             \n              Methods \n              Cross-sectional survey data from two sites in South Africa was used - the rural Vulindlela community in KZN and the peri-urban Philippi East community in the WC. Study inclusion criteria included being sexually active with at least one male partner, and not planning to relocate in the next 12 months. The PHQ-9 scale was used to determine depressive symptomology, a socio-behavioural questionnaire was used to determine sexual behaviours, odds ratios and confidence intervals derived from logistic regression models were used to explore the associations between depressive symptomology and socio-behavioural factors associated with HIV acquisition. \n             \n             \n              Results \n              The cohort consisted of 274 adolescent girls, 38.6\\% from the WC site and 61.4\\% from the KZN site. Overall, 15.7\\% (43/274) of AGYW reported depressive symptoms. Participants from the peri-urban WC site were more likely to experience depressive symptoms (OR 8.34; 95\\% CI 3.80–18.30) compared to those living in the rural KZN site. Depressive symptoms were less likely to occur in adolescent girls between the ages of 14 to 17 as compared to those between the ages of 18 and 19 (OR 0.44; 95\\% CI 0.22–0.90). Socio-behavioural HIV risk factors associated with depressive symptoms include: age disparate relationships (OR 2.98; 95\\% CI 1.52–5.84), high (four or more) numbers of lifetime partners (OR 8.15; 95\\% CI 3.60–18.45) and engaging in sex under the influence of alcohol (OR 2.58; 95\\% CI 1.32–5.04). Multivariate analysis showed that participants from the WC site (AOR 5.25; 95\\% CI 1.95–14.17) had higher odds of experiencing depressive symptoms while participants with four or more lifetime partners (AOR 3.46; 95\\% CI 1.24–9.60) were at higher odds of experiencing depressive symptoms. \n             \n             \n              Conclusion \n              In this cross-sectional study, depressive symptomology is associated with certain HIV risk behaviours. Longitudinal studies are required to test the causal relationship between depression and HIV acquisition and to better understand the geospatial differences observed.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {PLOS ONE},\n\tauthor = {Gumbi, Zanenhlanhla and Mehou-Loko, Celia and Masson, Lindi and Mdladla, Makhosazana and Maphumulo, Nokuthula and Passmore, Jo-Ann and Mbeje, Sanele and Bekker, Linda Gail and Potloane, Disebo and Jaspan, Heather and Radzey, Nina and Abrahams, Andrea and Harryparsad, Rushil and Mkhize, Pamela and Humphries, Hilton},\n\teditor = {Evans, Denise},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {e0317732},\n}\n\n\n\n

\n

\n\n\n

\n Purpose Adolescent girls are at high risk for depression and human immunodeficiency virus (HIV) acquisition. Poor mental health can increase vulnerability to risky sexual behaviours. Therefore, this study aims to determine the prevalence of depressive symptomology and explore the convergence of HIV risk factors with depressive symptoms amongst cis-gender adolescent girls and young women (AGYW) in rural KwaZulu-Natal (KZN) and peri-urban Western Cape (WC) communities in South Africa. Methods Cross-sectional survey data from two sites in South Africa was used - the rural Vulindlela community in KZN and the peri-urban Philippi East community in the WC. Study inclusion criteria included being sexually active with at least one male partner, and not planning to relocate in the next 12 months. The PHQ-9 scale was used to determine depressive symptomology, a socio-behavioural questionnaire was used to determine sexual behaviours, odds ratios and confidence intervals derived from logistic regression models were used to explore the associations between depressive symptomology and socio-behavioural factors associated with HIV acquisition. Results The cohort consisted of 274 adolescent girls, 38.6% from the WC site and 61.4% from the KZN site. Overall, 15.7% (43/274) of AGYW reported depressive symptoms. Participants from the peri-urban WC site were more likely to experience depressive symptoms (OR 8.34; 95% CI 3.80–18.30) compared to those living in the rural KZN site. Depressive symptoms were less likely to occur in adolescent girls between the ages of 14 to 17 as compared to those between the ages of 18 and 19 (OR 0.44; 95% CI 0.22–0.90). Socio-behavioural HIV risk factors associated with depressive symptoms include: age disparate relationships (OR 2.98; 95% CI 1.52–5.84), high (four or more) numbers of lifetime partners (OR 8.15; 95% CI 3.60–18.45) and engaging in sex under the influence of alcohol (OR 2.58; 95% CI 1.32–5.04). Multivariate analysis showed that participants from the WC site (AOR 5.25; 95% CI 1.95–14.17) had higher odds of experiencing depressive symptoms while participants with four or more lifetime partners (AOR 3.46; 95% CI 1.24–9.60) were at higher odds of experiencing depressive symptoms. Conclusion In this cross-sectional study, depressive symptomology is associated with certain HIV risk behaviours. Longitudinal studies are required to test the causal relationship between depression and HIV acquisition and to better understand the geospatial differences observed.\n

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\n \n\n \n \n \n \n \n \n Data simulation to optimize frameworks for genome-wide association studies in diverse populations.\n \n \n \n \n\n\n \n Mugo, J. W.; Mulder, N.; and Chimusa, E. R.\n\n\n \n\n\n\n Frontiers in Genetics, 16: 1559496. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Data$ Paper\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{mugo_data_2025,\n\ttitle = {Data simulation to optimize frameworks for genome-wide association studies in diverse populations},\n\tvolume = {16},\n\tissn = {1664-8021},\n\turl = {https://www.frontiersin.org/articles/10.3389/fgene.2025.1559496/full},\n\tdoi = {10.3389/fgene.2025.1559496},\n\tabstract = {Whole-genome or genome-wide association studies (GWAS) have become a fundamental part of modern genetic studies and methods for dissecting the genetic architecture of common traits based on common polymorphisms in random populations. It is hoped that there would be many potential uses of these identified variants, including a better understanding of the pathogenesis of traits, disease risk prediction, discovery of biomarkers, and clinical prediction of drug treatments for populations and global health. Questions have been raised about whether associations that are largely discovered in European ancestry populations are replicable in diverse populations, can inform medical decision-making globally, and how efficiently current GWAS tools perform in populations of high genetic diversity, multi-wave genetic admixture, and low linkage disequilibrium, such as African populations. Here, we discuss some of the challenges in association mapping and leverage genomic data simulation to mimic structured African, European, and multi-way admixed populations to evaluate the replicability of association signals from current state-of-the-art GWAS tools. We use the results to discuss optimized frameworks for the analysis of GWAS data in diverse populations. Finally, we outline the implications, challenges, and opportunities these studies present for populations of non-European descent.},\n\turldate = {2026-05-28},\n\tjournal = {Frontiers in Genetics},\n\tauthor = {Mugo, Jacquiline W. and Mulder, Nicola and Chimusa, Emile R.},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {1559496},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Subcellular Fractionation and Metaproteogenomic Identification and Validation of Key Differentially Expressed Molecular Targets for Keloid Disease.\n \n \n \n \n\n\n \n Kidzeru, E. B.; Sinkala, M.; Chalwa, T.; Matobole, R.; Alkelani, M.; Ghasemishahrestani, Z.; Mbandi, S. K.; Blackburn, J.; Tabb, D. L.; Adeola, H. A.; Khumalo, N. P.; and Bayat, A.\n\n\n \n\n\n\n Journal of Investigative Dermatology, 145(3): 660–677.e8. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Subcellular$ Paper\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{kidzeru_subcellular_2025,\n\ttitle = {Subcellular {Fractionation} and {Metaproteogenomic} {Identification} and {Validation} of {Key} {Differentially} {Expressed} {Molecular} {Targets} for {Keloid} {Disease}},\n\tvolume = {145},\n\tissn = {0022202X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0022202X24019729},\n\tdoi = {10.1016/j.jid.2024.07.010},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Investigative Dermatology},\n\tauthor = {Kidzeru, Elvis B. and Sinkala, Musalula and Chalwa, Temwani and Matobole, Relebohile and Alkelani, Madeha and Ghasemishahrestani, Zeinab and Mbandi, Stanley K. and Blackburn, Jonathan and Tabb, David L. and Adeola, Henry Ademola and Khumalo, Nonhlanhla P. and Bayat, Ardeshir},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {660--677.e8},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Implementation outcomes of the IMARA-South Africa mother-daughter HIV/STI prevention intervention: A mixed-methods study.\n \n \n \n \n\n\n \n Merrill, K. G.; Atujuna, M.; Ahmed, S.; Emerson, E.; Ngcuka, A.; Jaworski, E.; Bekker, L.; Crooks, N.; Debra, A.; and Donenberg, G.\n\n\n \n\n\n\n Journal of Clinical and Translational Science, 9(1): e231. 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Implementation$ Paper\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{merrill_implementation_2025,\n\ttitle = {Implementation outcomes of the {IMARA}-{South} {Africa} mother-daughter {HIV}/{STI} prevention intervention: {A} mixed-methods study},\n\tvolume = {9},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2059-8661},\n\tshorttitle = {Implementation outcomes of the {IMARA}-{South} {Africa} mother-daughter {HIV}/{STI} prevention intervention},\n\turl = {https://www.cambridge.org/core/product/identifier/S2059866125101581/type/journal_article},\n\tdoi = {10.1017/cts.2025.10158},\n\tabstract = {Abstract \n             \n              Background: \n              IMARA-South Africa (SA) is an HIV/STI prevention program for adolescent girls and young women (AGYW) and their female caregivers (FC). We examined six implementation outcomes of IMARA-SA (acceptability, appropriateness, feasibility, reach, adoption, and sustainability) from the perspectives of study staff, investigators, and collaborators. \n             \n             \n              Methods: \n               \n                We used a sequential explanatory mixed-methods design. We administered surveys, hosted three focus group discussions with study staff/facilitators ( \n                n \n                = 5), clinic staff ( \n                n \n                = 3), and community advisory board members ( \n                n \n                = 5), and conducted seven key informant interviews with investigators and study staff. We used descriptive statistics and rapid qualitative analyses, merging quantitative and qualitative data by implementation outcome to achieve triangulation. \n               \n             \n             \n              Results: \n              On 27 surveys analyzed, mean scores were highest for acceptability (2.8/3, SD = 0.6), appropriateness (2.7/3, SD = 0.5), and reach (2.7/3, SD = 0.5), followed by feasibility (2.1/3, SD = 0.5), adoption (3.8/5, SD = 0.3), and sustainability (5.9/7, SD = 0.8). All perceived the AGYW and FC to love the program, which fit well with South African culture and addressed AGYW’s needs. The delivery site was deemed highly appropriate for reaching vulnerable populations. The lowest scoring items concerned time constraints (2.2/3, SD = 0.9), safety concerns (1.4/3, SD = 0.7), complexity (2.9/5, SD = 1.3), and cost (2.8/5, SD = 0.9). Qualitative participants attributed complexity and cost challenges to the research procedures, not the intervention. Participants proposed potential avenues for future implementation (e.g., schools, clinics) and interest in engaging males. \n             \n             \n              Conclusion: \n              IMARA-SA is implementable. Findings reveal challenges with navigating trade-offs between implementation outcomes and surveys distinguishing between intervention and research activities. Findings can inform future delivery of IMARA-SA and similar programs regionally.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Clinical and Translational Science},\n\tauthor = {Merrill, Katherine G. and Atujuna, Millicent and Ahmed, Saba and Emerson, Erin and Ngcuka, Anelisiwe and Jaworski, Erin and Bekker, Linda-Gail and Crooks, Natasha and Debra, Alyssa and Donenberg, Geri},\n\tyear = {2025},\n\tpages = {e231},\n}\n\n\n\n

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\n Abstract Background: IMARA-South Africa (SA) is an HIV/STI prevention program for adolescent girls and young women (AGYW) and their female caregivers (FC). We examined six implementation outcomes of IMARA-SA (acceptability, appropriateness, feasibility, reach, adoption, and sustainability) from the perspectives of study staff, investigators, and collaborators. Methods: We used a sequential explanatory mixed-methods design. We administered surveys, hosted three focus group discussions with study staff/facilitators ( n = 5), clinic staff ( n = 3), and community advisory board members ( n = 5), and conducted seven key informant interviews with investigators and study staff. We used descriptive statistics and rapid qualitative analyses, merging quantitative and qualitative data by implementation outcome to achieve triangulation. Results: On 27 surveys analyzed, mean scores were highest for acceptability (2.8/3, SD = 0.6), appropriateness (2.7/3, SD = 0.5), and reach (2.7/3, SD = 0.5), followed by feasibility (2.1/3, SD = 0.5), adoption (3.8/5, SD = 0.3), and sustainability (5.9/7, SD = 0.8). All perceived the AGYW and FC to love the program, which fit well with South African culture and addressed AGYW’s needs. The delivery site was deemed highly appropriate for reaching vulnerable populations. The lowest scoring items concerned time constraints (2.2/3, SD = 0.9), safety concerns (1.4/3, SD = 0.7), complexity (2.9/5, SD = 1.3), and cost (2.8/5, SD = 0.9). Qualitative participants attributed complexity and cost challenges to the research procedures, not the intervention. Participants proposed potential avenues for future implementation (e.g., schools, clinics) and interest in engaging males. Conclusion: IMARA-SA is implementable. Findings reveal challenges with navigating trade-offs between implementation outcomes and surveys distinguishing between intervention and research activities. Findings can inform future delivery of IMARA-SA and similar programs regionally.\n

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\n \n\n \n \n \n \n \n \n Recent Antiretroviral Therapy Initiation Is Associated With Increased Mortality Risk in Human Immunodeficiency Virus–associated Cryptococcal Meningitis: An Analysis of Clinical Trial Data From Africa.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Clinical Infectious Diseases. January 2025.\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

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@article{noauthor_recent_2025,\n\ttitle = {Recent {Antiretroviral} {Therapy} {Initiation} {Is} {Associated} {With} {Increased} {Mortality} {Risk} in {Human} {Immunodeficiency} {Virus}–associated {Cryptococcal} {Meningitis}: {An} {Analysis} of {Clinical} {Trial} {Data} {From} {Africa}},\n\tissn = {1537-6591},\n\tshorttitle = {Recent {Antiretroviral} {Therapy} {Initiation} {Is} {Associated} {With} {Increased} {Mortality} {Risk} in {Human} {Immunodeficiency} {Virus}–associated {Cryptococcal} {Meningitis}},\n\turl = {https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciae586/7954113},\n\tdoi = {10.1093/cid/ciae586},\n\turldate = {2026-05-28},\n\tjournal = {Clinical Infectious Diseases},\n\tmonth = jan,\n\tyear = {2025},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Delayed correct diagnoses in emerging disease outbreaks: historical patterns and lessons for contemporary responses.\n \n \n \n \n\n\n \n Pellejero-Sagastizábal, G.; Bulescu, C.; Gupta, N.; Jokelainen, P.; Gkrania-Klotsas, E.; Barac, A.; Goorhuis, A.; Jacob, S. T.; Agnandji, S. T.; Ntoumi, F.; Mora-Rillo, M.; Paño-Pardo, J. R.; Lescure, F.; and Grobusch, M. P.\n\n\n \n\n\n\n Clinical Microbiology and Infection, 31(8): 1298–1306. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Delayed$ Paper\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{pellejero-sagastizabal_delayed_2025,\n\ttitle = {Delayed correct diagnoses in emerging disease outbreaks: historical patterns and lessons for contemporary responses},\n\tvolume = {31},\n\tissn = {1198743X},\n\tshorttitle = {Delayed correct diagnoses in emerging disease outbreaks},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1198743X25001697},\n\tdoi = {10.1016/j.cmi.2025.04.007},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-28},\n\tjournal = {Clinical Microbiology and Infection},\n\tauthor = {Pellejero-Sagastizábal, Galadriel and Bulescu, Casandra and Gupta, Nitin and Jokelainen, Pikka and Gkrania-Klotsas, Effrossyni and Barac, Aleksandra and Goorhuis, Abraham and Jacob, Shevin T. and Agnandji, Selidji T. and Ntoumi, Francine and Mora-Rillo, Marta and Paño-Pardo, José Ramón and Lescure, F.-Xavier and Grobusch, Martin P.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {1298--1306},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Targeting Aurora Kinases as Essential Cell‐Cycle Regulators to Deliver Multi‐Stage Antimalarials Against Plasmodium Falciparum.\n \n \n \n \n\n\n \n Langeveld, H.; Maepa, K.; Maree, M.; Thibaud, J. L.; Salomane, N.; Bridgwater, R.; Famodimu, M. T.; Godoy, L. C.; Pasaje, C. F. A.; Boonyalai, N.; De Souza, M. L.; Fong, J.; Rabie, T.; Van Der Watt, M.; Theart, R. P.; Ghidelli‐Disse, S.; Niles, J. C.; Lee, M. C. S.; Winzeler, E. A.; Delves, M. J.; Chibale, K.; Wicht, K. J.; Coulson, L. B.; and Birkholtz, L.\n\n\n \n\n\n\n Angewandte Chemie International Edition, 64(51): e202518493. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Targeting$ Paper\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{langeveld_targeting_2025,\n\ttitle = {Targeting {Aurora} {Kinases} as {Essential} {Cell}‐{Cycle} {Regulators} to {Deliver} {Multi}‐{Stage} {Antimalarials} {Against} \\textit{{Plasmodium} {Falciparum}}},\n\tvolume = {64},\n\tissn = {1433-7851, 1521-3773},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/anie.202518493},\n\tdoi = {10.1002/anie.202518493},\n\tabstract = {Abstract \n             \n              Kinases play critical roles in the development and adaptation of \n              Plasmodium falciparum \n              and present novel opportunities for chemotherapeutic intervention. Mitotic kinases that regulate the proliferation of the parasites by controlling nuclear division, segregation, and cytokinesis. We evaluated the potential of human Aurora kinase (Aur) inhibitors to prevent \n              P. falciparum \n              development by targeting members of the Aurora‐related kinase (Ark) family in this parasite. Several human AurB inhibitors exhibited multistage potency ({\\textless} 250 nM) against all proliferative stages of parasite development, including asexual blood stages, liver schizonts, and male gametes. The most potent compounds, hesperadin, TAE684, and AT83, exhibited {\\textgreater} 1000x selectivity towards the parasite. Importantly, we identified \n              Pf \n              Ark1 as the principal vulnerable Ark family member, with specific inhibition of \n              Pf \n              Ark1 as the primary target for hesperadin. Hesperadin's whole‐cell and protein activity validates it as a unique \n              Pf \n              Ark1 tool compound. Inhibition of \n              Pf \n              Ark1 results in the parasite's inability to complete mitotic processes, presenting with unsegregated, multi‐lobed nuclei caused by aberrant microtubule organization. This suggests \n              Pf \n              Ark1 is the main Aur mitotic kinase in proliferative stages of \n              Plasmodium \n              , characterized by bifunctional AurA and B activity. This paves the way for drug‐discovery campaigns based on hesperadin targeting \n              Pf \n              Ark1.},\n\tlanguage = {en},\n\tnumber = {51},\n\turldate = {2026-05-28},\n\tjournal = {Angewandte Chemie International Edition},\n\tauthor = {Langeveld, Henrico and Maepa, Keletso and Maree, Marché and Thibaud, Jessica L. and Salomane, Nicolaas and Bridgwater, Rosie and Famodimu, Mufuliat T. and Godoy, Luiz C. and Pasaje, Charisse Flerida A. and Boonyalai, Nonlawat and De Souza, Mariana Laureano and Fong, Justin and Rabie, Tayla and Van Der Watt, Mariëtte and Theart, Rensu P. and Ghidelli‐Disse, Sonja and Niles, Jacquin C. and Lee, Marcus C. S. and Winzeler, Elizabeth A. and Delves, Michael J. and Chibale, Kelly and Wicht, Kathryn J. and Coulson, Lauren B. and Birkholtz, Lyn‐Marié},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e202518493},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Heme processing in the malaria parasite, Plasmodium falciparum: a time-dependent basal-level analysis.\n \n \n \n \n\n\n \n Garnie, L. F.; Egan, T. J.; and Wicht, K. J.\n\n\n \n\n\n\n Communications Biology, 8(1): 1564. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Heme$ Paper\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{garnie_heme_2025,\n\ttitle = {Heme processing in the malaria parasite, {Plasmodium} falciparum: a time-dependent basal-level analysis},\n\tvolume = {8},\n\tissn = {2399-3642},\n\tshorttitle = {Heme processing in the malaria parasite, {Plasmodium} falciparum},\n\turl = {https://www.nature.com/articles/s42003-025-08991-z},\n\tdoi = {10.1038/s42003-025-08991-z},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Communications Biology},\n\tauthor = {Garnie, Larnelle F. and Egan, Timothy J. and Wicht, Kathryn J.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {1564},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Metabolic Activation versus Masked Prodrugs: Bisubstrate Mimic Inhibitors of CoaBC’s PPCS Activity in Mycobacterium tuberculosis and Staphylococcus aureus.\n \n \n \n \n\n\n \n Kotzé, T. J.; Mostert, K. J.; Domingo, R.; Wang, X.; Moolman, W. J. A.; Butman, H. S.; Pepin, A.; McKay, K. T.; Neveling, D. P.; Evans, J. C.; Mizrahi, V.; Van Otterlo, W. A. L.; Dowd, C. S.; and Strauss, E.\n\n\n \n\n\n\n ACS Infectious Diseases, 11(6): 1508–1517. June 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kotze_metabolic_2025,\n\ttitle = {Metabolic {Activation} versus {Masked} {Prodrugs}: {Bisubstrate} {Mimic} {Inhibitors} of {CoaBC}’s {PPCS} {Activity} in \\textit{{Mycobacterium} tuberculosis} and \\textit{{Staphylococcus} aureus}},\n\tvolume = {11},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2373-8227, 2373-8227},\n\tshorttitle = {Metabolic {Activation} versus {Masked} {Prodrugs}},\n\turl = {https://pubs.acs.org/doi/10.1021/acsinfecdis.5c00047},\n\tdoi = {10.1021/acsinfecdis.5c00047},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {ACS Infectious Diseases},\n\tauthor = {Kotzé, Timothy J. and Mostert, Konrad J. and Domingo, Riyad and Wang, Xu and Moolman, Wessel J. A. and Butman, Hailey S. and Pepin, Abigail and McKay, Kyle T. and Neveling, Deon P. and Evans, Joanna C. and Mizrahi, Valerie and Van Otterlo, Willem A. L. and Dowd, Cynthia S. and Strauss, Erick},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {1508--1517},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Can hair concentrations of artemether-lumefantrine be used as a tool to retrospectively determine drug exposure during malaria treatment?.\n \n \n \n \n\n\n \n Schnyder, J. L.; Vos-van Der Meer, M.; Van Hest, R. M.; Mathot, R.; Schlagenhauf, P.; De Jong, H. K.; and Grobusch, M. P.\n\n\n \n\n\n\n New Microbes and New Infections, 67: 101617. October 2025.\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{schnyder_can_2025,\n\ttitle = {Can hair concentrations of artemether-lumefantrine be used as a tool to retrospectively determine drug exposure during malaria treatment?},\n\tvolume = {67},\n\tissn = {20522975},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2052297525000563},\n\tdoi = {10.1016/j.nmni.2025.101617},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {New Microbes and New Infections},\n\tauthor = {Schnyder, Jenny L. and Vos-van Der Meer, Marloes and Van Hest, Reinier M. and Mathot, Ron and Schlagenhauf, Patricia and De Jong, Hanna K. and Grobusch, Martin P.},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {101617},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Global health at crossroads: uniting together to overcome challenges, restore trust and advance priorities for a sustainable future.\n \n \n \n \n\n\n \n Sartelli, M.; Mossialos, E.; Coccolini, F.; Jammer, I.; Labricciosa, F. M.; Barie, P.; Biffl, W. L.; Memish, Z. A.; Maeurer, M.; Kobinger, G. P.; Ippolito, G.; Zumla, A.; Catena, F.; Global Consortium for Solidarity to Overcome Challenges, Restore Trustand Advance Science for a Sustainable Future; Abbo, L. M.; Abraham, Y.; Abu-Zidan, F. M.; Adamou, H.; Agastra, E.; Agodi, A.; Ahmed, R.; Aklillu, E.; Ala, A.; Alex-Wele, M. A.; Alfouzan, W.; Al-Hasan, M. N.; Ali, S.; Ali, S. M.; Al-Omari, A.; Al-Omari, J. A. K.; Al-Shehari, M.; Amir, A.; Amponsah, O. K. O.; Anis, H.; Ansaloni, L.; Ansari, S.; Arauz, A. B.; Aruyaru, S.; Augustin, G.; Awazi, B.; Azfar, M.; Azhar, E. I.; Bains, L.; Bala, M.; Baral, S.; Baraket, O.; Barchitta, M.; Murguía, M. E. B.; Barkema, H.; Barreda, R. L.; Basher, A.; Bassetti, M.; Beilman, G.; Beka, S. G.; Benboubker, M.; Beović, B.; Biemba, G.; Bignami, E. G.; Blanchet, K.; Blot, S.; Bonomo, R. A.; Brink, A.; Brusaferro, S.; Bueno, J.; Bulanauca, M.; Buonomo, L.; Caínzos, M. A.; Camacho-Ortiz, A.; Canton, R.; Cantürk, A. Ö.; Carlini, M.; Cascio, A.; Casini, B.; Cassini, A.; Catena, R.; Cavaillon, J.; Ceschi, P.; Cheadle, W. G.; Olinyo, D. C.; Chiara, F.; Chikowe, I.; Chimatiro, S.; Chioti, A.; Chiwodza, Z.; Chowdhury, S.; Cocuz, M.; Coimbra, R.; Correia, T.; Cortese, F.; Cricca, M.; Cui, Y.; Czepiel, J.; Dahal, E. R.; Dar, O.; De Angelis, G.; Delibegovic, S.; Dellinger, E. P.; Demetrashvili, Z.; De Palma, A.; De Simone, B.; De Silva, D.; Detanac, D.; Dhingra, S.; Diaz, J. J.; Dima, C.; Diwan, V.; Dogjani, A.; Dorj, G.; Dulskas, A.; Eckmann, C.; Erdene, S.; Egyir, B.; Elhassi, A.; Elmangory, M. M.; Omer, H. F. E.; Ergonul, O.; Antezana, J. P. E.; Everett, D. B.; Fabbri, E.; Fadare, J. O.; Fantoni, M.; Farsakoury, R.; Fassari, A.; Ferrada, P.; Ferreres, A.; Filipescu, D.; Foghetti, D.; Gandhi, C.; Gastaldi, S.; Gemmi, F.; Gerardi, C.; Ghannam, W.; Giamarellou, H.; Giordano, A.; Gkiokas, G.; Glasbey, J.; Glushkova, N.; Gomes, C. A.; Herrera, M. N. G.; Gomi, H.; Gonullu, E.; Granata, G.; Griffiths, E.; Grynchuk, F.; Gualano, M. R.; Guirao, X.; Haddadin, R.; Hajhamad, M. M. H.; Hakemi-Vala, M.; Halle-Ekane, G. E.; Hansen, S.; Haque, M.; Hardcastle, T. C.; Hecker, A.; Hui, D. S.; Inaba, K.; Isik, A.; Ishimwe, M.; Iskandar, K.; Itani, K.; Jaffar, S.; Jaidane, N.; Jeschke, M. G.; Jensen, P. Ø.; Johnson, W.; Kamara, I. F.; Kamarulzaman, A.; Kanj, S. S.; Kaplan, L.; Keikha, M.; Khalid, A.; Khamis, F.; Khokha, V.; Kiguba, R.; Kilpatrick, C.; Kim, H. B.; Kirkpatrick, A. W.; Ko, W.; Kok, K. Y. Y.; Korzh, O.; Kotecha, V.; Kouma, I.; Krasniqi, J.; Kruger, V. F.; Kryvoruchko, I.; Kullar, R.; Kuriyama, A.; Kyota, S.; Lakanwall, M. N.; Lakatos, B.; Lakoh, S.; Lansang, M. A.; Latifi, R.; Lee, J. G.; Lee, S. S.; Leone, M.; Leppaniemi, A.; Hara, G. L.; Litvin, A.; López-Vidal, Y.; Machain, G. M.; Macias, A. E.; Mbamalu, O.; Mahomoodally, F.; Maiti, S.; Majumder, M. A. A.; Malama, S.; Manasa, J.; Manzano-Nunez, R.; Marmorale, C.; Martínez-Pérez, A.; Marwah, S.; Maves, R. C.; McHugh, T. D.; McLay, C.; Juan José Meléndez, L.; Meschiari, M.; Metan, G.; Mfinanga, S.; Mierzejewska, A.; Miranda-Novales, M. G.; Mikic, M.; Mishra, S. K.; Mohammed, Y.; Molina, G.; Molla, L. S.; Montravers, P.; Monzani, R.; Moro, M. L.; Motta, F.; M’Pelé, P. K.; Mudenda, S.; Mugisha, M. J. M.; Murri, R.; Muşină, A.; Mutters, N. T.; Mwaba, P.; Nabyonga-Orem, J.; Naeem, J.; Navsaria, P. H.; Negoi, I.; Nyeko, D.; Ntoumi, F.; Nouwen, J.; Ochoa-Hein, E.; O’Connor, D.; Olausson, M.; Onyeaghala, C.; Ordoñez, C.; Orozco, H. G. H.; Ouadii, M.; Ouedraogo, A.; Pagani, L.; Paiva, J. A.; Pan, A.; Panyko, A.; Paolillo, C.; Pasero, D.; Patel, J.; Petersen, E.; Petrone, P.; Petrosillo, N.; Pintar, T.; Pipitone, G.; Pikoulis, E.; Plaudis, H.; Podda, M.; De León, A. P.; De León, S. P.; Guerrero, A. P.; Rasa, K.; Reichert, M.; Rello, J.; Reynolds-Campbell, G.; Resanovic, V.; Rezza, G.; Ribeiro, J.; Rickard, J.; Ripabelli, G.; Rodrigues, G. S.; Rodriguez-Morales, A. J.; Villamil, G. E. R.; Różańska-Walędziak, A.; Rubio-Perez, I.; Rwegerera, G.; Sabbatucci, M.; Terrazas, J. M. S.; Saguil, E.; Sakakushev, B. E.; Saladžinskas, Ž.; Salile, S. S.; Sall, I.; Kafil, H. S.; Santillan-Doherty, P.; Satta, G.; Sawyer, R. G.; Schizas, D.; Lohse, H. A. S.; Seni, J.; Septimus, E. J.; Sganga, G.; Shabaan, V.; Shabanzadeh, D. M.; Hussein, M. S.; Shelat, V. G.; Shibabaw, A.; Shlyapnikov, S. A.; Singh, I.; Singh, K.; Siribumrungwong, B.; Somville, F.; Shor, E.; Soreide, K.; Stefani, S.; Storr, J.; Sydorchuk, L.; Sydorchuk, R.; Szabo, B. G.; Tan, B. K.; Tartari, E.; Tattevin, P.; Almenares, O. T.; Tian, B. W. C. A.; Tochie, J. N.; Todorovic, Z.; Bifa, K. T.; Tolonen, M.; Torres, M.; Traore, T.; Trostchansky, I.; Trueba, G.; Tsioutis, C.; Tsogbale, N.; Tumietto, F.; Turrado-Rodríguez, V.; Udoh, U.; Ulrych, J.; Umo, I.; Uranues, S.; Van Dongen, M.; Varghese, C.; Vasilescu, A. M.; Vasiljev, K. D.; Velmahos, G. C.; Viaggi, B.; Vila, J.; Walędziak, M.; Waruingi, D.; Watkins, R. R.; Wechsler-Fördös, A.; Waworuntu, O.; Wesangula, E.; Yadgarova, K.; Yeboah-Manu, D.; Yepez, R.; Willcox, M.; Younis, M. U.; Yuan, K.; Zakaria, A. D.; Zakrison, T. L.; Mesia, V. Z.; Zamudio-Lugo, I.; Zhang, G.; Zorzet, A.; Zubareva, N.; Zughaier, S. M.; Zuidema, W. P.; and Zumla, A.\n\n\n \n\n\n\n World Journal of Emergency Surgery, 20(1): 84. November 2025.\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

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@article{sartelli_global_2025,\n\ttitle = {Global health at crossroads: uniting together to overcome challenges, restore trust and advance priorities for a sustainable future},\n\tvolume = {20},\n\tissn = {1749-7922},\n\tshorttitle = {Global health at crossroads},\n\turl = {https://wjes.biomedcentral.com/articles/10.1186/s13017-025-00656-w},\n\tdoi = {10.1186/s13017-025-00656-w},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {World Journal of Emergency Surgery},\n\tauthor = {Sartelli, Massimo and Mossialos, Elias and Coccolini, Federico and Jammer, Ib and Labricciosa, Francesco M. and Barie, Philip and Biffl, Walter L. and Memish, Ziad A. and Maeurer, Markus and Kobinger, Gary P. and Ippolito, Giuseppe and Zumla, Alimuddin and Catena, Fausto and {Global Consortium for Solidarity to Overcome Challenges, Restore Trustand Advance Science for a Sustainable Future} and Abbo, Lilian M. and Abraham, Yishak and Abu-Zidan, Fikri M. and Adamou, Harissou and Agastra, Ervis and Agodi, Antonella and Ahmed, Rizwan and Aklillu, Eleni and Ala, Aftab and Alex-Wele, Mary A. and Alfouzan, Wadha and Al-Hasan, Majdi N. and Ali, Sajjad and Ali, Syed Muhammad and Al-Omari, Abdelkarim and Al-Omari, Jamal A. K. and Al-Shehari, Mohammed and Amir, Afreenish and Amponsah, Obed Kwabena Offe and Anis, Hasnaoui and Ansaloni, Luca and Ansari, Shamshul and Arauz, Ana Belen and Aruyaru, Stanley and Augustin, Goran and Awazi, Bih and Azfar, Mohammad and Azhar, Esam I. and Bains, Lovenish and Bala, Miklosh and Baral, Suman and Baraket, Oussema and Barchitta, Martina and Murguía, Maria E. Baridó and Barkema, Herman and Barreda, Rodrigo López and Basher, Ariful and Bassetti, Matteo and Beilman, Gregory and Beka, Solomon Gurmu and Benboubker, Moussa and Beović, Bojana and Biemba, Godfrey and Bignami, Elena Giovanna and Blanchet, Karl and Blot, Stijn and Bonomo, Robert A. and Brink, Adrian and Brusaferro, Silvio and Bueno, Juan and Bulanauca, Maloni and Buonomo, Luis and Caínzos, Miguel A. and Camacho-Ortiz, Adrian and Canton, Rafael and Cantürk, Alp Ömer and Carlini, Massimo and Cascio, Antonio and Casini, Beatrice and Cassini, Alessandro and Catena, Rodolfo and Cavaillon, Jean-Marc and Ceschi, Piera and Cheadle, William G. and Olinyo, Diana Chebet and Chiara, Francesca and Chikowe, Ibrahim and Chimatiro, Syrold and Chioti, Anna and Chiwodza, Zororai and Chowdhury, Sharfuddin and Cocuz, Maria-Elena and Coimbra, Raul and Correia, Tiago and Cortese, Francesco and Cricca, Monica and Cui, Yunfeng and Czepiel, Jacek and Dahal, Ek Raj and Dar, Osman and De Angelis, Giulia and Delibegovic, Samir and Dellinger, E. Patchen and Demetrashvili, Zaza and De Palma, Alessandra and De Simone, Belinda and De Silva, Danushka and Detanac, Dzemail and Dhingra, Sameer and Diaz, Jose J. and Dima, Claudia and Diwan, Vinod and Dogjani, Agron and Dorj, Gereltuya and Dulskas, Audrius and Eckmann, Christian and Erdene, Sarnai and Egyir, Beverly and Elhassi, Ahmed and Elmangory, Mutasim M. and Omer, Hala Fathi EmamElkhir and Ergonul, Onder and Antezana, Juan Pablo Escalera and Everett, Dean B. and Fabbri, Elisa and Fadare, Joseph O. and Fantoni, Massimo and Farsakoury, Rana and Fassari, Alessia and Ferrada, Paula and Ferreres, Alberto and Filipescu, Daniela and Foghetti, Domitilla and Gandhi, Chinmay and Gastaldi, Silvana and Gemmi, Fabrizio and Gerardi, Chiara and Ghannam, Wagih and Giamarellou, Helen and Giordano, Alessio and Gkiokas, George and Glasbey, James and Glushkova, Natalya and Gomes, Carlos Augusto and Herrera, María Norma Gómez and Gomi, Harumi and Gonullu, Emre and Granata, Guido and Griffiths, Ewen and Grynchuk, Fedir and Gualano, Maria Rosaria and Guirao, Xavier and Haddadin, Ruba and Hajhamad, Mohammed M. H. and Hakemi-Vala, Mojdeh and Halle-Ekane, Gregory Edie and Hansen, Sonja and Haque, Mainul and Hardcastle, Timothy C. and Hecker, Andreas and Hui, David S. and Inaba, Kenji and Isik, Arda and Ishimwe, Marcel and Iskandar, Katia and Itani, Kamal and Jaffar, Shabbar and Jaidane, Nadia and Jeschke, Marc G. and Jensen, Peter Østrup and Johnson, Walt and Kamara, Ibrahim Franklyn and Kamarulzaman, Adeeba and Kanj, Souha S. and Kaplan, Lewis and Keikha, Masoud and Khalid, Abdullahi and Khamis, Faryal and Khokha, Vladimir and Kiguba, Ronald and Kilpatrick, Claire and Kim, Hong Bin and Kirkpatrick, Andrew W. and Ko, Wen-Chien and Kok, Kenneth Y. Y. and Korzh, Oleksii and Kotecha, Vihar and Kouma, Ibrahima and Krasniqi, Jehona and Kruger, Vitor Favali and Kryvoruchko, Igor and Kullar, Ravina and Kuriyama, Akira and Kyota, Steve and Lakanwall, Mohammad Naeem and Lakatos, Botond and Lakoh, Sulaiman and Lansang, Mary Ann and Latifi, Rifat and Lee, Jae Gil and Lee, Shui Shan and Leone, Marc and Leppaniemi, Ari and Hara, Gabriel Levy and Litvin, Andrey and López-Vidal, Yolanda and Machain, Gustavo M. and Macias, Alejandro E. and Mbamalu, Oluchi and Mahomoodally, Fawzi and Maiti, Sourav and Majumder, Md Anwarul Azim and Malama, Sydney and Manasa, Justen and Manzano-Nunez, Ramiro and Marmorale, Cristina and Martínez-Pérez, Aleix and Marwah, Sanjay and Maves, Ryan C. and McHugh, Timothy D. and McLay, Carol and Juan José Meléndez, L. and Meschiari, Marianna and Metan, Gokhan and Mfinanga, Sayoki and Mierzejewska, Anna and Miranda-Novales, María Guadalupe and Mikic, Margareta and Mishra, Shyam Kumar and Mohammed, Yahaya and Molina, Gabriel and Molla, Lindita Salia and Montravers, Philippe and Monzani, Roberta and Moro, Maria Luisa and Motta, Fabrizio and M’Pelé, Pierre K. and Mudenda, Steward and Mugisha, Mc Juan Muco and Murri, Rita and Muşină, Ana-Maria and Mutters, Nico T. and Mwaba, Peter and Nabyonga-Orem, Juliet and Naeem, Junaid and Navsaria, Pradeep H. and Negoi, Ionut and Nyeko, David and Ntoumi, Francine and Nouwen, Jan and Ochoa-Hein, Eric and O’Connor, Donald and Olausson, Maria and Onyeaghala, Chizaram and Ordoñez, Carlos and Orozco, Hilda Gpe Hernandez and Ouadii, Mouaqit and Ouedraogo, Abdoul-Salam and Pagani, Leonardo and Paiva, José Artur and Pan, Angelo and Panyko, Arpád and Paolillo, Ciro and Pasero, Daniela and Patel, Jay and Petersen, Eskild and Petrone, Patrizio and Petrosillo, Nicola and Pintar, Tadeja and Pipitone, Giuseppe and Pikoulis, Emmamouil and Plaudis, Haurald and Podda, Mauro and De León, Alfredo Ponce and De León, Samuel Ponce and Guerrero, Adrián Puello and Rasa, Kemal and Reichert, Martin and Rello, Jordi and Reynolds-Campbell, Glendee and Resanovic, Vladimir and Rezza, Giovanni and Ribeiro, Julival and Rickard, Jennifer and Ripabelli, Giancarlo and Rodrigues, Gabriel Sunil and Rodriguez-Morales, Alfonso Javier and Villamil, Gustavo Eduardo Roncancio and Różańska-Walędziak, Anna and Rubio-Perez, Ines and Rwegerera, Godfrey and Sabbatucci, Michela and Terrazas, Jesús Manuel Sáenz and Saguil, Esther and Sakakushev, Boris E. and Saladžinskas, Žilvinas and Salile, Samson Sahile and Sall, Ibrahima and Kafil, Hossein Samadi and Santillan-Doherty, Patricio and Satta, Giovanni and Sawyer, Robert G. and Schizas, Dimitrios and Lohse, Helmut Alfredo Segovia and Seni, Jeremiah and Septimus, Edward J. and Sganga, Gabriele and Shabaan, Vivian and Shabanzadeh, Daniel Mønsted and Hussein, Mohamud Sheek and Shelat, Vishal G. and Shibabaw, Agumas and Shlyapnikov, Sergei A. and Singh, Iqbal and Singh, Keerti and Siribumrungwong, Boonying and Somville, Francis and Shor, Elina and Soreide, Kjetil and Stefani, Stefania and Storr, Jules and Sydorchuk, Larysa and Sydorchuk, Ruslan and Szabo, Balint Gergely and Tan, Boun Kim and Tartari, Ermira and Tattevin, Pierre and Almenares, Orlando Téllez and Tian, Brian W. C. A. and Tochie, Joel Noutakdie and Todorovic, Zoran and Bifa, Kasu Tola and Tolonen, Matti and Torres, Margarida and Traore, Tieble and Trostchansky, Ivan and Trueba, Gabriel and Tsioutis, Constantinos and Tsogbale, Novissi and Tumietto, Fabio and Turrado-Rodríguez, Víctor and Udoh, Ubong and Ulrych, Jan and Umo, Ian and Uranues, Selman and Van Dongen, Maarten and Varghese, Chris and Vasilescu, Alin Mihai and Vasiljev, Krstina Doklestic and Velmahos, George C. and Viaggi, Bruno and Vila, Jordi and Walędziak, Maciej and Waruingi, Daniel and Watkins, Richard R. and Wechsler-Fördös, Agnes and Waworuntu, Olivia and Wesangula, Evelyn and Yadgarova, Klara and Yeboah-Manu, Dorothy and Yepez, Raul and Willcox, Mark and Younis, Muhammad Umar and Yuan, Kuo-Ching and Zakaria, Andee Dzulkarnaen and Zakrison, Tanya L. and Mesia, Victor Zamora and Zamudio-Lugo, Irma and Zhang, Guixi and Zorzet, Anna and Zubareva, Nadezhda and Zughaier, Susu M. and Zuidema, Wietse P. and Zumla, Adam},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {84},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Tuberculosis and HIV coinfection: Progress and challenges towards reducing incidence and mortality.\n \n \n \n \n\n\n \n Sossen, B.; Kubjane, M.; and Meintjes, G.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 155: 107876. June 2025.\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{sossen_tuberculosis_2025,\n\ttitle = {Tuberculosis and {HIV} coinfection: {Progress} and challenges towards reducing incidence and mortality},\n\tvolume = {155},\n\tissn = {12019712},\n\tshorttitle = {Tuberculosis and {HIV} coinfection},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971225000992},\n\tdoi = {10.1016/j.ijid.2025.107876},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Sossen, Bianca and Kubjane, Mmamapudi and Meintjes, Graeme},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {107876},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Kisspeptin fiber and receptor distribution analysis suggests its potential role in central sensorial processing and behavioral state control.\n \n \n \n \n\n\n \n Zhang, L.; Hernández, V. S.; Zetter, M. A.; Hernández‐Pérez, O. R.; Hernández‐González, R.; Camacho‐Arroyo, I.; Eiden, L. E.; and Millar, R. P.\n\n\n \n\n\n\n Journal of Neuroendocrinology, 37(5): e70007. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Kisspeptin$ Paper\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{zhang_kisspeptin_2025,\n\ttitle = {Kisspeptin fiber and receptor distribution analysis suggests its potential role in central sensorial processing and behavioral state control},\n\tvolume = {37},\n\tissn = {0953-8194, 1365-2826},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/jne.70007},\n\tdoi = {10.1111/jne.70007},\n\tabstract = {Abstract \n             \n              Kisspeptin (KP) signaling in the brain is defined by the anatomical distribution of KP‐producing neurons, their fibers, receptors, and connectivity. Technological advances have prompted a re‐evaluation of these chemoanatomical aspects, originally studied in the early years after the discovery of KP and its receptor \n              Kiss1r. \n              Previously, we characterized (Hernández et al. bioRxiv 2024) seven KP neuronal populations in the mouse brain at the mRNA level, including two novel populations, and examined their response to gonadectomy. In this study, we mapped KP fiber distribution in rats and mice using immunohistochemistry under intact as well as short‐ and long‐term post‐gonadectomy conditions. \n              Kiss1r \n              mRNA expression was examined via RNAscope, in relation to vesicular GABA transporter ( \n              Slc32a1 \n              ) in whole mouse brain, and to KP and vesicular glutamate transporter 2 ( \n              Slc17a6 \n              ), \n              Kiss1 \n              , and \n              Slc32a1 \n              in hypothalamic RP3V and arcuate regions. We identified KP fibers in 118 brain regions, primarily in extra‐hypothalamic areas associated with sensorial processing and behavioral state control. KP‐immunoreactive fiber density and distribution were largely unchanged by gonadectomy. \n              Kiss1r \n              was expressed prominently in sensorial and state control regions such as the septal nuclei, the suprachiasmatic nucleus, locus coeruleus, hippocampal layers, thalamic nuclei, and cerebellar structures. Co‐expression of \n              Kiss1r \n              and \n              Kiss1 \n              was observed in hypothalamic neurons, suggesting both autocrine and paracrine KP signaling mechanisms. These findings enhance our understanding of KP signaling beyond reproductive functions, particularly in sensorial processing and behavioral state regulation. This study opens new avenues for investigating KP's role in controlling complex physiological processes, including those unrelated to reproduction.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Neuroendocrinology},\n\tauthor = {Zhang, Limei and Hernández, Vito Salvador and Zetter, Mario Alberto and Hernández‐Pérez, Oscar Rene and Hernández‐González, Rafael and Camacho‐Arroyo, Ignacio and Eiden, Lee E. and Millar, Robert P.},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {e70007},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Advancing the course of HIV genomics research in Africa.\n \n \n \n \n\n\n \n Agamah, F. E; Arbuthnot, P.; Tindana, P.; Munung, N. S.; Kasule, M.; Ghansah, A.; Mosepele, M.; Gaolathe, T.; Kekitiinwa, A.; Nduati, E.; Jumare, J.; Gómez-Olivé, F. X.; Liebenberg, L.; Dandara, C.; Osawe, S.; Julius, R.; Muzambi, T.; Natus, T.; Omumbo, J.; Mayne, E.; Abimiku, A.; Richardson, S.; Matshaba, M.; and Skelton, M.\n\n\n \n\n\n\n BMJ Global Health, 10(8): e019094. August 2025.\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{agamah_advancing_2025,\n\ttitle = {Advancing the course of {HIV} genomics research in {Africa}},\n\tvolume = {10},\n\tissn = {2059-7908},\n\turl = {https://gh.bmj.com/lookup/doi/10.1136/bmjgh-2025-019094},\n\tdoi = {10.1136/bmjgh-2025-019094},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-28},\n\tjournal = {BMJ Global Health},\n\tauthor = {Agamah, Francis E and Arbuthnot, Patrick and Tindana, Paulina and Munung, Nchangwi Synthia and Kasule, Mary and Ghansah, Anita and Mosepele, Mosepele and Gaolathe, Tendani and Kekitiinwa, Adeodata and Nduati, Eunice and Jumare, Jibreel and Gómez-Olivé, Francesc Xavier and Liebenberg, Lenine and Dandara, Collet and Osawe, Sophia and Julius, Rolanda and Muzambi, Tino and Natus, Tanian and Omumbo, Judith and Mayne, Elizabeth and Abimiku, Alash’le and Richardson, Simone and Matshaba, Mogomotsi and Skelton, Michelle},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {e019094},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Pre-existing adipose tissue signaling profile related to obesity determines disease outcome of COVID-19: addressing obesity should be a priority for future pandemic preparedness.\n \n \n \n \n\n\n \n Parker, A.; Petersen-Ross, K.; Maponga, T.; Parkar, S.; Ahmed, N.; Snyders, C. I.; Kidd, M.; Taljaard, J. J.; Meintjes, G.; Koegelenberg, C. F. N.; Kleynhans, L.; and Smith, C.\n\n\n \n\n\n\n Frontiers in Endocrinology, 16: 1506065. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Pre-existing$ Paper\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{parker_pre-existing_2025,\n\ttitle = {Pre-existing adipose tissue signaling profile related to obesity determines disease outcome of {COVID}-19: addressing obesity should be a priority for future pandemic preparedness},\n\tvolume = {16},\n\tissn = {1664-2392},\n\tshorttitle = {Pre-existing adipose tissue signaling profile related to obesity determines disease outcome of {COVID}-19},\n\turl = {https://www.frontiersin.org/articles/10.3389/fendo.2025.1506065/full},\n\tdoi = {10.3389/fendo.2025.1506065},\n\tabstract = {Objectives \n              Obesity is associated with COVID-19 severity and mortality. We investigated relationships between adipokines, cytokines and redox parameters with obesity, human immunodeficiency virus (HIV), severity and outcome. \n             \n             \n              Methods \n               \n                In the exploratory study, adipose tissue (AT) was sampled in patients with COVID-19 on admission. Concentrations of leptin, adiponectin, resistin, interleukin 1 beta (IL-1b), IL-2, IL-6, IL-10, IL-17, tumor necrosis factor alpha (TNF-a), monocyte chemoattractant protein 1 (MCP-1), Trolox equivalent antioxidant capacity (TEAC), oxidative stress (H \n                2 \n                0 \n                2 \n                ) and malonaldehyde (MDA) were determined. \n               \n             \n             \n              Results \n              Thirty-eight biopsies of subcutaneous adipose tissue were obtained (prevalence of HIV was 39\\% and of obesity 61\\%). Higher IL-6 serum concentrations (p=0.03) were associated with more severe COVID-19, and higher serum IL-10 concentrations, (p=0.03) with mortality. People with obesity had higher leptin concentrations (p=0.03, and p\\&lt;0.01), lower adiponectin/leptin (p=0.03 and p\\&lt;0.01), and higher leptin/resistin ratios (p=0.09 and p\\&lt;0.01) in both AT and serum respectively. Higher leptin/resistin (p=0.04) and lower adiponectin/resistin (p=0.05) ratios in AT, but not serum, were predictive of mortality. HIV was not associated with any differences. Relationships between resistin and redox indicators, TEAC and MDA, suggest a dysregulation of metabolic vs immune-relevant effect of resistin, which differentially predicted severity and mortality. SARS-CoV-2 RNA was detected in the subcutaneous AT in 3/8 patients who demised, but only in 1/30 who survived. \n             \n             \n              Conclusion \n              Given the significant link demonstrated between leptin dysregulation in obesity and mortal severity of COVID-19, addressing obesity should be a priority therapeutic target in terms of future pandemic preparedness. Mechanistic studies are recommended to further elucidate the importance of metabolic vs immune modulation by resistin in COVID-19, to identify future therapeutic targets.},\n\turldate = {2026-05-28},\n\tjournal = {Frontiers in Endocrinology},\n\tauthor = {Parker, Arifa and Petersen-Ross, Kelly and Maponga, Tongai and Parkar, Samina and Ahmed, Nadiya and Snyders, Candice I. and Kidd, Martin and Taljaard, Jantjie J. and Meintjes, Graeme and Koegelenberg, Coenraad F. N. and Kleynhans, Léanie and Smith, Carine},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {1506065},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Marburg virus disease outbreak in Rwanda, 2024.\n \n \n \n \n\n\n \n Grobusch, M. P.; Jokelainen, P.; Wyllie, A. L.; Gupta, N.; Paño-Pardo, J. R.; Barac, A.; Bulescu, C.; Pellejero-Sagastizábal, G.; Goorhuis, A.; Lescure, F.; Gkrania-Klotsas, E.; and Mora-Rillo, M.\n\n\n \n\n\n\n Clinical Microbiology and Infection, 31(2): 161–163. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Marburg$ Paper\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{grobusch_marburg_2025,\n\ttitle = {Marburg virus disease outbreak in {Rwanda}, 2024},\n\tvolume = {31},\n\tissn = {1198743X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1198743X24005585},\n\tdoi = {10.1016/j.cmi.2024.11.027},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {Clinical Microbiology and Infection},\n\tauthor = {Grobusch, Martin P. and Jokelainen, Pikka and Wyllie, Anne L. and Gupta, Nitin and Paño-Pardo, José Ramón and Barac, Aleksandra and Bulescu, Casandra and Pellejero-Sagastizábal, Galadriel and Goorhuis, Abraham and Lescure, F-Xavier and Gkrania-Klotsas, Effrossyni and Mora-Rillo, Marta},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {161--163},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n What it takes to become a physician scientist in a low- and middle-income country.\n \n \n \n \n\n\n \n Barreto-Duarte, B.; Mendelsohn, S. C.; Bruyn, E. D.; and Andrade, B. B.\n\n\n \n\n\n\n PLOS Global Public Health, 5(4): e0004234. April 2025.\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 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{barreto-duarte_what_2025,\n\ttitle = {What it takes to become a physician scientist in a low- and middle-income country},\n\tvolume = {5},\n\tissn = {2767-3375},\n\turl = {https://dx.plos.org/10.1371/journal.pgph.0004234},\n\tdoi = {10.1371/journal.pgph.0004234},\n\tabstract = {Physician-scientists, who have dual medical and advanced research training, are a scarce and valuable asset. They bridge clinical practice and research, address critical medical challenges with a scientific perspective, and drive innovation by translating discoveries into patient care. Physicians with research expertise are particularly adept at critically evaluating scientific literature to improve their practice and ensure that they provide up-to-date, individualised, and evidence-based care to their patients. However, the path to becoming a physician-scientist in Low- and Middle-Income Countries (LMICs) is fraught with challenges. In this article, we explore the difficulties faced by physician-scientists in LMICs, including lengthy and arduous training, systems that favour eminence-based over evidence-based medicine, and financial disincentives for pursuing a dual career in medicine and research. The article also highlights the significant underrepresentation of women in medical and scientific fields, compounded by gender-specific challenges such as balancing motherhood with career demands, gender pay gaps, and the lack of supportive and affirmative policies. We advocate for reforms in medical education to create a more supportive environment for aspiring physician-scientists. Addressing these issues can help LMICs enhance the contribution of physician-scientists to global health and scientific advancement.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-28},\n\tjournal = {PLOS Global Public Health},\n\tauthor = {Barreto-Duarte, Beatriz and Mendelsohn, Simon C. and Bruyn, Elsa Du and Andrade, Bruno B.},\n\teditor = {Zeinali, Zahra},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {e0004234},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Recombination Analysis of Geminiviruses Using Recombination Detection Program (RDP).\n \n \n \n \n\n\n \n Crespo-Bellido, A.; Martin, D. P.; and Duffy, S.\n\n\n \n\n\n\n In Zerbini, F. M.; Fiallo-Olivé, E.; and Navas-Castillo, J., editor(s), Geminiviruses, volume 2912, pages 125–143. Springer US, New York, NY, 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Recombination$ Paper\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{zerbini_recombination_2025,\n\taddress = {New York, NY},\n\ttitle = {Recombination {Analysis} of {Geminiviruses} {Using} {Recombination} {Detection} {Program} ({RDP})},\n\tvolume = {2912},\n\tisbn = {9781071644539 9781071644546},\n\turl = {https://link.springer.com/10.1007/978-1-0716-4454-6_11},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tbooktitle = {Geminiviruses},\n\tpublisher = {Springer US},\n\tauthor = {Crespo-Bellido, Alvin and Martin, Darren Patrick and Duffy, Siobain},\n\teditor = {Zerbini, Francisco Murilo and Fiallo-Olivé, Elvira and Navas-Castillo, Jesús},\n\tyear = {2025},\n\tdoi = {10.1007/978-1-0716-4454-6_11},\n\tpages = {125--143},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n 6-Phenoxyl-4-aminoquinoline: synthesis and preliminary antitubercular-structure activity relationship analyses.\n \n \n \n \n\n\n \n Beteck, R. M.; Legoabe, L. J.; Dube, P. S.; Jordaan, A.; and Warner, D. F.\n\n\n \n\n\n\n Medicinal Chemistry Research, 34(5): 1065–1073. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"6-Phenoxyl-4-aminoquinoline:$ Paper\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{beteck_6-phenoxyl-4-aminoquinoline_2025,\n\ttitle = {6-{Phenoxyl}-4-aminoquinoline: synthesis and preliminary antitubercular-structure activity relationship analyses},\n\tvolume = {34},\n\tissn = {1054-2523, 1554-8120},\n\tshorttitle = {6-{Phenoxyl}-4-aminoquinoline},\n\turl = {https://link.springer.com/10.1007/s00044-025-03402-8},\n\tdoi = {10.1007/s00044-025-03402-8},\n\tabstract = {Abstract \n             \n              Diphenyl ether and quinoline based compounds have been reported to show antibacterial activity. Against \n              Mycobacterium tuberculosis \n              , drug targets inhibited by diphenyl ether compounds are reportedly different from those perturbed by quinoline based antitubercular hits/drugs. Herein, we conceptualized and synthesized novel molecules incorporating quinoline and diphenyl ether moieties. The antitubercular property of the synthesized compounds were measured in vitro using Tween 80 and Tyloxapol supplemented growth media. Compounds in this study generally showed sub micromolar antitubercular activity in tween 80/albumin supplemented growth medium, and moderate to poor activity in tyloxapol/casitone supplemented growth medium. Compound \n              4e \n              , havin a trimethylenediamine moiety and low melting point of 68 °C, emerged as the hit compound, possessing MIC \n              90 \n              value of 0.2 µM. \n              4e \n              is non-cytotoxic when tested against normal human cell line, exhibiting CC \n              50 \n              value {\\textgreater} 20 µM.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {Medicinal Chemistry Research},\n\tauthor = {Beteck, Richard M. and Legoabe, Lesetja J. and Dube, Phelelisiwe S. and Jordaan, Audrey and Warner, Digby F.},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {1065--1073},\n}\n\n\n\n

\n

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

\n \n\n \n \n \n \n \n \n Artificial intelligence coupled to pharmacometrics modelling to tailor malaria and tuberculosis treatment in Africa.\n \n \n \n \n\n\n \n Turon, G.; Mulubwa, M.; Montaner, A.; Njoroge, M.; Chibale, K.; and Duran-Frigola, M.\n\n\n \n\n\n\n Nature Communications, 16(1): 9258. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Artificial$ Paper\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{turon_artificial_2025,\n\ttitle = {Artificial intelligence coupled to pharmacometrics modelling to tailor malaria and tuberculosis treatment in {Africa}},\n\tvolume = {16},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-025-64304-2},\n\tdoi = {10.1038/s41467-025-64304-2},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Nature Communications},\n\tauthor = {Turon, Gemma and Mulubwa, Mwila and Montaner, Anna and Njoroge, Mathew and Chibale, Kelly and Duran-Frigola, Miquel},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {9258},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Personalised risk-prediction tools for cryptococcal meningitis mortality to guide treatment stratification in sub-Saharan Africa: a prognostic modelling study based on pooled analysis of two randomised controlled trials.\n \n \n \n \n\n\n \n Samuels, T. H A; Molloy, S. F; Lawrence, D. S; Loyse, A.; Kanyama, C.; Heyderman, R. S; Lai, W. S.; Mfinanga, S.; Lesikari, S.; Chanda, D.; Kouanfack, C.; Temfack, E.; Lortholary, O.; Hosseinipour, M. C; Chan, A. K; Meya, D. B; Boulware, D. R; Mwandumba, H. C; Meintjes, G.; Muzoora, C.; Mosepele, M.; Ndhlovu, C. E; Youssouf, N.; Harrison, T. S; Jarvis, J. N; and Gupta, R. K\n\n\n \n\n\n\n The Lancet Global Health, 13(5): e920–e930. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Personalised$ Paper\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{samuels_personalised_2025,\n\ttitle = {Personalised risk-prediction tools for cryptococcal meningitis mortality to guide treatment stratification in sub-{Saharan} {Africa}: a prognostic modelling study based on pooled analysis of two randomised controlled trials},\n\tvolume = {13},\n\tissn = {2214109X},\n\tshorttitle = {Personalised risk-prediction tools for cryptococcal meningitis mortality to guide treatment stratification in sub-{Saharan} {Africa}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X25000105},\n\tdoi = {10.1016/S2214-109X(25)00010-5},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Global Health},\n\tauthor = {Samuels, Thomas H A and Molloy, Sile F and Lawrence, David S and Loyse, Angela and Kanyama, Cecilia and Heyderman, Robert S and Lai, Wai Shing and Mfinanga, Sayoki and Lesikari, Sokoine and Chanda, Duncan and Kouanfack, Charles and Temfack, Elvis and Lortholary, Olivier and Hosseinipour, Mina C and Chan, Adrienne K and Meya, David B and Boulware, David R and Mwandumba, Henry C and Meintjes, Graeme and Muzoora, Conrad and Mosepele, Mosepele and Ndhlovu, Chiratidzo E and Youssouf, Nabila and Harrison, Thomas S and Jarvis, Joseph N and Gupta, Rishi K},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {e920--e930},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n SARS-CoV-2 vaccines elicit differential Fc effector functions.\n \n \n \n \n\n\n \n Manamela, N. P.; Motsoeneng, B. M.; Spencer, H.; Hermanus, T.; Mzindle, N.; Ayres, F.; Makhado, Z.; Serage, R.; Gray, G. G.; Bekker, L.; Madhi, S. A.; Moore, P. L.; and Richardson, S. I.\n\n\n \n\n\n\n iScience, 28(8): 113084. August 2025.\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{manamela_sars-cov-2_2025,\n\ttitle = {{SARS}-{CoV}-2 vaccines elicit differential {Fc} effector functions},\n\tvolume = {28},\n\tissn = {25890042},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2589004225013458},\n\tdoi = {10.1016/j.isci.2025.113084},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-28},\n\tjournal = {iScience},\n\tauthor = {Manamela, Nelia P. and Motsoeneng, Boitumelo M. and Spencer, Holly and Hermanus, Tandile and Mzindle, Nonkululeko and Ayres, Frances and Makhado, Zanele and Serage, Rudolph and Gray, Glenda G. and Bekker, Linda-Gail and Madhi, Shabir A. and Moore, Penny L. and Richardson, Simone I.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {113084},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Anti-CD64(scFv)-SNAP-Auristatin F: An in vitro proof of concept study for a recombinant antibody conjugate targeting CD64+ acute monocytic leukemia.\n \n \n \n \n\n\n \n Akinrinmade, O. A.; Fajemisin, E. A.; Daramola, A. K.; Huysamen, A.; Fadeyi, O.; Dogbey, D. M.; Biteghe, F. A.; Hunter, R.; and Barth, S.\n\n\n \n\n\n\n European Journal of Medicinal Chemistry, 290: 117520. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Anti-CD64(scFv)-SNAP-Auristatin$ Paper\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{akinrinmade_anti-cd64scfv-snap-auristatin_2025,\n\ttitle = {Anti-{CD64}({scFv})-{SNAP}-{Auristatin} {F}: {An} in vitro proof of concept study for a recombinant antibody conjugate targeting {CD64}+ acute monocytic leukemia},\n\tvolume = {290},\n\tissn = {02235234},\n\tshorttitle = {Anti-{CD64}({scFv})-{SNAP}-{Auristatin} {F}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0223523425002855},\n\tdoi = {10.1016/j.ejmech.2025.117520},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {European Journal of Medicinal Chemistry},\n\tauthor = {Akinrinmade, Olusiji Alex and Fajemisin, Emmanuel Adebowale and Daramola, Adebukola Kemi and Huysamen, Allan and Fadeyi, Olaolu and Dogbey, Dennis Makafui and Biteghe, Fleury A.N. and Hunter, Roger and Barth, Stefan},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {117520},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Malaria recrudescence after artemether-lumefantrine treatment in travellers– a hospital-based observational study and literature review.\n \n \n \n \n\n\n \n Schnyder, J. L.; Bache, B. E.; Hoogakker, M.; Van De Ruit, M.; Zonneveld, R.; Hermans, S. M.; Stijnis, C.; Van Vugt, M.; Hänscheid, T.; Van Hest, R. M.; Goorhuis, A.; De Jong, H. K.; and Grobusch, M. P.\n\n\n \n\n\n\n Tropical Diseases, Travel Medicine and Vaccines, 11(1): 19. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Malaria$ Paper\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{schnyder_malaria_2025,\n\ttitle = {Malaria recrudescence after artemether-lumefantrine treatment in travellers– a hospital-based observational study and literature review},\n\tvolume = {11},\n\tissn = {2055-0936},\n\turl = {https://tdtmvjournal.biomedcentral.com/articles/10.1186/s40794-025-00256-1},\n\tdoi = {10.1186/s40794-025-00256-1},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Tropical Diseases, Travel Medicine and Vaccines},\n\tauthor = {Schnyder, Jenny L. and Bache, Bache E. and Hoogakker, Mika and Van De Ruit, Mabel and Zonneveld, Rens and Hermans, Sabine M. and Stijnis, Cornelis and Van Vugt, Michèle and Hänscheid, Thomas and Van Hest, Reinier M. and Goorhuis, Abraham and De Jong, Hanna K. and Grobusch, Martin P.},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {19},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n COVID-19 pandemic reclassification and implications for continuing uptake of COVID-19 vaccination: The case of Savannah Region, Ghana, 2023.\n \n \n \n \n\n\n \n Adjei, M. R.; Sarfo, K. A.; Azornu, C. K.; Kwarteng, P. G.; Osei-Sarpong, F.; Baafi, J. V.; Bafana, N. A. A.; Kubio, C.; Ohene, S.; and Grobusch, M. P.\n\n\n \n\n\n\n IJID Regions, 16: 100694. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"COVID-19$ Paper\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{adjei_covid-19_2025,\n\ttitle = {{COVID}-19 pandemic reclassification and implications for continuing uptake of {COVID}-19 vaccination: {The} case of {Savannah} {Region}, {Ghana}, 2023},\n\tvolume = {16},\n\tissn = {27727076},\n\tshorttitle = {{COVID}-19 pandemic reclassification and implications for continuing uptake of {COVID}-19 vaccination},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2772707625001298},\n\tdoi = {10.1016/j.ijregi.2025.100694},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {IJID Regions},\n\tauthor = {Adjei, Michael Rockson and Sarfo, Kwabena Adjei and Azornu, Cyril Kwami and Kwarteng, Peter Gyamfi and Osei-Sarpong, Felix and Baafi, Janet Vanessa and Bafana, Nana Akua Afriyie and Kubio, Chrysantus and Ohene, Sally-Ann and Grobusch, Martin Peter},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {100694},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Live-attenuated Mycobacterium tuberculosis vaccine, MTBVAC, in adults with or without M tuberculosis sensitisation: a single-centre, phase 1b–2a, double-blind, dose-escalation, randomised controlled trial.\n \n \n \n \n\n\n \n Luabeya, A. K. K.; Rozot, V.; Imbratta, C.; Ratangee, F.; Shenje, J.; Tameris, M.; Mendelsohn, S. C; Geldenhuys, H.; Fisher, M.; Musvosvi, M.; Young, C.; Mulenga, H.; Bilek, N.; Mabwe, S.; Jelsbak, I. M.; Rodríguez, E.; Puentes, E.; Doce, J.; Aguilo, N.; Martin, C.; Pillay, C.; Tait, D.; Russell, M.; Van Der Merve, A.; Rutkowski, K.; Hunt, D.; Ginsberg, A.; Scriba, T. J; Hatherill, M.; Swanepoel, L.; Davids, I.; De Kock, M.; Botes, N.; Rossouw, S.; Barnard, L.; Verster, E.; Veldsman, A.; Meyer, F.; Kaskar, M.; Leopeng, T.; Noble, J.; Africa, H.; Valley, H.; Steyn, M.; Makhete, L.; Mangali, S.; Nkambule, H.; Erasmus, M.; Jaxa, L.; Raphela, R.; Schreuder, C.; Cloete, Y.; Nambida, O.; Companie, A.; Khomba, G.; Abrahams, C.; Magawu, P.; Mactavie, L.; Erasmus, M.; Van Rooyen, J.; Mouton, A.; Opperman, F.; Segelaar, C.; Tyambetyu, P.; Diamond, B.; Veldtsman, H.; and Reid, T.\n\n\n \n\n\n\n The Lancet Global Health, 13(6): e1030–e1042. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Live-attenuated$ Paper\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{luabeya_live-attenuated_2025,\n\ttitle = {Live-attenuated {Mycobacterium} tuberculosis vaccine, {MTBVAC}, in adults with or without {M} tuberculosis sensitisation: a single-centre, phase 1b–2a, double-blind, dose-escalation, randomised controlled trial},\n\tvolume = {13},\n\tissn = {2214109X},\n\tshorttitle = {Live-attenuated {Mycobacterium} tuberculosis vaccine, {MTBVAC}, in adults with or without {M} tuberculosis sensitisation},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X25000464},\n\tdoi = {10.1016/S2214-109X(25)00046-4},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Global Health},\n\tauthor = {Luabeya, Angelique Kany Kany and Rozot, Virginie and Imbratta, Claire and Ratangee, Frances and Shenje, Justin and Tameris, Michele and Mendelsohn, Simon C and Geldenhuys, Hennie and Fisher, Michelle and Musvosvi, Munyaradzi and Young, Carly and Mulenga, Humphrey and Bilek, Nicole and Mabwe, Simbarashe and Jelsbak, Ingrid Murillo and Rodríguez, Esteban and Puentes, Eugenia and Doce, Juana and Aguilo, Nacho and Martin, Carlos and Pillay, Cadwill and Tait, Dereck and Russell, Marisa and Van Der Merve, Arrie and Rutkowski, Kathryn and Hunt, Devin and Ginsberg, Ann and Scriba, Thomas J and Hatherill, Mark and Swanepoel, Liticia and Davids, Ilse and De Kock, Marwou and Botes, Natasja and Rossouw, Susan and Barnard, Liezl and Verster, Elmien and Veldsman, Ashley and Meyer, Faheemah and Kaskar, Masooda and Leopeng, Thelma and Noble, Julia and Africa, Hadn and Valley, Habibullah and Steyn, Marcia and Makhete, Lebohgang and Mangali, Sandisiwe and Nkambule, Hlengiwe and Erasmus, Mzwandile and Jaxa, Lungisa and Raphela, Rodney and Schreuder, Constance and Cloete, Yolundi and Nambida, Onke and Companie, Alessandro and Khomba, Gloria and Abrahams, Charmaine and Magawu, Patricia and Mactavie, Lauren and Erasmus, Margareth and Van Rooyen, Johanna and Mouton, Angelique and Opperman, Fajwa and Segelaar, Carmen and Tyambetyu, Petrus and Diamond, Bongani and Veldtsman, Helen and Reid, Tim},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {e1030--e1042},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n c-Myc, AKT, Hsc70, and the T-Box Transcription Factor TBX3 Form an Important Oncogenic Signaling Axis in Breast Cancer.\n \n \n \n \n\n\n \n Ncube, S. M.; Nagarajan, A.; Lang, D.; Sinkala, M.; Burmeister, C. A.; Serala, K.; Blackburn, J.; and Prince, S.\n\n\n \n\n\n\n Molecular Cancer Research, 23(1): 20–32. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"c-Myc,$ Paper\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{ncube_c-myc_2025,\n\ttitle = {c-{Myc}, {AKT}, {Hsc70}, and the {T}-{Box} {Transcription} {Factor} {TBX3} {Form} an {Important} {Oncogenic} {Signaling} {Axis} in {Breast} {Cancer}},\n\tvolume = {23},\n\tissn = {1541-7786, 1557-3125},\n\turl = {https://aacrjournals.org/mcr/article/23/1/20/750582/c-Myc-AKT-Hsc70-and-the-T-Box-Transcription-Factor},\n\tdoi = {10.1158/1541-7786.MCR-23-1031},\n\tabstract = {Abstract \n             \n               \n              Breast cancer is the second leading cause of death in women globally, and it remains a health burden due to poor therapy response, cancer cell drug resistance, and the debilitating side effects associated with most therapies. One approach to addressing the need to improve breast cancer therapies has been to elucidate the mechanism(s) underpinning this disease to identify key drivers that can be targeted in molecular therapies. The T-box transcription factor, TBX3, is upregulated in breast cancer, in which it contributes to important oncogenic processes, and it has been validated as a potential therapeutic target. Here, we investigated the molecular mechanisms that upregulate TBX3 in breast cancer, and we show that it involves transcriptional activation by c-Myc, post-translational modification by AKT1 and AKT3, and interaction with the molecular chaperone Hsc70. Together, the results from this study provide evidence that c-Myc, AKT, Hsc70, and TBX3 form part of an important oncogenic pathway in breast cancer and thus reveal versatile ways of interfering with the oncogenic activity of TBX3 for the treatment of this neoplasm. \n             \n             \n              Implications: \n              Targeting the c-Myc/AKT/TBX3/Hsc70 signaling axis may be an effective treatment strategy for TBX3-driven breast cancer.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Molecular Cancer Research},\n\tauthor = {Ncube, Stephanie M. and Nagarajan, ArulJothi and Lang, Dirk and Sinkala, Musalula and Burmeister, Carly A. and Serala, Karabo and Blackburn, Jonathan and Prince, Sharon},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {20--32},\n}\n\n\n\n

\n

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

\n \n\n \n \n \n \n \n \n Implementing health economics for pharmacogenomics research translation in Africa.\n \n \n \n \n\n\n \n Alimohamed, M. Z.; Obeng, G. D.; Csanadi, M.; Masimirembwa, C.; and Dandara, C.\n\n\n \n\n\n\n Communications Medicine, 5(1): 241. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Implementing$ Paper\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{alimohamed_implementing_2025,\n\ttitle = {Implementing health economics for pharmacogenomics research translation in {Africa}},\n\tvolume = {5},\n\tissn = {2730-664X},\n\turl = {https://www.nature.com/articles/s43856-025-00955-y},\n\tdoi = {10.1038/s43856-025-00955-y},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Communications Medicine},\n\tauthor = {Alimohamed, Mohamed Zahir and Obeng, George Dennis and Csanadi, Marcell and Masimirembwa, Collen and Dandara, Collet},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {241},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n The participation of people deprived of liberty in tuberculosis vaccine trials: should they be protected from research, or through research?.\n \n \n \n \n\n\n \n Andrews, J. R; Charalambous, S.; Churchyard, G.; Cobelens, F.; Fernández-Escobar, C.; Frick, M.; Hanekom, W.; Hatherill, M.; Hill, P. C; Pandey, S.; Rangaka, M. X; White, R. G; Lemos, E. F; Da Silva, A. M.; Croda, J.; and Garcia-Basteiro, A. L\n\n\n \n\n\n\n The Lancet Infectious Diseases, 25(12): e722–e729. December 2025.\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{andrews_participation_2025,\n\ttitle = {The participation of people deprived of liberty in tuberculosis vaccine trials: should they be protected from research, or through research?},\n\tvolume = {25},\n\tissn = {14733099},\n\tshorttitle = {The participation of people deprived of liberty in tuberculosis vaccine trials},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1473309925003056},\n\tdoi = {10.1016/S1473-3099(25)00305-6},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Infectious Diseases},\n\tauthor = {Andrews, Jason R and Charalambous, Salome and Churchyard, Gavin and Cobelens, Frank and Fernández-Escobar, Carlos and Frick, Mike and Hanekom, Willem and Hatherill, Mark and Hill, Philip C and Pandey, Surabhi and Rangaka, Molebogeng X and White, Richard G and Lemos, Everton F and Da Silva, Alessandra Moura and Croda, Julio and Garcia-Basteiro, Alberto L},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e722--e729},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Effects of M. tuberculosis and HIV-1 infection on in vitro blood-brain barrier function.\n \n \n \n \n\n\n \n Proust, A.; Wilkinson, K. A.; and Wilkinson, R. J.\n\n\n \n\n\n\n Journal of Neuroinflammation, 22(1): 141. May 2025.\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

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@article{proust_effects_2025,\n\ttitle = {Effects of {M}. tuberculosis and {HIV}-1 infection on in vitro blood-brain barrier function},\n\tvolume = {22},\n\tissn = {1742-2094},\n\turl = {https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-025-03467-7},\n\tdoi = {10.1186/s12974-025-03467-7},\n\tabstract = {Abstract \n             \n              Background \n               \n                Tuberculous meningitis is the most severe form of tuberculosis and HIV-1 co-infection worsens the already poor prognosis. However, how \n                Mycobacterium tuberculosis \n                crosses the blood-brain barrier and how HIV-1 influences tuberculous meningitis pathogenesis remains unclear. \n               \n             \n             \n              Methods \n               \n                Using human pericytes, astrocytes, endothelial cells, and microglia alone and combined in an in vitro blood-brain barrier model, we investigated the effect of \n                Mycobacterium tuberculosis \n                +/- HIV-1 co-infection on central nervous system cell entry and function. Cells and the blood-brain barrier model were infected with \n                Mycobacterium tuberculosis \n                and/or HIV-1 and we evaluated the effects of both infection on (i) cells susceptibility to \n                Mycobacterium tuberculosis \n                and its growth in cells by flow cytometry; (ii) modulation of blood-brain barrier permeability and \n                Mycobacterium tuberculosis \n                passage through it; (iii) viral and bacterial cytopathogenicity using the xCELLigence system; (iv) cell metabolic activity and ROS release using colorimetric assays; (v) extracellular glutamate concentration by fluorometric assay; (vi) the inflammatory response by Luminex; and (vii) endoplasmic reticulum stress by quantitative PCR. \n               \n             \n             \n              Results \n               \n                We demonstrated that \n                Mycobacterium tuberculosis \n                infects and multiplies in all cell types with HIV-1 increasing entry to astrocytes and pericytes, and growth in HIV-1 positive pericytes and endothelial cells. \n                Mycobacterium \n                tuberculosis \n                also induces an increase of the blood-brain barrier permeability resulting in translocation of bacilli across it. Cytopathic effects include (i) increased markers of cellular stress (mitochondrial metabolic activity, unfolded protein response); (ii) ROS release; (iii) the induction of neurotoxic astrocytes; (iv) and the secretion of the excitotoxic neurotransmitter glutamate. Lastly, we observed distinct cell-type specific production of inflammatory and effector mediators. \n               \n             \n             \n              Conclusion \n               \n                These results indicate that \n                Mycobacterium tuberculosis \n                can translocate the blood-brain barrier directly to initiate meningitis.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Neuroinflammation},\n\tauthor = {Proust, Alizé and Wilkinson, Katalin A. and Wilkinson, Robert J.},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {141},\n}\n\n\n\n

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\n Abstract Background Tuberculous meningitis is the most severe form of tuberculosis and HIV-1 co-infection worsens the already poor prognosis. However, how Mycobacterium tuberculosis crosses the blood-brain barrier and how HIV-1 influences tuberculous meningitis pathogenesis remains unclear. Methods Using human pericytes, astrocytes, endothelial cells, and microglia alone and combined in an in vitro blood-brain barrier model, we investigated the effect of Mycobacterium tuberculosis +/- HIV-1 co-infection on central nervous system cell entry and function. Cells and the blood-brain barrier model were infected with Mycobacterium tuberculosis and/or HIV-1 and we evaluated the effects of both infection on (i) cells susceptibility to Mycobacterium tuberculosis and its growth in cells by flow cytometry; (ii) modulation of blood-brain barrier permeability and Mycobacterium tuberculosis passage through it; (iii) viral and bacterial cytopathogenicity using the xCELLigence system; (iv) cell metabolic activity and ROS release using colorimetric assays; (v) extracellular glutamate concentration by fluorometric assay; (vi) the inflammatory response by Luminex; and (vii) endoplasmic reticulum stress by quantitative PCR. Results We demonstrated that Mycobacterium tuberculosis infects and multiplies in all cell types with HIV-1 increasing entry to astrocytes and pericytes, and growth in HIV-1 positive pericytes and endothelial cells. Mycobacterium tuberculosis also induces an increase of the blood-brain barrier permeability resulting in translocation of bacilli across it. Cytopathic effects include (i) increased markers of cellular stress (mitochondrial metabolic activity, unfolded protein response); (ii) ROS release; (iii) the induction of neurotoxic astrocytes; (iv) and the secretion of the excitotoxic neurotransmitter glutamate. Lastly, we observed distinct cell-type specific production of inflammatory and effector mediators. Conclusion These results indicate that Mycobacterium tuberculosis can translocate the blood-brain barrier directly to initiate meningitis.\n

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\n \n\n \n \n \n \n \n \n Comparison of plant- and mammalian cell-produced human papillomavirus pseudovirions.\n \n \n \n \n\n\n \n Van Zyl, A. R.; Lindsay, S.; Schäfer, G.; Rybicki, E. P.; and Hitzeroth, I. I.\n\n\n \n\n\n\n Journal of Virological Methods, 338: 115215. December 2025.\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

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@article{van_zyl_comparison_2025,\n\ttitle = {Comparison of plant- and mammalian cell-produced human papillomavirus pseudovirions},\n\tvolume = {338},\n\tissn = {01660934},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0166093425001089},\n\tdoi = {10.1016/j.jviromet.2025.115215},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Virological Methods},\n\tauthor = {Van Zyl, Albertha R. and Lindsay, Sarah and Schäfer, Georgia and Rybicki, Edward P. and Hitzeroth, Inga I.},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {115215},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Circulating Short-Chain Fatty Acids: Association with Vaginal Microbiota, Genital Inflammation, and HIV Acquisition.\n \n \n \n \n\n\n \n Shivakoti, R.; Letsoalo, M.; Lewis, L.; Mckinnon, L. R.; Passmore, J. S.; Karim, S. S. A.; and Liebenberg, L. J.\n\n\n \n\n\n\n AIDS Research and Human Retroviruses, 41(12): 559–566. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Circulating$ Paper\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{shivakoti_circulating_2025,\n\ttitle = {Circulating {Short}-{Chain} {Fatty} {Acids}: {Association} with {Vaginal} {Microbiota}, {Genital} {Inflammation}, and {HIV} {Acquisition}},\n\tvolume = {41},\n\tissn = {0889-2229, 1931-8405},\n\tshorttitle = {Circulating {Short}-{Chain} {Fatty} {Acids}},\n\turl = {https://journals.sagepub.com/doi/10.1177/08892229251366174},\n\tdoi = {10.1177/08892229251366174},\n\tabstract = {Little is known about the relationships between circulating short-chain fatty acids (SCFAs) and genital microbiota, inflammation, and the risk for HIV infection in women. As circulating SCFAs are potentially modifiable, for example, through dietary fiber or probiotics, we investigated association of circulating SCFA levels with these outcomes. We carried out a nested matched case–control study within a randomized trial of an antiretroviral microbicide to prevent HIV infection to study the association between circulating SCFAs and HIV acquisition (primary outcome for case definition), vaginal microbiota, and genital inflammation. Levels of the SCFAs butyrate, acetate, and propionate were quantified in plasma using mass spectrometry. Vaginal microbiota was assessed using metaproteomics and characterized as \n              Lactobacillus \n              dominant (LD) or low \n              Lactobacillus \n              (LL). Genital inflammation was measured using multiplex immunoassays. Logistic regression models were used to study the association of SCFAs with each outcome. Study population ( \n              N \n              = 99) characteristics were similar between cases (33 who acquired HIV) and controls (66 who did not acquire HIV). We did not observe any associations between any of the circulating SCFAs with HIV acquisition or with LL vaginal microbiota status. However, there was an inverse association between circulating SCFAs and several pro-inflammatory genital cytokines, including interleukin-6 (IL-6), IL-1α, and IL-8. In our study of women with high risk of HIV infection, higher levels of circulating SCFAs were associated with lower levels of various genital inflammatory markers, but not with HIV acquisition or a LL microbiota profile. Future larger studies, including genital SCFA assessment, are needed to confirm these findings.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2026-05-28},\n\tjournal = {AIDS Research and Human Retroviruses},\n\tauthor = {Shivakoti, Rupak and Letsoalo, Marothi and Lewis, Lara and Mckinnon, Lyle R. and Passmore, Jo-Ann S. and Karim, Salim S. Abdool and Liebenberg, Lenine J.P.},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {559--566},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n In-house assays for detecting anti-SARS-CoV-2 antibodies in serum and urine: Correlation with COVID-19 severity from a cohort study in Qatar.\n \n \n \n \n\n\n \n Vaikath, N. N.; Al-Nesf, M. A.; Majbour, N.; Abdesselem, H. B.; Gupta, V.; Bensmail, I.; Abdi, I. Y.; Elmagarmid, K. A.; Shabani, S.; Sudhakaran, I. P.; Ghanem, S. S.; Al-Maadheed, M.; Mohamed-Ali, V.; Blackburn, J. M.; Decock, J.; and El-Agnaf, O. M.\n\n\n \n\n\n\n Journal of Infection and Public Health, 18(6): 102744. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"In-house$ Paper\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{vaikath_-house_2025,\n\ttitle = {In-house assays for detecting anti-{SARS}-{CoV}-2 antibodies in serum and urine: {Correlation} with {COVID}-19 severity from a cohort study in {Qatar}},\n\tvolume = {18},\n\tissn = {18760341},\n\tshorttitle = {In-house assays for detecting anti-{SARS}-{CoV}-2 antibodies in serum and urine},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1876034125000930},\n\tdoi = {10.1016/j.jiph.2025.102744},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Infection and Public Health},\n\tauthor = {Vaikath, Nishant N. and Al-Nesf, Maryam Ali and Majbour, Nour and Abdesselem, Houari B. and Gupta, Vijay and Bensmail, Ilham and Abdi, Ilham Y. and Elmagarmid, Khalifa Ahmed and Shabani, Shadah and Sudhakaran, Indulekha P. and Ghanem, Simona S. and Al-Maadheed, Mohammed and Mohamed-Ali, Vidya and Blackburn, Jonathan M. and Decock, Julie and El-Agnaf, Omar M.A.},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {102744},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The BRILLIANT HIV Vaccine Consortium: Unfunded but not undone.\n \n \n \n \n\n\n \n Bekker, L.; and Gray, G. E.\n\n\n \n\n\n\n South African Journal of Science, 121(5/6). May 2025.\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{bekker_brilliant_2025,\n\ttitle = {The {BRILLIANT} {HIV} {Vaccine} {Consortium}: {Unfunded} but not undone},\n\tvolume = {121},\n\tissn = {1996-7489},\n\tshorttitle = {The {BRILLIANT} {HIV} {Vaccine} {Consortium}},\n\turl = {https://sajs.co.za/article/view/21985},\n\tdoi = {10.17159/sajs.2025/21985},\n\tlanguage = {en},\n\tnumber = {5/6},\n\turldate = {2026-05-28},\n\tjournal = {South African Journal of Science},\n\tauthor = {Bekker, Linda-Gail and Gray, Glenda E.},\n\tmonth = may,\n\tyear = {2025},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Serum norethisterone (NET) levels in NET-enanthate (NET-EN) injectable contraception users substantially interfere with testosterone immunoassay measurements and confound interpretation of biological outcomes.\n \n \n \n \n\n\n \n Avenant, C.; Moliki, J. M.; Bick, A. J.; Dlamini, S.; Singata-Madliki, M.; Hofmeyr, G. J.; Chen, P.; Storbeck, K.; Africander, D. J.; Erikson, D. W.; and Hapgood, J. P.\n\n\n \n\n\n\n Contraception and Reproductive Medicine, 10(1): 51. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Serum$ Paper\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{avenant_serum_2025,\n\ttitle = {Serum norethisterone ({NET}) levels in {NET}-enanthate ({NET}-{EN}) injectable contraception users substantially interfere with testosterone immunoassay measurements and confound interpretation of biological outcomes},\n\tvolume = {10},\n\tissn = {2055-7426},\n\turl = {https://contraceptionmedicine.biomedcentral.com/articles/10.1186/s40834-025-00388-x},\n\tdoi = {10.1186/s40834-025-00388-x},\n\tabstract = {Abstract \n             \n              Background \n              The progestin norethisterone (NET), which is structurally related to testosterone, and its enanthate form (NET-EN), are used in contraception in women. Oral NET has been shown to interfere with testosterone measurements by some chemiluminescence microparticle immunoassays (CMIA). However, whether serum NET in NET-EN users interferes with these assays is unknown. \n             \n             \n              Methods \n              Serum samples were obtained from women randomized to the injectable contraceptives NET-EN or depo medroxyprogesterone acetate intramuscular (DMPA-IM) in a clinical trial conducted in South Africa. Testosterone concentrations were compared after measurement by Abbott Architect CMIA and ultra-high performance liquid chromatography tandem mass spectrometry (UHPLC-MS/MS), from matched samples collected at baseline (D0) and 25 weeks (25W) after initiation. \n             \n             \n              Results \n              At 25W, testosterone concentrations in the NET-EN arm were significantly higher (271\\%) using the CMIA compared to the UHPLC-MS/MS method. Contrary to the UHPLC-MS/MS results showing a significant decrease in testosterone concentrations in the NET-EN arm from D0 to 25W, a significant increase was determined by CMIA. Conversely, in the DMPA-IM arm at 25W, no significant difference in testosterone concentrations between the two methods was detected, and both methods showed a significant decrease in testosterone from D0 to 25W. \n             \n             \n              Conclusions \n              We show for the first time that physiological concentrations of NET in premenopausal NET-EN users interfere with testosterone quantification using a CMIA method. The degree of interference is much higher and occurs at lower concentrations of NET than has previously been reported for oral NET and confounds the biological outcome of NET-EN use on testosterone concentrations, individually and relative to DMPA-IM. \n             \n             \n              Trial registration \n              The WHICH trial was retrospectively registered with the Pan African Clinical Trials Registry (PACTR 202009758229976).},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Contraception and Reproductive Medicine},\n\tauthor = {Avenant, Chanel and Moliki, Johnson Mosoko and Bick, Alexis J. and Dlamini, Sigcinile and Singata-Madliki, Mandisa and Hofmeyr, G. Justus and Chen, Pai-Lien and Storbeck, Karl-Heinz and Africander, Donita J. and Erikson, David W. and Hapgood, Janet P.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {51},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Elevated Plasma Matrix Metalloproteinases Are Associated With Mycobacterium tuberculosis Bloodstream Infection and Mortality in Human Immunodeficiency Virus–Associated Tuberculosis.\n \n \n \n \n\n\n \n Walker, N. F; Schutz, C.; Ward, A.; Barr, D.; Opondo, C.; Shey, M.; Elkington, P. T; Wilkinson, K. A; Wilkinson, R. J; and Meintjes, G.\n\n\n \n\n\n\n The Journal of Infectious Diseases, 231(1): 109–114. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Elevated$ Paper\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{walker_elevated_2025,\n\ttitle = {Elevated {Plasma} {Matrix} {Metalloproteinases} {Are} {Associated} {With} \\textit{{Mycobacterium} tuberculosis} {Bloodstream} {Infection} and {Mortality} in {Human} {Immunodeficiency} {Virus}–{Associated} {Tuberculosis}},\n\tvolume = {231},\n\tcopyright = {https://academic.oup.com/pages/standard-publication-reuse-rights},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/231/1/109/7747364},\n\tdoi = {10.1093/infdis/jiae296},\n\tabstract = {Abstract \n            Mortality from human immunodeficiency virus (HIV)–associated tuberculosis (TB) is high, particularly among hospitalized patients. In 433 people with HIV hospitalized with symptoms of TB, we investigated plasma matrix metalloproteinases (MMP) and matrix-derived biomarkers in relation to TB diagnosis, mortality, and Mycobacterium tuberculosis (Mtb) bloodstream infection (BSI). Compared to other diagnoses, MMP-8 was elevated in confirmed TB and in Mtb-BSI, positively correlating with extracellular matrix breakdown products. Baseline MMP-3, -7, -8, -10, and PIIINP were associated with Mtb-BSI and 12-week mortality. These findings implicate MMP dysregulation in pathophysiology of advanced HIV-TB and support MMP inhibition as a host-directed therapeutic strategy for HIV-TB.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Walker, Naomi F and Schutz, Charlotte and Ward, Amy and Barr, David and Opondo, Charles and Shey, Muki and Elkington, Paul T and Wilkinson, Katalin A and Wilkinson, Robert J and Meintjes, Graeme},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {109--114},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Evaluation of point‐of‐care diagnostics for sexually transmitted infection on oral PrEP initiation and persistence among young people in South Africa: a randomized controlled study.\n \n \n \n \n\n\n \n Joseph Davey, D.; Fynn, L.; Rousseau, E.; Macdonald, P.; Leonard, B.; Lebelo, K.; Kolisa, A.; Little, F.; and Bekker, L.\n\n\n \n\n\n\n Journal of the International AIDS Society, 28(5): e26488. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Evaluation$ Paper\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_davey_evaluation_2025,\n\ttitle = {Evaluation of point‐of‐care diagnostics for sexually transmitted infection on oral {PrEP} initiation and persistence among young people in {South} {Africa}: a randomized controlled study},\n\tvolume = {28},\n\tissn = {1758-2652, 1758-2652},\n\tshorttitle = {Evaluation of point‐of‐care diagnostics for sexually transmitted infection on oral {PrEP} initiation and persistence among young people in {South} {Africa}},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/jia2.26488},\n\tdoi = {10.1002/jia2.26488},\n\tabstract = {Abstract \n             \n              Introduction \n              Pre‐exposure prophylaxis (PrEP) services are linked to increased sexually transmitted infection (STI) diagnoses, which may facilitate PrEP uptake. We hypothesized that point‐of‐care (POC) STI testing and treatment would improve PrEP initiation and persistence. \n             \n             \n              Methods \n               \n                Between September 2023 and November 2024, we conducted a single‐centre, open‐label, unblinded, randomized controlled trial among adolescent girls and young women (15−29 years old) or male partners (any age). Participants were randomized 1:1 to standard syndromic STI management (SOC) or POC testing for \n                C. trachomatis \n                , \n                N. gonorrhoeae \n                , syphilis and \n                T. vaginalis \n                (women only). All participants received standard HIV prevention counselling, including the offer of oral PrEP. The primary outcome was effect of POC STI testing versus syndromic management on PrEP initiation; secondary outcomes included persistence at 1 and 4 months (PrEP prescription), verified in the secondary analysis of tenofovir diphosphate (TFV‐DP) in dried blood spots (DBS) in a random subset. TFV‐DP in DBS was analysed in a subset. Analysis was intention‐to‐treat, adjusted for age and sex. \n               \n             \n             \n              Results \n               \n                We enrolled and randomized 900 participants (452 in intervention; 448 in SOC). The mean age was 20.4 years (SD = 4.2); 48\\% were female. In the intervention arm, 435 received POC STI testing (96\\%); 25\\% (110 of 435 tested) were diagnosed with ={\\textgreater}1 STIs; 84\\% were treated. In SOC, 7\\% of participants reported symptoms of STIs (31); 88\\% were treated (27). Overall, 64\\% of participants in SOC versus 62\\% in intervention‐initiated PrEP (RR = 0.98, 95\\% CI = 0.88ng women and partners1.08). In the intervention, 41\\% persisted on PrEP at 1 month and 25\\% through 4 months, compared to 46\\% and 19\\%, respectively, in SOC (aRR intervention = 1.39; 95\\% CI = 0.93−2.09; \n                p \n                = 0.08). In participants treated for STIs or syndromically, 77\\% initiated PrEP versus 60\\% untreated/diagnosed (aRR = 1.14; 95\\% CI = 1.02−1.27); 19\\% versus 14\\% persisted on PrEP at 4 months (aRR STI/syndrome treated = 1.41; 95\\% CI = 0.79−2.51). Overall, 30\\% of 64 DBS had any TFV‐DP levels present with no difference by study arm (RR = 0.74; 95\\% CI: 0.38−1.41). \n               \n             \n             \n              Conclusions \n              POC STI testing did not increase PrEP initiation or 1‐month persistence but showed a moderate association with 4‐month persistence. STI treatment (syndromic or confirmed) was linked to higher PrEP uptake and persistence. Integrating STI management may improve PrEP persistence among youth.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {Journal of the International AIDS Society},\n\tauthor = {Joseph Davey, Dvora and Fynn, Lauren and Rousseau, Elzette and Macdonald, Pippa and Leonard, Bryan and Lebelo, Keitumetse and Kolisa, Ande and Little, Francesca and Bekker, Linda‐Gail},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {e26488},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Introduction Pre‐exposure prophylaxis (PrEP) services are linked to increased sexually transmitted infection (STI) diagnoses, which may facilitate PrEP uptake. We hypothesized that point‐of‐care (POC) STI testing and treatment would improve PrEP initiation and persistence. Methods Between September 2023 and November 2024, we conducted a single‐centre, open‐label, unblinded, randomized controlled trial among adolescent girls and young women (15−29 years old) or male partners (any age). Participants were randomized 1:1 to standard syndromic STI management (SOC) or POC testing for C. trachomatis , N. gonorrhoeae , syphilis and T. vaginalis (women only). All participants received standard HIV prevention counselling, including the offer of oral PrEP. The primary outcome was effect of POC STI testing versus syndromic management on PrEP initiation; secondary outcomes included persistence at 1 and 4 months (PrEP prescription), verified in the secondary analysis of tenofovir diphosphate (TFV‐DP) in dried blood spots (DBS) in a random subset. TFV‐DP in DBS was analysed in a subset. Analysis was intention‐to‐treat, adjusted for age and sex. Results We enrolled and randomized 900 participants (452 in intervention; 448 in SOC). The mean age was 20.4 years (SD = 4.2); 48% were female. In the intervention arm, 435 received POC STI testing (96%); 25% (110 of 435 tested) were diagnosed with =\\textgreater1 STIs; 84% were treated. In SOC, 7% of participants reported symptoms of STIs (31); 88% were treated (27). Overall, 64% of participants in SOC versus 62% in intervention‐initiated PrEP (RR = 0.98, 95% CI = 0.88ng women and partners1.08). In the intervention, 41% persisted on PrEP at 1 month and 25% through 4 months, compared to 46% and 19%, respectively, in SOC (aRR intervention = 1.39; 95% CI = 0.93−2.09; p = 0.08). In participants treated for STIs or syndromically, 77% initiated PrEP versus 60% untreated/diagnosed (aRR = 1.14; 95% CI = 1.02−1.27); 19% versus 14% persisted on PrEP at 4 months (aRR STI/syndrome treated = 1.41; 95% CI = 0.79−2.51). Overall, 30% of 64 DBS had any TFV‐DP levels present with no difference by study arm (RR = 0.74; 95% CI: 0.38−1.41). Conclusions POC STI testing did not increase PrEP initiation or 1‐month persistence but showed a moderate association with 4‐month persistence. STI treatment (syndromic or confirmed) was linked to higher PrEP uptake and persistence. Integrating STI management may improve PrEP persistence among youth.\n

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\n \n\n \n \n \n \n \n \n Prevalence and characterization of carbapenem-resistant gram-negative bacteria from poultry in Tamil Nadu, India.\n \n \n \n \n\n\n \n Sivasankar, S.; Grobusch, M. P.; Schaumburg, F.; and Jeyaraj, S.\n\n\n \n\n\n\n One Health, 21: 101192. December 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{sivasankar_prevalence_2025,\n\ttitle = {Prevalence and characterization of carbapenem-resistant gram-negative bacteria from poultry in {Tamil} {Nadu}, {India}},\n\tvolume = {21},\n\tissn = {23527714},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352771425002289},\n\tdoi = {10.1016/j.onehlt.2025.101192},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {One Health},\n\tauthor = {Sivasankar, Seshan and Grobusch, Martin Peter and Schaumburg, Frieder and Jeyaraj, Sankarganesh},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {101192},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Immune, metabolic, anatomical, and functional features of people after successful tuberculosis treatment: an exploratory analysis.\n \n \n \n \n\n\n \n Webber, T.; Macdonald, C.; Tameris, M.; Tredoux, N.; Bierman, A.; Gutschmidt, A.; Tönsing, S.; Hiemstra, A.; Noor, F.; Snyders, C.; Richardson, T.; Fransman, B.; Allwood, B.; Hatherill, M.; Kleynhans, L.; Loxton, A. G.; Walzl, G.; Chegou, N.; Du Plessis, N.; Shaw, J. A; and Malherbe, S. T.\n\n\n \n\n\n\n Scientific Reports, 15(1): 18392. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Immune,$ Paper\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{webber_immune_2025,\n\ttitle = {Immune, metabolic, anatomical, and functional features of people after successful tuberculosis treatment: an exploratory analysis},\n\tvolume = {15},\n\tissn = {2045-2322},\n\tshorttitle = {Immune, metabolic, anatomical, and functional features of people after successful tuberculosis treatment},\n\turl = {https://www.nature.com/articles/s41598-025-01656-1},\n\tdoi = {10.1038/s41598-025-01656-1},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Scientific Reports},\n\tauthor = {Webber, Tariq and Macdonald, Candice and Tameris, Michele and Tredoux, Nicolette and Bierman, Anandi and Gutschmidt, Andrea and Tönsing, Susanne and Hiemstra, Andriëtte and Noor, Firdows and Snyders, Candice and Richardson, Tracy and Fransman, Bernadine and Allwood, Brian and Hatherill, Mark and Kleynhans, Leanie and Loxton, André G. and Walzl, Gerhard and Chegou, Novel and Du Plessis, Nelita and Shaw, Jane A and Malherbe, Stephanus T.},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {18392},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Mining the CD4 antigen repertoire for next-generation tuberculosis vaccines.\n \n \n \n \n\n\n \n Vidal, S. J.; Lasrado, N.; Tostanoski, L. H.; Chaudhari, J.; Mbiwan, E. R.; Neka, G. D.; Strutton, E. A.; Espinosa Perez, A. A.; Sellers, D.; Barrett, J.; Lifton, M.; Wakabayashi, S.; Eshaghi, B.; Borducchi, E. N.; Aid, M.; Li, W.; Scriba, T. J.; Jaklenec, A.; Langer, R.; and Barouch, D. H.\n\n\n \n\n\n\n Cell, 188(24): 6791–6803.e13. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Mining$ Paper\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{vidal_mining_2025,\n\ttitle = {Mining the {CD4} antigen repertoire for next-generation tuberculosis vaccines},\n\tvolume = {188},\n\tissn = {00928674},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0092867425009821},\n\tdoi = {10.1016/j.cell.2025.08.027},\n\tlanguage = {en},\n\tnumber = {24},\n\turldate = {2026-05-28},\n\tjournal = {Cell},\n\tauthor = {Vidal, Samuel J. and Lasrado, Ninaad and Tostanoski, Lisa H. and Chaudhari, Jayeshbhai and Mbiwan, Esther R. and Neka, Ganad D. and Strutton, Ellis A. and Espinosa Perez, Alejandro A. and Sellers, Daniel and Barrett, Julia and Lifton, Michelle and Wakabayashi, Shoko and Eshaghi, Behnaz and Borducchi, Erica N. and Aid, Malika and Li, Wenjun and Scriba, Thomas J. and Jaklenec, Ana and Langer, Robert and Barouch, Dan H.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {6791--6803.e13},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Physiologically Based Pharmacokinetic Modelling of Serum 25-Hydroxyvitamin D Concentrations in Schoolchildren Receiving Weekly Oral Vitamin D3 Supplementation.\n \n \n \n \n\n\n \n Muhamad, N.; Walker, N.; Middelkoop, K.; Ganmaa, D.; Martineau, A.; and You, T.\n\n\n \n\n\n\n Nutrients, 17(19): 3028. September 2025.\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

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@article{muhamad_physiologically_2025,\n\ttitle = {Physiologically {Based} {Pharmacokinetic} {Modelling} of {Serum} 25-{Hydroxyvitamin} {D} {Concentrations} in {Schoolchildren} {Receiving} {Weekly} {Oral} {Vitamin} {D3} {Supplementation}},\n\tvolume = {17},\n\tissn = {2072-6643},\n\turl = {https://www.mdpi.com/2072-6643/17/19/3028},\n\tdoi = {10.3390/nu17193028},\n\tabstract = {Background: Following vitamin D3 oral administration, attained serum concentrations of its metabolite 25-hydroxyvitamin D3 (25(OH)D3) are variable among children. Methods: We developed physiologically based pharmacokinetic (PBPK) modelling using annually measured serum 25(OH)D3 concentrations in 77 Cape Town schoolchildren aged 6–11 years who received weekly oral doses of 10,000 IU vitamin D3 for 3 years during a clinical trial (Δ25(OH)D = 32.2 nmol/L, 95\\% CI: [−3.2, 65.8] nmol/L). Simulations were performed to test the model on 463 other participants in the same trial, and in a cohort of 1756 Mongolian schoolchildren aged 6–11 years who received weekly oral doses of 14,000 IU vitamin D3 for 3 years in another trial. Results: The best model attributed most of the variability in post-supplementation 25(OH)D3 concentrations to hepatic clearance and covariates including weight (ΔAIC = −21) and ZBMI (body mass index Z-score, ΔAIC = −34). For 463 other children from the Cape Town trial (Δ25(OH)D = 25.8 nmol/L, 95\\% CI: [8.3, 47.2] nmol/L), mean estimation error was 5.3 nmol/L, and 76.7\\% of observations were within the 95\\% prediction intervals. Our simulation supported the previous proposal that serum 25(OH)D3 should exceed 50 nmol/L among 97.5\\% of European children at 24.4 μg/day vitamin D3 dosing. At a higher weekly dose (14,000 IU), the Mongolian children demonstrated a higher average increase in serum 25(OH)D3 (40.6 [−2.9, 88.9] nmol/L) but were overestimated by the model. Conclusion: We developed the first PBPK model to successfully predict the long-term serum 25(OH)D3 increases in healthy schoolchildren in Cape Town who received orally administered vitamin D3 and exhibited higher relative increases than Mongolian children.},\n\tlanguage = {en},\n\tnumber = {19},\n\turldate = {2026-05-28},\n\tjournal = {Nutrients},\n\tauthor = {Muhamad, Nadda and Walker, Neil and Middelkoop, Keren and Ganmaa, Davaasambuu and Martineau, Adrian and You, Tao},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {3028},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Cross-sectional versus longitudinal estimates of annual risk of TB infection.\n \n \n \n \n\n\n \n Jolliffe, D.; Middelkoop, K.; Ganmaa, D.; Dowdy, D.; and Martineau, A.\n\n\n \n\n\n\n The International Journal of Tuberculosis and Lung Disease, 29(3): 146–147. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Cross-sectional$ Paper\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{jolliffe_cross-sectional_2025,\n\ttitle = {Cross-sectional versus longitudinal estimates of annual risk of {TB} infection},\n\tvolume = {29},\n\tissn = {1027-3719},\n\turl = {https://www.ingentaconnect.com/content/10.5588/ijtld.24.0492},\n\tdoi = {10.5588/ijtld.24.0492},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {The International Journal of Tuberculosis and Lung Disease},\n\tauthor = {Jolliffe, D.A. and Middelkoop, K. and Ganmaa, D. and Dowdy, D.W. and Martineau, A.R.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {146--147},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Oral Rinse versus Facemask Capture for Nonsputum Diagnosis of Pulmonary Tuberculosis.\n \n \n \n \n\n\n \n Mendelsohn, S. C.; Jackson, G. T.; Wessels, E.; Beyers, E.; Visagie, S.; Steyn, M.; Sivarasu, S.; Kana, B. D.; Scriba, T. J.; and Hatherill, M.\n\n\n \n\n\n\n American Journal of Respiratory and Critical Care Medicine, 211(11): 2139–2142. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Oral$ Paper\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{mendelsohn_oral_2025,\n\ttitle = {Oral {Rinse} versus {Facemask} {Capture} for {Nonsputum} {Diagnosis} of {Pulmonary} {Tuberculosis}},\n\tvolume = {211},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1073-449X, 1535-4970},\n\turl = {https://academic.oup.com/ajrccm/article/211/11/2139/8444194},\n\tdoi = {10.1164/rccm.202506-1477RL},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-28},\n\tjournal = {American Journal of Respiratory and Critical Care Medicine},\n\tauthor = {Mendelsohn, Simon C. and Jackson, Gabriella T. and Wessels, Edmund and Beyers, Elizabeth and Visagie, Suzette and Steyn, Marcia and Sivarasu, Sudesh and Kana, Bavesh D. and Scriba, Thomas J. and Hatherill, Mark},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {2139--2142},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Zika virus: an overview update.\n \n \n \n \n\n\n \n De Jong, H. K.; and Grobusch, M. P.\n\n\n \n\n\n\n Current Opinion in HIV and AIDS, 20(3): 294–302. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Zika$ Paper\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_zika_2025,\n\ttitle = {Zika virus: an overview update},\n\tvolume = {20},\n\tissn = {1746-630X, 1746-6318},\n\tshorttitle = {Zika virus},\n\turl = {https://journals.lww.com/10.1097/COH.0000000000000926},\n\tdoi = {10.1097/COH.0000000000000926},\n\tabstract = {Purpose of review \n              Although cases of Zika virus disease (ZVD) have declined globally since 2017, new outbreaks have been reported, such as in Asia in 2024. As there is no vaccine or treatment available to date, both vaccines and mAbs neutralizing Zika virus would be of great interest, especially for pregnant women and immunocompromised patients such as those living with HIV. This review focuses on new insights regarding ZVD in the last two years and summarizes the key literature on global epidemiology, transmission, diagnostics, clinical features, preventive measures, and treatment options. \n             \n             \n              Recent findings \n              At the time of writing, ZVD is endemic across tropical and subtropical regions of the world, with the highest risk of infection in Latin America and the Caribbean, but no significant peaks in outbreak activity across endemic regions. There are ongoing efforts to further investigate the clinical and epidemiological long-term sequelae of the large outbreak in the Americas 2015–2018; further refinement of diagnostic tools to improve specificity in view of significant cross-reactivity potential, particularly with dengue virus. Multiple vaccines are in different clinical development stages; however, phase 3 trials are awaiting the next epidemic. \n             \n             \n              Summary \n              While there is no current major zika virus outbreak, progress has been made in the epidemiological work-up of clinical-epidemiological data, refinement of diagnostic tools, and mainly preventive (vaccines) rather than curative (drugs) tools.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {Current Opinion in HIV and AIDS},\n\tauthor = {De Jong, Hanna K. and Grobusch, Martin P.},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {294--302},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Medicinal Chemistry Progression of Sapanisertib, the Anticancer and Dual Plasmodium Phosphatidylinositol 4-Kinase Beta and cGMP-Dependent Protein Kinase Inhibitor, for Malaria.\n \n \n \n \n\n\n \n Gachuhi, S.; Kamunya, S.; Fienberg, S.; Wambua, L.; Salomane, N.; Mayoka, G.; Taylor, D.; Coertzen, D.; Van Der Watt, M.; Reader, J.; Birkholtz, L.; Wittlin, S.; Krugmann, L.; Coulson, L. B.; and Chibale, K.\n\n\n \n\n\n\n Journal of Medicinal Chemistry, 68(11): 10757–10770. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Medicinal$ Paper\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{gachuhi_medicinal_2025,\n\ttitle = {Medicinal {Chemistry} {Progression} of {Sapanisertib}, the {Anticancer} and {Dual} \\textit{{Plasmodium}} {Phosphatidylinositol} 4-{Kinase} {Beta} and {cGMP}-{Dependent} {Protein} {Kinase} {Inhibitor}, for {Malaria}},\n\tvolume = {68},\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.4c02799},\n\tdoi = {10.1021/acs.jmedchem.4c02799},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Medicinal Chemistry},\n\tauthor = {Gachuhi, Samuel and Kamunya, Stephanie and Fienberg, Stephen and Wambua, Lynn and Salomane, Nicolaas and Mayoka, Godfrey and Taylor, Dale and Coertzen, Dina and Van Der Watt, Mariette and Reader, Janette and Birkholtz, Lyn-Marié and Wittlin, Sergio and Krugmann, Liezl and Coulson, Lauren B. and Chibale, Kelly},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {10757--10770},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The evolution of health data ecosystems: An international survey.\n \n \n \n \n\n\n \n Lerner-Ellis, J. P.; Price, E. M.; Subhani, S.; Boughtwood, T.; Brion, M.; Rendon, A.; Cividanes, L.; Gemmer, J.; Ciofani, D.; Bertin, N.; Wee, S. S.; Robertson, S.; Baz, B.; Crameri, K.; Österle, S.; Wirta, V.; Sikora, P.; Lindstrand, A.; Nowak, F.; Amado, I.; Mulder, N. J.; Ganna, A.; Goodhand, P.; Smith, L. D.; Marshall, C. R.; Zawati, M.; Ferretti, V.; Michaud, J. L.; Bulman, D.; Bernier, F.; and Boycott, K. M.\n\n\n \n\n\n\n The American Journal of Human Genetics, 112(8): 1769–1777. August 2025.\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{lerner-ellis_evolution_2025,\n\ttitle = {The evolution of health data ecosystems: {An} international survey},\n\tvolume = {112},\n\tissn = {00029297},\n\tshorttitle = {The evolution of health data ecosystems},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0002929725002484},\n\tdoi = {10.1016/j.ajhg.2025.06.017},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-28},\n\tjournal = {The American Journal of Human Genetics},\n\tauthor = {Lerner-Ellis, Jordan P. and Price, E. Magda and Subhani, Shazia and Boughtwood, Tiffany and Brion, Marie-Jo and Rendon, Augusto and Cividanes, Lene and Gemmer, Jacob and Ciofani, Danielle and Bertin, Nicolas and Wee, Seow Shih and Robertson, Stephen and Baz, Batoul and Crameri, Katrin and Österle, Sabine and Wirta, Valtteri and Sikora, Per and Lindstrand, Anna and Nowak, Frédérique and Amado, Inês and Mulder, Nicola Jane and Ganna, Andrea and Goodhand, Peter and Smith, Lindsay D. and Marshall, Christian R. and Zawati, Ma’n and Ferretti, Vincent and Michaud, Jacques L. and Bulman, Dennis and Bernier, Francois and Boycott, Kym M.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {1769--1777},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A Prospective Evaluation of the Diagnostic Accuracy of the Point-of-Care VISITECT CD4 Advanced Disease Test in 7 Countries.\n \n \n \n \n\n\n \n Gils, T.; Hella, J.; Jacobs, B. K M; Sossen, B.; Mukoka, M.; Muyoyeta, M.; Nakabugo, E.; Van Nguyen, H.; Ubolyam, S.; Macé, A.; Vermeulen, M.; Nyangu, S.; Sanjase, N.; Sasamalo, M.; Dinh, H. T.; Ngo, T. A.; Manosuthi, W.; Jirajariyavej, S.; Denkinger, C. M; Nguyen, N. V.; Avihingsanon, A.; Nakiyingi, L.; Székely, R.; Kerkhoff, A. D; MacPherson, P.; Meintjes, G.; Reither, K.; and Ruhwald, M.\n\n\n \n\n\n\n The Journal of Infectious Diseases, 231(1): e82–e90. February 2025.\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{gils_prospective_2025,\n\ttitle = {A {Prospective} {Evaluation} of the {Diagnostic} {Accuracy} of the {Point}-of-{Care} {VISITECT} {CD4} {Advanced} {Disease} {Test} in 7 {Countries}},\n\tvolume = {231},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/231/1/e82/7719076},\n\tdoi = {10.1093/infdis/jiae374},\n\tabstract = {Abstract \n             \n              Background \n              CD4 measurement is pivotal in the management of advanced human immunodeficiency virus (HIV) disease. VISITECT CD4 Advanced Disease (VISITECT; AccuBio, Ltd) is an instrument-free, point-of-care, semiquantitative test allowing visual identification of CD4 ≤ 200 cells/µL or \\&gt;200 cells/ µL from finger-prick or venous blood. \n             \n             \n              Methods \n              As part of a diagnostic accuracy study of FUJIFILM SILVAMP TB LAM, people with HIV ≥18 years old were prospectively recruited in 7 countries from outpatient departments if a tuberculosis symptom was present, and from inpatient departments. Participants provided venous blood for CD4 measurement using flow cytometry (reference standard) and finger-prick blood for VISITECT (index text), performed at point-of-care. Sensitivity, specificity, and positive and negative predictive values of VISITECT to determine CD4 ≤ 200 cells/ µL were evaluated. \n             \n             \n              Results \n              Among 1604 participants, the median flow cytometry CD4 was 367 cells/µL (interquartile range, 128–626 cells/µL) and 521 (32.5\\%) had CD4 ≤ 200 cells/µL. VISITECT sensitivity was 92.7\\% (483/521; 95\\% confidence interval [CI], 90.1\\%–94.7\\%) and specificity was 61.4\\% (665/1083; 95\\% CI, 58.4\\%–64.3\\%). For participants with CD4 0–100, 101–200, 201–300, 301–500, and \\&gt;500 cells/µL, VISITECT misclassified 4.5\\% (95\\% CI, 2.5\\%–7.2\\%), 12.5 (95\\% CI, 8.0\\%–18.2\\%), 74.1\\% (95\\% CI, 67.0\\%–80.5\\%), 48.0\\% (95\\% CI, 42.5\\%–53.6\\%), and 22.6\\% (95\\% CI, 19.3\\%–26.3\\%), respectively. \n             \n             \n              Conclusions \n              VISITECT's sensitivity, but not specificity, met the World Health Organization's minimal sensitivity and specificity threshold of 80\\% for point-of-care CD4 tests. VISITECT's quality needs to be assessed and its accuracy optimized. VISITECT’s utility as CD4 triage test should be investigated. \n              Clinical Trials Registration. NCT04089423.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Gils, Tinne and Hella, Jerry and Jacobs, Bart K M and Sossen, Bianca and Mukoka, Madalo and Muyoyeta, Monde and Nakabugo, Elizabeth and Van Nguyen, Hung and Ubolyam, Sasiwimol and Macé, Aurélien and Vermeulen, Marcia and Nyangu, Sarah and Sanjase, Nsala and Sasamalo, Mohamed and Dinh, Huong Thi and Ngo, The Anh and Manosuthi, Weerawat and Jirajariyavej, Supunnee and Denkinger, Claudia M and Nguyen, Nhung Viet and Avihingsanon, Anchalee and Nakiyingi, Lydia and Székely, Rita and Kerkhoff, Andrew D and MacPherson, Peter and Meintjes, Graeme and Reither, Klaus and Ruhwald, Morten},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {e82--e90},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Recombination Between Bubaline Alphaherpesvirus 1 and Bovine Alphaherpesvirus 1 as a Possible Origin of Bovine Alphaherpesvirus 5.\n \n \n \n \n\n\n \n Paredes-Galarza, B. S.; Campos, F. S.; Oliveira, M. T.; Prandi, B. A.; De Souza, U. J. B.; Junqueira, D. M.; Martin, D. P.; Spilki, F. R.; Franco, A. C.; and Roehe, P. M.\n\n\n \n\n\n\n Viruses, 17(2): 198. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Recombination$ Paper\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{paredes-galarza_recombination_2025,\n\ttitle = {Recombination {Between} {Bubaline} {Alphaherpesvirus} 1 and {Bovine} {Alphaherpesvirus} 1 as a {Possible} {Origin} of {Bovine} {Alphaherpesvirus} 5},\n\tvolume = {17},\n\tissn = {1999-4915},\n\turl = {https://www.mdpi.com/1999-4915/17/2/198},\n\tdoi = {10.3390/v17020198},\n\tabstract = {Bovine alphaherpesvirus 1 (BoAHV1) is prevalent in cattle throughout the world, whereas bovine alphaherpesvirus 5 (BoAHV5) prevalence seems restricted to some countries in South America, Australia, and other regions, mainly in the Southern Hemisphere. BoAHV5 infections occur where water buffalo (Bubalus bubalis) farming is practiced, often close to cattle (Bos taurus) farms. Bubaline alphaherpesvirus 1 (BuAHV1), a virus whose natural host is believed to be the water buffaloes, usually causes asymptomatic infections in that species. Here, evidence is provided confirming the close relationship between BuAHV1 and BoAHV5. Phylogenetic and recombination analyses were used to reveal the evolutionary relationship between all whole-genome sequences of BoAHV1 (n = 52), BoAHV5 (n = 7), and BuAHV1 (n = 6) available to date. It is proposed here that BoAHV5 most likely resulted from multiple recombination events between a BuAHV1-like ancestor and BoAHV1-like viruses. The BoAHV5 whole unique short (US) region and most of the unique long (UL) genomic regions seem to have been derived from a BuAHV1-like parental genome, whereas at least six small segments of the UL (corresponding to nucleotides 8287 to 8624; 10,658 to 14,496; 48,013 to 48,269; 71,379 to 71,927; 81,426 to 85,003; and 94,012 to 96,841 of the BoAHV5 genome) and two small segments of the US (corresponding to nucleotides 107,039 to 107,581 and 131,267 to 131,810) have been derived from a BoAHV1-like parental genome. The hypothesis that the BoAHV5 species may have originated following a series of recombination events between BuAHV1 and BoAHV1 variants is consistent with the geographical distribution of BoAHV5, which seems to be prevalent in the regions where cattle and water buffalo farming overlap.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {Viruses},\n\tauthor = {Paredes-Galarza, Bruna S. and Campos, Fabrício S. and Oliveira, Martha T. and Prandi, Bruno A. and De Souza, Ueric J. B. and Junqueira, Dennis M. and Martin, Darren P. and Spilki, Fernando R. and Franco, Ana C. and Roehe, Paulo M.},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {198},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Peptide receptor radionuclide therapy ( \\textlessspan style=\"font-variant:small-caps;\"\\textgreaterPRRT\\textless/span\\textgreater ) special issue.\n \n \n \n \n\n\n \n Navalkissoor, S.; and Millar, R. P.\n\n\n \n\n\n\n Journal of Neuroendocrinology, 37(3): e70014. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Peptide$ Paper\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{navalkissoor_peptide_2025,\n\ttitle = {Peptide receptor radionuclide therapy ( {\\textless}span style="font-variant:small-caps;"{\\textgreater}{PRRT}{\\textless}/span{\\textgreater} ) special issue},\n\tvolume = {37},\n\tissn = {0953-8194, 1365-2826},\n\tshorttitle = {Peptide receptor radionuclide therapy ( {\\textless}span style="font-variant},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/jne.70014},\n\tdoi = {10.1111/jne.70014},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Neuroendocrinology},\n\tauthor = {Navalkissoor, Shaunak and Millar, Robert P.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {e70014},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Rare twin cysteine residues in the HIV-1 envelope variable region 1 link to neutralization escape and breadth development.\n \n \n \n \n\n\n \n Hesselman, M. C.; Zeeb, M.; Rusert, P.; Pasin, C.; Mamrosh, J.; Kariuki, S.; Pichler, I.; Sickmann, M.; Kaufmann, M. M.; Schmidt, D.; Friedrich, N.; Metzner, K. J.; Rindler, A.; Kuster, H.; Adams, C.; Thebus, R.; Huber, M.; Yerly, S.; Leuzinger, K.; Perreau, M.; Koller, R.; Dollenmaier, G.; Frigerio, S.; Westfall, D. H.; Deng, W.; deCamp , A. C.; Juraska, M.; Edupuganti, S.; Mgodi, N.; Murrell, H.; Garrett, N.; Wagh, K.; Mullins, J. I.; Williamson, C.; Moore, P. L.; Günthard, H. F.; Kouyos, R. D.; and Trkola, A.\n\n\n \n\n\n\n Cell Host & Microbe, 33(2): 279–293.e6. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Rare$ Paper\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{hesselman_rare_2025,\n\ttitle = {Rare twin cysteine residues in the {HIV}-1 envelope variable region 1 link to neutralization escape and breadth development},\n\tvolume = {33},\n\tissn = {19313128},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1931312825000228},\n\tdoi = {10.1016/j.chom.2025.01.004},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {Cell Host \\& Microbe},\n\tauthor = {Hesselman, Maria C. and Zeeb, Marius and Rusert, Peter and Pasin, Chloé and Mamrosh, Jennifer and Kariuki, Samuel and Pichler, Ian and Sickmann, Michèle and Kaufmann, Masako M. and Schmidt, Daniel and Friedrich, Nikolas and Metzner, Karin J. and Rindler, Audrey and Kuster, Herbert and Adams, Craig and Thebus, Ruwayhida and Huber, Michael and Yerly, Sabine and Leuzinger, Karoline and Perreau, Matthieu and Koller, Roger and Dollenmaier, Günter and Frigerio, Simona and Westfall, Dylan H. and Deng, Wenjie and deCamp, Allan C. and Juraska, Michal and Edupuganti, Srilatha and Mgodi, Nyaradzo and Murrell, Hugh and Garrett, Nigel and Wagh, Kshitij and Mullins, James I. and Williamson, Carolyn and Moore, Penny L. and Günthard, Huldrych F. and Kouyos, Roger D. and Trkola, Alexandra},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {279--293.e6},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Thalidomide as an Adjunctive Therapy for HIV-Tuberculosis–Associated Immune Reconstitution Inflammatory Syndrome: A Case Series.\n \n \n \n \n\n\n \n Lee-Jones, S; Rebe, K; Marais, S; Meintjes, G; Parker, A; and Van Der Plas, H\n\n\n \n\n\n\n Open Forum Infectious Diseases, 12(11): ofaf617. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Thalidomide$ Paper\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{lee-jones_thalidomide_2025,\n\ttitle = {Thalidomide as an {Adjunctive} {Therapy} for {HIV}-{Tuberculosis}–{Associated} {Immune} {Reconstitution} {Inflammatory} {Syndrome}: {A} {Case} {Series}},\n\tvolume = {12},\n\tcopyright = {https://creativecommons.org/licenses/by-nc-nd/4.0/},\n\tissn = {2328-8957},\n\tshorttitle = {Thalidomide as an {Adjunctive} {Therapy} for {HIV}-{Tuberculosis}–{Associated} {Immune} {Reconstitution} {Inflammatory} {Syndrome}},\n\turl = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofaf617/8269507},\n\tdoi = {10.1093/ofid/ofaf617},\n\tabstract = {Abstract \n             \n              Background \n              A small proportion of people living with human immunodeficiency virus (HIV) who have tuberculosis-related immune reconstitution inflammatory syndrome (tuberculosis-IRIS) have prolonged and complicated courses and experience poor response to corticosteroid therapy, relapse after withdrawing, or intolerability demonstrating a need for alternative immunomodulatory options. Thalidomide has been shown to have immunomodulatory effects, primarily in neurological tuberculosis in children, but there is little description of its use in adult patients. \n             \n             \n              Methods \n              We describe the clinical course in 7 adult patients with complicated HIV-associated tuberculosis-IRIS treated with thalidomide. \n             \n             \n              Results \n              The clinical manifestations included central nervous system tuberculosis (n = 4) , tuberculous adenitis (n = 2), and recurrent tuberculous psoas collection (n = 1). All patients were given thalidomide (100 mg) for 6–12 months, with favorable clinical outcomes and no adverse effects. \n             \n             \n              Conclusions \n              Thalidomide dosed at 100 mg/d remains an agent with clinical utility in this small subset of patients, and further research to determine optimal dosing and duration could be beneficial.},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-28},\n\tjournal = {Open Forum Infectious Diseases},\n\tauthor = {Lee-Jones, S and Rebe, K and Marais, S and Meintjes, G and Parker, A and Van Der Plas, H},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {ofaf617},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Effect of contraceptive methods on the vaginal microbiome and host immune factors.\n \n \n \n \n\n\n \n Serrano, M. G.; Edwards, D.; Ahmed, K.; Bailey, V. C.; Beksinska, M.; Edupuganti, L.; Harryparsad, R.; D'Hellencourt, F. L.; Meyer, B.; Mehou-Loko, C.; Radzey, N.; Taku, O.; Williamson, A.; Smit, J.; Spaine, K.; Zhu, B.; Jefferson, K. K.; Nanda, K.; Strauss Iii, J. F.; Morrison, C. S.; Deese, J.; Masson, L.; and Buck, G. A.\n\n\n \n\n\n\n Contraception, 148: 110936. August 2025.\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

\n

@article{serrano_effect_2025,\n\ttitle = {Effect of contraceptive methods on the vaginal microbiome and host immune factors},\n\tvolume = {148},\n\tissn = {00107824},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0010782425001271},\n\tdoi = {10.1016/j.contraception.2025.110936},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Contraception},\n\tauthor = {Serrano, Myrna G. and Edwards, David and Ahmed, Khatija and Bailey, Veronique C. and Beksinska, Mags and Edupuganti, Laahirie and Harryparsad, Rushil and D'Hellencourt, Florence L. and Meyer, Bahiah and Mehou-Loko, Celia and Radzey, Nina and Taku, Ongeziwe and Williamson, Anna-Lise and Smit, Jennifer and Spaine, Katherine and Zhu, Bin and Jefferson, Kimberly K. and Nanda, Kavita and Strauss Iii, Jerome F. and Morrison, Charles S. and Deese, Jennifer and Masson, Lindi and Buck, Gregory A.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {110936},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Conserved recombination patterns across hepatitis B genotypes: a retrospective study.\n \n \n \n \n\n\n \n Tshiabuila, D.; San, J. E.; Wilkinson, E.; Dor, G.; Tegally, H.; Maponga, T. G.; Delphin, M.; Matthews, P. C.; Martin, D. P.; Baxter, C.; and De Oliveira, T.\n\n\n \n\n\n\n Virology Journal, 22(1): 220. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Conserved$ Paper\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{tshiabuila_conserved_2025,\n\ttitle = {Conserved recombination patterns across hepatitis {B} genotypes: a retrospective study},\n\tvolume = {22},\n\tissn = {1743-422X},\n\tshorttitle = {Conserved recombination patterns across hepatitis {B} genotypes},\n\turl = {https://virologyj.biomedcentral.com/articles/10.1186/s12985-025-02829-0},\n\tdoi = {10.1186/s12985-025-02829-0},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Virology Journal},\n\tauthor = {Tshiabuila, Derek and San, James E. and Wilkinson, Eduan and Dor, Graeme and Tegally, Houriiyah and Maponga, Tongai G. and Delphin, Marion and Matthews, Philippa C. and Martin, Darren P. and Baxter, Cheryl and De Oliveira, Tulio},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {220},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Escitalopram alters tryptophan metabolism, plasma lipopolysaccharide, and the inferred functional potential of the gut microbiome in deer mice showing compulsive-like rigidity.\n \n \n \n \n\n\n \n Karsten, L.; Harvey, B. H.; Stein, D. J.; Valderrama, B.; Bastiaanssen, T. F.; Clarke, G.; Cryan, J. F.; Van Der Sluis, R.; Jaspan, H.; Happel, A.; and Wolmarans, D. W.\n\n\n \n\n\n\n Acta Neuropsychiatrica, 37: e60. 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Escitalopram$ Paper\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{karsten_escitalopram_2025,\n\ttitle = {Escitalopram alters tryptophan metabolism, plasma lipopolysaccharide, and the inferred functional potential of the gut microbiome in deer mice showing compulsive-like rigidity},\n\tvolume = {37},\n\tissn = {0924-2708, 1601-5215},\n\turl = {https://www.cambridge.org/core/product/identifier/S092427082500016X/type/journal_article},\n\tdoi = {10.1017/neu.2025.16},\n\tabstract = {Abstract \n             \n              Objective: \n               \n                Compulsive-like rigidity may be associated with hyposerotonergia and increased kynurenine (KYN) pathway activity. Conversion of tryptophan (TRP) to KYN, which may contribute to hyposerotonergia, is bolstered by inflammation and could be related to altered gut microbiota composition. Here, we studied these mechanisms in a naturalistic animal model of compulsive-like behavioural rigidity, that is, large nest building (LNB) in deer mice ( \n                Peromyscus \n                sp.). \n               \n             \n             \n              Methods: \n              Twenty-four (24) normal nest building (NNB) and 24 LNB mice (both sexes) were chronically administered either escitalopram (a selective serotonin reuptake inhibitor; 50 mg/kg/day) or a control solution, with nesting behaviour analysed before and after intervention. After endpoint euthanising, frontal cortices and striata were analysed for TRP and its metabolites, plasma for microbiota-derived lipopolysaccharide (LPS) and its binding protein (lipopolysaccharide binding protein), and stool samples for microbial DNA. \n             \n             \n              Results: \n              LNB, but not NNB, decreased after escitalopram exposure. At baseline, LNB was associated with reduced frontal cortical TRP concentrations and hyposerotonergia that was unrelated to altered KYN pathway activity. In LNB mice, escitalopram significantly increased frontal-cortical and striatal TRP without altering serotonin concentrations. Treated LNB, compared to untreated LNB and treated NNB mice, had significantly reduced plasma LPS as well as a microbiome showing a decreased inferred potential to synthesise short-chain fatty acids and degrade TRP. \n             \n             \n              Conclusions: \n              These findings support the role of altered serotonergic mechanisms, inflammatory processes, and gut microbiome involvement in compulsive-like behavioural rigidity. Our results also highlight the importance of gut-brain crosstalk mechanisms at the level of TRP metabolism in the spontaneous development of such behaviour.},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Acta Neuropsychiatrica},\n\tauthor = {Karsten, Larissa and Harvey, Brian H. and Stein, Dan J. and Valderrama, Benjamín and Bastiaanssen, Thomaz F.S. and Clarke, Gerard and Cryan, John F. and Van Der Sluis, Rencia and Jaspan, Heather and Happel, Anna-Ursula and Wolmarans, De Wet},\n\tyear = {2025},\n\tpages = {e60},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Pyrroloquinolone-Based Compounds as a Novel Antimycobacterial Chemotype.\n \n \n \n \n\n\n \n Clariano, M.; Nunes, D.; Canudo, D.; Maçãs, D.; Castro, B. J. L.; Jordaan, A.; Gomes, P.; Contini, A.; Perdigão, J.; Portugal, I.; Madureira, M.; Warner, D. F.; Pieroni, M.; Perry, M. D. J.; and Lopes, F.\n\n\n \n\n\n\n ACS Medicinal Chemistry Letters, 16(6): 1139–1146. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Pyrroloquinolone-Based$ 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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{clariano_pyrroloquinolone-based_2025,\n\ttitle = {Pyrroloquinolone-{Based} {Compounds} as a {Novel} {Antimycobacterial} {Chemotype}},\n\tvolume = {16},\n\tcopyright = {https://doi.org/10.15223/policy-029},\n\tissn = {1948-5875, 1948-5875},\n\turl = {https://pubs.acs.org/doi/10.1021/acsmedchemlett.5c00183},\n\tdoi = {10.1021/acsmedchemlett.5c00183},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {ACS Medicinal Chemistry Letters},\n\tauthor = {Clariano, Marta and Nunes, Diogo and Canudo, Daniela and Maçãs, Daniela and Castro, Bruno J. L. and Jordaan, Audrey and Gomes, Pedro and Contini, Anna and Perdigão, João and Portugal, Isabel and Madureira, Margarida and Warner, Digby F. and Pieroni, Marco and Perry, Maria De Jesus and Lopes, Francisca},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {1139--1146},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Immunomodulatory effects of atorvastatin on peripheral blood mononuclear cells infected with Mycobacterium tuberculosis.\n \n \n \n \n\n\n \n Sabeel, S.; Motaung, B.; Ozturk, M.; Mafu, T. S.; Wilkinson, R. J.; Thienemann, F.; and Guler, R.\n\n\n \n\n\n\n Frontiers in Immunology, 16: 1597534. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Immunomodulatory$ Paper\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{sabeel_immunomodulatory_2025,\n\ttitle = {Immunomodulatory effects of atorvastatin on peripheral blood mononuclear cells infected with {Mycobacterium} tuberculosis},\n\tvolume = {16},\n\tissn = {1664-3224},\n\turl = {https://www.frontiersin.org/articles/10.3389/fimmu.2025.1597534/full},\n\tdoi = {10.3389/fimmu.2025.1597534},\n\tabstract = {Background \n               \n                Tuberculosis (TB) remains a major global health threat, contributing substantially to high morbidity and mortality rates. This underscores the urgent need for more effective interventions. Recent studies highlight the potential of host-directed therapy approaches to enhance immune defences against TB. Atorvastatin, recognized for both its lipid-lowering properties and its immunomodulatory effects, has emerged as a compelling candidate for host-directed therapy against TB. Here, we investigated the \n                ex vivo \n                efficacy of atorvastatin in inducing immunomodulatory activities (phagosome maturation, autophagy, and apoptosis) and enhancing the mycobacterial killing capacity in \n                Mycobacterium tuberculosis \n                ( \n                Mtb \n                )-infected peripheral blood mononuclear cells (PBMCs). \n               \n             \n             \n              Method \n               \n                Blood samples from healthy donors were collected for PBMC isolation. PBMCs were then treated overnight with or without atorvastatin, followed by infection with \n                Mtb \n                strains (H37Rv, HN878, and CDC1551) to evaluate intracellular mycobacterial growth by colony-forming units enumeration. Furthermore, co-localization of late endosomal marker (Rab-7), lysosomal markers (Cathepsin-D and LAMP-3), and autophagy marker (LC3B) with GFP- \n                Mtb \n                was investigated in infected PBMCs using laser scanning confocal microscopy. Moreover, multiple apoptotic assays were performed, including the TUNEL assay for DNA fragmentation, quantification of caspase-3 activity, and the expression levels of the pro-apoptotic gene ( \n                Bax \n                ) and anti-apoptotic gene ( \n                Bcl2 \n                ). \n               \n             \n             \n              Results \n               \n                Treatment with atorvastatin significantly reduced intracellular mycobacterial replication compared to untreated controls in \n                Mtb \n                -infected PBMCs. Moreover, atorvastatin enhanced co-localization between \n                Mtb \n                and late endosomal marker (Rab-7), lysosomal markers (Cathepsin-D and LAMP-3), and autophagy marker (LC3B) in \n                Mtb \n                -infected PBMCs. Furthermore, atorvastatin robustly promoted apoptosis in \n                Mtb \n                -infected PBMCs, as demonstrated by TUNEL assay and caspase-3 activation. \n               \n             \n             \n              Conclusion \n               \n                Our findings highlight atorvastatin’s potential as a crucial modulator of the immune response in \n                Mtb \n                -infected PBMCs, supporting its role in host-directed therapy.},\n\turldate = {2026-05-28},\n\tjournal = {Frontiers in Immunology},\n\tauthor = {Sabeel, Solima and Motaung, Bongani and Ozturk, Mumin and Mafu, Trevor S. and Wilkinson, Robert J. and Thienemann, Friedrich and Guler, Reto},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {1597534},\n}\n\n\n\n

\n

\n\n\n

\n Background Tuberculosis (TB) remains a major global health threat, contributing substantially to high morbidity and mortality rates. This underscores the urgent need for more effective interventions. Recent studies highlight the potential of host-directed therapy approaches to enhance immune defences against TB. Atorvastatin, recognized for both its lipid-lowering properties and its immunomodulatory effects, has emerged as a compelling candidate for host-directed therapy against TB. Here, we investigated the ex vivo efficacy of atorvastatin in inducing immunomodulatory activities (phagosome maturation, autophagy, and apoptosis) and enhancing the mycobacterial killing capacity in Mycobacterium tuberculosis ( Mtb )-infected peripheral blood mononuclear cells (PBMCs). Method Blood samples from healthy donors were collected for PBMC isolation. PBMCs were then treated overnight with or without atorvastatin, followed by infection with Mtb strains (H37Rv, HN878, and CDC1551) to evaluate intracellular mycobacterial growth by colony-forming units enumeration. Furthermore, co-localization of late endosomal marker (Rab-7), lysosomal markers (Cathepsin-D and LAMP-3), and autophagy marker (LC3B) with GFP- Mtb was investigated in infected PBMCs using laser scanning confocal microscopy. Moreover, multiple apoptotic assays were performed, including the TUNEL assay for DNA fragmentation, quantification of caspase-3 activity, and the expression levels of the pro-apoptotic gene ( Bax ) and anti-apoptotic gene ( Bcl2 ). Results Treatment with atorvastatin significantly reduced intracellular mycobacterial replication compared to untreated controls in Mtb -infected PBMCs. Moreover, atorvastatin enhanced co-localization between Mtb and late endosomal marker (Rab-7), lysosomal markers (Cathepsin-D and LAMP-3), and autophagy marker (LC3B) in Mtb -infected PBMCs. Furthermore, atorvastatin robustly promoted apoptosis in Mtb -infected PBMCs, as demonstrated by TUNEL assay and caspase-3 activation. Conclusion Our findings highlight atorvastatin’s potential as a crucial modulator of the immune response in Mtb -infected PBMCs, supporting its role in host-directed therapy.\n

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\n \n\n \n \n \n \n \n \n The identification of novel missense variant in ChAT gene in a patient with gestational diabetes denotes plausible genetic association.\n \n \n \n \n\n\n \n Oluwole, O. G.; Arowolo, A.; Musa, E.; Levitt, N.; and Matjila, M.\n\n\n \n\n\n\n Open Medicine, 20(1): 20251225. July 2025.\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{oluwole_identification_2025,\n\ttitle = {The identification of novel missense variant in \\textit{{ChAT}} gene in a patient with gestational diabetes denotes plausible genetic association},\n\tvolume = {20},\n\tcopyright = {http://creativecommons.org/licenses/by/4.0},\n\tissn = {2391-5463},\n\turl = {https://www.degruyterbrill.com/document/doi/10.1515/med-2025-1225/html},\n\tdoi = {10.1515/med-2025-1225},\n\tabstract = {Abstract \n             \n              Introduction \n               \n                Gestational diabetes mellitus (GDM), the most common metabolic complication of pregnancy, is associated with a 50\\% increase in subsequent risk for type 2 diabetes. There is increasing interest in identifying biomarkers that may facilitate the stratification of subsequent type 2 diabetes risk among women with GDM. In this study, we considered the choline acetyltransferase ( \n                ChAT \n                ) gene. CHAT plays a critical role in acetylcholine synthesis and regulates insulin secretion from the pancreatic islet to maintain glucose homeostasis. \n               \n             \n             \n              Methods \n               \n                We screened for deleterious variants in the \n                ChAT \n                gene in 12 GDM patients and 10 ethnically matched controls from a South African cohort. We isolated DNA from the placental samples of these patients and performed DNA sequencing of the protein-coding region of the \n                ChAT \n                gene. Sequence alignments and variant annotations were done using UGENE software and Ensembl VEP. \n               \n             \n             \n              Results \n               \n                A novel heterozygous missense variant in exon 8 of the \n                ChAT \n                gene was identified. The plausible phenotypic impact of the variant \n                ChAT \n                (NM\\_020549.5):c.1213C{\\textgreater}G (p.Leu405Val) can be explained by haploinsufficiency, changing protein activities, strong transcription activity, and epigenetic repression activities of the variant. Also, structurally, the variant is located 18bp in-frame to a stop-gained variant (p.Gly411Ter). The RegulomeDB DNase expression data clearly show the identified variant in a peak expression in the spleen and placenta. This observation corroborates that the \n                ChAT \n                gene may play an essential role in GDM. \n               \n             \n             \n              Conclusion \n               \n                Taken together, the metric scores for this variant show that it could affect the functions of the gene, but more functional studies are necessary to validate these effects. Consequently, this study sets the stage for the future screening of a larger cohort and functional validation of deleterious variants to underpin the \n                ChAT \n                gene and GDM association.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Open Medicine},\n\tauthor = {Oluwole, Oluwafemi G. and Arowolo, Afolake and Musa, Ezekiel and Levitt, Naomi and Matjila, Mushi},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {20251225},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Ferrocenyl Quinoline-Benzimidazole Hybrids: A Multistage Strategy to Combat Drug-Resistant Malaria.\n \n \n \n \n\n\n \n Golding, T. M.; Garnie, L. F.; Rabie, T.; Reader, J.; Birkholtz, L.; Wicht, K. J.; and Smith, G. S.\n\n\n \n\n\n\n Inorganic Chemistry, 64(31): 16152–16167. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Ferrocenyl$ Paper\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{golding_ferrocenyl_2025,\n\ttitle = {Ferrocenyl {Quinoline}-{Benzimidazole} {Hybrids}: {A} {Multistage} {Strategy} to {Combat} {Drug}-{Resistant} {Malaria}},\n\tvolume = {64},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0020-1669, 1520-510X},\n\tshorttitle = {Ferrocenyl {Quinoline}-{Benzimidazole} {Hybrids}},\n\turl = {https://pubs.acs.org/doi/10.1021/acs.inorgchem.5c02689},\n\tdoi = {10.1021/acs.inorgchem.5c02689},\n\tlanguage = {en},\n\tnumber = {31},\n\turldate = {2026-05-28},\n\tjournal = {Inorganic Chemistry},\n\tauthor = {Golding, Taryn M. and Garnie, Larnelle F. and Rabie, Tayla and Reader, Janette and Birkholtz, Lyn-Marié and Wicht, Kathryn J. and Smith, Gregory S.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {16152--16167},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Fluorescent acid-fast stains for diagnosing mycobacteria and beyond: back to the future?.\n \n \n \n \n\n\n \n Hänscheid, T.; Mahomed, S.; Oliveira, L.; Pereira, D. S.; and Grobusch, M. P\n\n\n \n\n\n\n The Lancet Microbe, 6(12): 101233. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Fluorescent$ Paper\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{hanscheid_fluorescent_2025,\n\ttitle = {Fluorescent acid-fast stains for diagnosing mycobacteria and beyond: back to the future?},\n\tvolume = {6},\n\tissn = {26665247},\n\tshorttitle = {Fluorescent acid-fast stains for diagnosing mycobacteria and beyond},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524725001612},\n\tdoi = {10.1016/j.lanmic.2025.101233},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Hänscheid, Thomas and Mahomed, Sara and Oliveira, Laila and Pereira, Danielle Segóvia and Grobusch, Martin P},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {101233},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Diagnostic Accuracy of Chest X-ray Computer-Aided Detection Software for Detection of Prevalent and Incident Tuberculosis in Household Contacts.\n \n \n \n \n\n\n \n Macpherson, L.; Kik, S. V; Quartagno, M.; Lakay, F.; Jaftha, M.; Yende, N.; Galant, S.; Aziz, S.; Daroowala, R.; Court, R.; Taliep, A.; Serole, K.; Goliath, R. T; Davies, N. O.; Jackson, A.; Douglass, E.; Sossen, B.; Mukasa, S.; Thienemann, F.; Song, T.; Ruhwald, M.; Wilkinson, R. J; Coussens, A. K; Esmail, H.; Imaging of TB Household Contacts Group; Barry, C. E; Ellner, J. J; Flynn, J. L; Heinsohn, T.; Horsburgh, C R.; Jacobson, K. R; Malherbe, S. T; Salgame, P.; Sheerin, D.; Streicher, E.; Tlala, M.; Via, L. E; Walzl, G.; Warren, R.; and Warwick, J.\n\n\n \n\n\n\n Clinical Infectious Diseases, 80(3): 626–636. March 2025.\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{macpherson_diagnostic_2025,\n\ttitle = {Diagnostic {Accuracy} of {Chest} {X}-ray {Computer}-{Aided} {Detection} {Software} for {Detection} of {Prevalent} and {Incident} {Tuberculosis} in {Household} {Contacts}},\n\tvolume = {80},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1058-4838, 1537-6591},\n\turl = {https://academic.oup.com/cid/article/80/3/626/7925268},\n\tdoi = {10.1093/cid/ciae528},\n\tabstract = {Abstract \n             \n              Background \n              World Health Organization (WHO) tuberculosis (TB) screening guidelines recommend computer-aided detection (CAD) software for chest radiograph (CXR) interpretation. However, studies evaluating their diagnostic and prognostic accuracy are limited. \n             \n             \n              Methods \n              We conducted a prospective cohort study of household contacts of rifampicin-resistant TB in South Africa. Participants underwent baseline CXR and sputum investigation (routine [single spontaneous] and enhanced [additionally 2–3 induced]) for prevalent TB and follow-up for incident TB. Three CXR-CAD software products (CAD4TBv7.0, qXRv3.0.0, and Lunit INSIGHT v3.1.4.111) were compared. We evaluated their performance to detect routine and enhanced prevalent and incident TB, comparing performance with blood tests (Xpert MTB host-response, erythrocyte sedimentation rate, C-reactive protein, QuantiFERON) in a subgroup. \n             \n             \n              Results \n              483 participants were followed up for 4.6 years (median). There were 23 prevalent (7 routinely diagnosed) and 38 incident TB cases. The AUC ROCs (95\\% CIs) to identify prevalent TB for CAD4TBv7.0, qXRv3.0.0, and Lunit INSIGHT v3.1.4.111 were .87 (.77–.96), .88 (.79–.97), and .91 (.83–.99), respectively. More than 30\\% with scores above recommended CAD thresholds who were bacteriologically negative on routine baseline sputum were subsequently diagnosed by enhanced sputum investigation or during follow-up. The AUC performance of baseline CAD to identify incident cases ranged between .60 and .65. Diagnostic performance of CAD for prevalent TB was superior to blood testing. \n             \n             \n              Conclusions \n              Our findings suggest that the potential of CAD-CXR screening for TB is not maximized as a high proportion of those above current thresholds, but with a negative routine confirmatory sputum, have true TB disease that may benefit intervention.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {Clinical Infectious Diseases},\n\tauthor = {Macpherson, Liana and Kik, Sandra V and Quartagno, Matteo and Lakay, Francisco and Jaftha, Marche and Yende, Nombuso and Galant, Shireen and Aziz, Saalikha and Daroowala, Remy and Court, Richard and Taliep, Arshad and Serole, Keboile and Goliath, Rene T and Davies, Nashreen Omar and Jackson, Amanda and Douglass, Emily and Sossen, Bianca and Mukasa, Sandra and Thienemann, Friedrich and Song, Taeksun and Ruhwald, Morten and Wilkinson, Robert J and Coussens, Anna K and Esmail, Hanif and {Imaging of TB Household Contacts Group} and Barry, Clifton E and Ellner, Jerrold J and Flynn, JoAnne L and Heinsohn, Torben and Horsburgh, C Robert and Jacobson, Karen R and Malherbe, Stephanus T and Salgame, Padmini and Sheerin, Dylan and Streicher, Elizabeth and Tlala, Mpho and Via, Laura E and Walzl, Gerhard and Warren, Robin and Warwick, James},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {626--636},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Network models incorporating chloride dynamics predict optimal strategies for terminating status epilepticus.\n \n \n \n \n\n\n \n Currin, C. B.; Burman, R. J.; Fedele, T.; Ramantani, G.; Rosch, R. E.; Sprekeler, H.; and Raimondo, J. V.\n\n\n \n\n\n\n Neurobiology of Disease, 212: 106966. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Network$ Paper\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{currin_network_2025,\n\ttitle = {Network models incorporating chloride dynamics predict optimal strategies for terminating status epilepticus},\n\tvolume = {212},\n\tissn = {09699961},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0969996125001822},\n\tdoi = {10.1016/j.nbd.2025.106966},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Neurobiology of Disease},\n\tauthor = {Currin, Christopher B. and Burman, Richard J. and Fedele, Tommaso and Ramantani, Georgia and Rosch, Richard E. and Sprekeler, Henning and Raimondo, Joseph V.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {106966},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Immunology of infants who are HIV-exposed uninfected in the parental combination antiretroviral therapy era.\n \n \n \n \n\n\n \n Gasper, M. A; Happel, A.; Dzanibe, S.; Slyker, J.; and Jaspan, H. B\n\n\n \n\n\n\n The Lancet HIV, 12(11): e789–e801. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Immunology$ Paper\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{gasper_immunology_2025,\n\ttitle = {Immunology of infants who are {HIV}-exposed uninfected in the parental combination antiretroviral therapy era},\n\tvolume = {12},\n\tissn = {23523018},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352301825001845},\n\tdoi = {10.1016/S2352-3018(25)00184-5},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet HIV},\n\tauthor = {Gasper, Melanie A and Happel, Anna-Ursula and Dzanibe, Sonwabile and Slyker, Jennifer and Jaspan, Heather B},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {e789--e801},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n High-sensitivity detection of Mycobacterium tuberculosis DNA in tongue swab samples.\n \n \n \n \n\n\n \n Olson, A. M.; Wood, R. C.; Weigel, K. M.; Yan, A. J.; Lochner, K. A.; Dragovich, R. B.; Luabeya, A. K.; Yager, P.; Hatherill, M.; and Cangelosi, G. A.\n\n\n \n\n\n\n Journal of Clinical Microbiology, 63(2): e01140–24. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"High-sensitivity$ Paper\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{olson_high-sensitivity_2025,\n\ttitle = {High-sensitivity detection of \\textit{{Mycobacterium} tuberculosis} {DNA} in tongue swab samples},\n\tvolume = {63},\n\tissn = {0095-1137, 1098-660X},\n\turl = {https://journals.asm.org/doi/10.1128/jcm.01140-24},\n\tdoi = {10.1128/jcm.01140-24},\n\tabstract = {ABSTRACT \n             \n               \n               \n                Tongue swab (TS) sampling combined with quantitative PCR (qPCR) to detect \n                Mycobacterium tuberculosis \n                (MTB) DNA is a promising alternative to sputum testing for tuberculosis (TB) diagnosis. In prior studies, the sensitivity of tongue swabbing has usually been lower than sputum. In this study, we evaluated two strategies to improve sensitivity. In one, centrifugation was used to concentrate tongue dorsum bacteria from 2-mL suspensions eluted from high-capacity foam swab samples. The pellets were resuspended as 500-µL suspensions, and then mechanically lysed prior to dual-target qPCR to detect MTB insertion elements IS \n                6110 \n                and IS \n                1081 \n                . Fractionation experiments demonstrated that most of the MTB DNA signal in clinical swab samples (99.22\\% ± 1.46\\%) was present in the sedimentable fraction. When applied to archived foam swabs collected from 124 South Africans with presumptive TB, this strategy exhibited 83\\% sensitivity (71/86) and 100\\% specificity (38/38) relative to sputum microbiological reference standard (MRS; sputum culture and/or Xpert Ultra). The second strategy used sequence-specific magnetic capture (SSMaC) to concentrate DNA released from MTB cells. This protocol was evaluated on archived Copan FLOQSwabs flocked swab samples collected from 128 South African participants with presumptive TB. Material eluted into 500 µL buffer was mechanically lysed. The suspensions were digested by proteinase K, hybridized to biotinylated dual-target oligonucleotide probes, and then concentrated {\\textasciitilde}20-fold using magnetic separation. Upon dual-target qPCR testing of concentrates, this strategy exhibited 90\\% sensitivity (83/92) and 97\\% specificity (35/36) relative to sputum MRS. These results point the way toward automatable, high-sensitivity methods for detecting MTB DNA in TS. \n               \n             \n             \n              IMPORTANCE \n              Improved testing for tuberculosis (TB) is needed. Using a more accessible sample type than sputum may enable the detection of more cases, but it is critical that alternative samples be tested appropriately. Here, we describe two new, highly accurate methods for testing tongue swabs for TB DNA. \n             \n          ,  \n            Improved testing for tuberculosis (TB) is needed. Using a more accessible sample type than sputum may enable the detection of more cases, but it is critical that alternative samples be tested appropriately. Here, we describe two new, highly accurate methods for testing tongue swabs for TB DNA.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Clinical Microbiology},\n\tauthor = {Olson, Alaina M. and Wood, Rachel C. and Weigel, Kris M. and Yan, Alexander J. and Lochner, Katherine A. and Dragovich, Rane B. and Luabeya, Angelique K. and Yager, Paul and Hatherill, Mark and Cangelosi, Gerard A.},\n\teditor = {Turenne, Christine Y.},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {e01140--24},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Tongue swab (TS) sampling combined with quantitative PCR (qPCR) to detect Mycobacterium tuberculosis (MTB) DNA is a promising alternative to sputum testing for tuberculosis (TB) diagnosis. In prior studies, the sensitivity of tongue swabbing has usually been lower than sputum. In this study, we evaluated two strategies to improve sensitivity. In one, centrifugation was used to concentrate tongue dorsum bacteria from 2-mL suspensions eluted from high-capacity foam swab samples. The pellets were resuspended as 500-µL suspensions, and then mechanically lysed prior to dual-target qPCR to detect MTB insertion elements IS 6110 and IS 1081 . Fractionation experiments demonstrated that most of the MTB DNA signal in clinical swab samples (99.22% ± 1.46%) was present in the sedimentable fraction. When applied to archived foam swabs collected from 124 South Africans with presumptive TB, this strategy exhibited 83% sensitivity (71/86) and 100% specificity (38/38) relative to sputum microbiological reference standard (MRS; sputum culture and/or Xpert Ultra). The second strategy used sequence-specific magnetic capture (SSMaC) to concentrate DNA released from MTB cells. This protocol was evaluated on archived Copan FLOQSwabs flocked swab samples collected from 128 South African participants with presumptive TB. Material eluted into 500 µL buffer was mechanically lysed. The suspensions were digested by proteinase K, hybridized to biotinylated dual-target oligonucleotide probes, and then concentrated ~20-fold using magnetic separation. Upon dual-target qPCR testing of concentrates, this strategy exhibited 90% sensitivity (83/92) and 97% specificity (35/36) relative to sputum MRS. These results point the way toward automatable, high-sensitivity methods for detecting MTB DNA in TS. IMPORTANCE Improved testing for tuberculosis (TB) is needed. Using a more accessible sample type than sputum may enable the detection of more cases, but it is critical that alternative samples be tested appropriately. Here, we describe two new, highly accurate methods for testing tongue swabs for TB DNA. , Improved testing for tuberculosis (TB) is needed. Using a more accessible sample type than sputum may enable the detection of more cases, but it is critical that alternative samples be tested appropriately. Here, we describe two new, highly accurate methods for testing tongue swabs for TB DNA.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Tracing the spatial origins and spread of SARS-CoV-2 Omicron lineages in South Africa.\n \n \n \n \n\n\n \n Dor, G.; Wilkinson, E.; Martin, D. P.; Moir, M.; Tshiabuila, D.; Kekana, D.; Ntozini, B.; Joseph, R.; Iranzadeh, A.; Nyaga, M. M.; Goedhals, D.; Maponga, T.; Maritz, J.; Laguda-Akingba, O.; Ramphal, Y.; MacIntyre, C.; Chabuka, L.; Pillay, S.; Giandhari, J.; Baxter, C.; Hsiao, N.; Preiser, W.; Bhiman, J. N.; Davies, M.; Venter, M.; Treurnicht, F. K.; Wolter, N.; Williamson, C.; Von Gottberg, A.; Lessells, R.; Tegally, H.; and De Oliveira, T.\n\n\n \n\n\n\n Nature Communications, 16(1): 4937. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Tracing$ Paper\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{dor_tracing_2025,\n\ttitle = {Tracing the spatial origins and spread of {SARS}-{CoV}-2 {Omicron} lineages in {South} {Africa}},\n\tvolume = {16},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-025-60081-0},\n\tdoi = {10.1038/s41467-025-60081-0},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Nature Communications},\n\tauthor = {Dor, Graeme and Wilkinson, Eduan and Martin, Darren P. and Moir, Monika and Tshiabuila, Derek and Kekana, Dikeledi and Ntozini, Buhle and Joseph, Rageema and Iranzadeh, Arash and Nyaga, Martin M. and Goedhals, Dominique and Maponga, Tongai and Maritz, Jean and Laguda-Akingba, Oluwakemi and Ramphal, Yajna and MacIntyre, Caitlin and Chabuka, Lucious and Pillay, Sureshnee and Giandhari, Jennifer and Baxter, Cheryl and Hsiao, Nei-yuan and Preiser, Wolfgang and Bhiman, Jinal N. and Davies, Mary-Anne and Venter, Marietjie and Treurnicht, Florette K. and Wolter, Nicole and Williamson, Carolyn and Von Gottberg, Anne and Lessells, Richard and Tegally, Houriiyah and De Oliveira, Tulio},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {4937},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Integrated renin angiotensin system dysregulation and immune profiles predict COVID-19 disease severity in a South African cohort.\n \n \n \n \n\n\n \n Müller, T.; Dzanibe, S.; Day, C.; Mpangase, P. T.; Chimbetete, T.; Pedretti, S.; Schwager, S.; Gray, C. M.; Sturrock, E.; and Peter, J.\n\n\n \n\n\n\n Scientific Reports, 15(1): 12799. April 2025.\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

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@article{muller_integrated_2025,\n\ttitle = {Integrated renin angiotensin system dysregulation and immune profiles predict {COVID}-19 disease severity in a {South} {African} cohort},\n\tvolume = {15},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-025-96161-w},\n\tdoi = {10.1038/s41598-025-96161-w},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Scientific Reports},\n\tauthor = {Müller, Talitha and Dzanibe, Sonwabile and Day, Cascia and Mpangase, Phelelani Thokozani and Chimbetete, Tafadzwa and Pedretti, Sarah and Schwager, Sylva and Gray, Clive M. and Sturrock, Edward and Peter, Jonny},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {12799},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Perimyocarditis in Dengue Shock Syndrome: A Primary Infection Challenging Traditional Paradigms — A Case Report.\n \n \n \n \n\n\n \n De Gaay Fortman, D. P. E.; Leopold, S. J.; Reeskamp, R. L. F.; De Weger, V. A.; Wagemakers, A.; He, M. C. T.; Grobusch, M. P.; and De Regt, M. J. E.\n\n\n \n\n\n\n SN Comprehensive Clinical Medicine, 7(1): 163. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Perimyocarditis$ Paper\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_gaay_fortman_perimyocarditis_2025,\n\ttitle = {Perimyocarditis in {Dengue} {Shock} {Syndrome}: {A} {Primary} {Infection} {Challenging} {Traditional} {Paradigms} — {A} {Case} {Report}},\n\tvolume = {7},\n\tissn = {2523-8973},\n\tshorttitle = {Perimyocarditis in {Dengue} {Shock} {Syndrome}},\n\turl = {https://link.springer.com/10.1007/s42399-025-01928-x},\n\tdoi = {10.1007/s42399-025-01928-x},\n\tabstract = {Abstract \n            Dengue virus infection is a leading cause of febrile illness in travellers returning from endemic regions. While most primary infections are mild and self-limiting, a small proportion progresses to severe disease, such as dengue shock syndrome (DSS). With the global rise in dengue incidence, clinicians should remain alert to rare but serious complications—including cardiac involvement—even in primary infections. We report a rare case of DSS complicated by perimyocarditis in a previously healthy traveller returning from Indonesia, highlighting the importance of early recognition of atypical presentations. A 55-year-old woman presented with malaise, rash, and weakness two weeks after returning from Bali, Indonesia. Serological testing confirmed dengue virus infection (IgM + , IgG − , NS1 +). Electrocardiogram (ECG), transthoracic echocardiography (TTE), and elevated troponin levels led to the diagnosis of perimyocarditis. Due to the suspicion of obstructive shock, given persistent hypotension, rising lactate, and a pulsus paradoxus, a pericardiocentesis was performed, but without hemodynamic improvement. The shock was ultimately attributed to distributive shock due to capillary leak in the context of DSS, supported by hypoalbuminaemia, peripheral oedema, and pleural effusion. The patient improved with supportive care and recovered fully. This case challenges the traditional dogma that severe dengue occurs primarily in secondary infections, demonstrating that life-threatening complications, including perimyocarditis, can arise even in primary infections.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {SN Comprehensive Clinical Medicine},\n\tauthor = {De Gaay Fortman, Duveke P. E. and Leopold, Stije J. and Reeskamp, Rens L. F. and De Weger, Vincent A. and Wagemakers, Alex and He, Marielle C. Tam and Grobusch, Martin P. and De Regt, Marieke J. E.},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {163},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Opportunistic Fungal Infections in Sub-Saharan Africa.\n \n \n \n \n\n\n \n Duvenage, L.; Higgitt, E. R.; Dangarembizi, R.; and Hoving, J. C.\n\n\n \n\n\n\n Annual Review of Microbiology, 79(1): 129–148. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Opportunistic$ Paper\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{duvenage_opportunistic_2025,\n\ttitle = {Opportunistic {Fungal} {Infections} in {Sub}-{Saharan} {Africa}},\n\tvolume = {79},\n\tcopyright = {http://creativecommons.org/licenses/by/4.0/},\n\tissn = {0066-4227, 1545-3251},\n\turl = {https://www.annualreviews.org/content/journals/10.1146/annurev-micro-121423-115959},\n\tdoi = {10.1146/annurev-micro-121423-115959},\n\tabstract = {Opportunistic fungal infections are a major cause of morbidity and mortality in sub-Saharan Africa. The high prevalence of advanced HIV disease, limited surveillance and reporting of fungal disease, and lack of access to healthcare lead to a disproportionate number of fungal-related deaths in this region. This review explores selected fungal pathogens associated with the highest mortality rates: \n              Cryptococcus neoformans \n              and \n              Pneumocystis jirovecii \n              , as well as endemic dimorphic fungal pathogens \n              Histoplasma \n              spp. and \n              Emergomyces africanus \n              , which are underreported in the region. Recent advances in our understanding of pathogenesis and how this knowledge may be exploited for the development of novel antifungals and therapies are discussed. We reflect on the risk factors unique to sub-Saharan Africa and on the diagnostic and treatment challenges, and we highlight the current research priorities that are needed to reduce the burden of fungal disease in this endemic region.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Annual Review of Microbiology},\n\tauthor = {Duvenage, Lucian and Higgitt, Emily Ruth and Dangarembizi, Rachael and Hoving, J. Claire},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {129--148},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Acute serum protein biomarker profile and prevalence of persistent (\\textgreater6 months) neuropsychiatric symptoms in a cohort of SARS-CoV-2 PCR positive patients in Cape Town, South Africa.\n \n \n \n \n\n\n \n Van Niekerk, I.; Panieri, M.; Müller, T.; Mapahla, L.; Dzanibe, S.; Day, C.; Stein, D. J.; and Peter, J.\n\n\n \n\n\n\n Brain, Behavior, & Immunity - Health, 46: 100990. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Acute$ Paper\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_niekerk_acute_2025,\n\ttitle = {Acute serum protein biomarker profile and prevalence of persistent ({\\textgreater}6 months) neuropsychiatric symptoms in a cohort of {SARS}-{CoV}-2 {PCR} positive patients in {Cape} {Town}, {South} {Africa}},\n\tvolume = {46},\n\tissn = {26663546},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666354625000481},\n\tdoi = {10.1016/j.bbih.2025.100990},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Brain, Behavior, \\& Immunity - Health},\n\tauthor = {Van Niekerk, Inette and Panieri, Monica and Müller, Talitha and Mapahla, Lovemore and Dzanibe, Sonwabile and Day, Cascia and Stein, Dan J. and Peter, Jonny},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {100990},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Comparative Performance of Urine Lipoarabinomannan and Urine Xpert MTB/RIF Ultra for Diagnosing Tuberculosis in Adult Inpatients With HIV in East London, South Africa.\n \n \n \n \n\n\n \n Stead, D.; Wasserman, S.; Steenkamp, E.; Parrish, A.; Barr, D.; and Meintjes, G.\n\n\n \n\n\n\n Clinical Infectious Diseases, 81(4): e146–e152. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Comparative$ Paper\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{stead_comparative_2025,\n\ttitle = {Comparative {Performance} of {Urine} {Lipoarabinomannan} and {Urine} {Xpert} {MTB}/{RIF} {Ultra} for {Diagnosing} {Tuberculosis} in {Adult} {Inpatients} {With} {HIV} in {East} {London}, {South} {Africa}},\n\tvolume = {81},\n\tcopyright = {https://creativecommons.org/licenses/by-nc-nd/4.0/},\n\tissn = {1058-4838, 1537-6591},\n\turl = {https://academic.oup.com/cid/article/81/4/e146/8102282},\n\tdoi = {10.1093/cid/ciaf080},\n\tabstract = {Abstract \n             \n              Background \n              Urine lateral flow lipoarabinomannan (LF-LAM) is a point-of-care tuberculosis (TB) test for patients with human immunodeficiency virus (HIV). Xpert MTB/RIF Ultra (Ultra) has improved sensitivity on sputum compared with the previous generation of Xpert and may improve diagnostic yield for TB on urine-based testing. \n             \n             \n              Methods \n              We conducted a diagnostic accuracy study in East London, South Africa. Adults with HIV hospitalized with ≥1 W4SS (World Health Organization–recommended 4-symptom screen) or clinical concern for TB were enrolled; TB cultures were performed on blood, sputum, and urine. Unprocessed urine was tested with LF-LAM and Ultra on the pellet of 15 mL centrifuged urine. The primary outcome was sensitivity of urine Ultra compared with LF-LAM, with microbiological TB (positive TB culture or molecular test, excluding urine Ultra) as the reference. Secondary outcomes included specificity and diagnostic yield. \n             \n             \n              Results \n              Two hundred thirty-eight participants were enrolled with a median CD4 count of 76 cells/mm3. Microbiological TB was diagnosed in 62 (26\\%). Using microbiological TB as the reference, sensitivity of LF-LAM and urine Ultra was 45\\% (95\\% confidence interval, 32–58) and 70\\% (95\\% CI, 57–81; McNemar P = .0013); specificity was 93\\% (95\\% CI, 81–99) and 100\\% (95\\% CI, 92–100; McNemar P = .25). Diagnostic yields for microbiological TB were 34\\% for sputum Ultra, 45\\% for urine LF-LAM, 68 for urine Ultra, and 73\\% for urine LF-LAM and urine Ultra combined. \n             \n             \n              Conclusions \n              Combined urine-based testing (Ultra + LF-LAM) identified nearly three-quarters of medical inpatients with HIV with microbiological TB. Urine Ultra had significantly improved sensitivity compared with LF-LAM.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-28},\n\tjournal = {Clinical Infectious Diseases},\n\tauthor = {Stead, David and Wasserman, Sean and Steenkamp, Ebrahim and Parrish, Andy and Barr, David and Meintjes, Graeme},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {e146--e152},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n How the DS-I Africa Consortium Is Harnessing the Power of Partnerships for Data Science in Africa.\n \n \n \n \n\n\n \n Agamah, F. E.; Mistry, A.; Muzambi, T.; Dankyi, G.; Povlich, L.; and Skelton, M.\n\n\n \n\n\n\n Data Science Journal, 24: 32. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"How$ Paper\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{agamah_how_2025,\n\ttitle = {How the {DS}-{I} {Africa} {Consortium} {Is} {Harnessing} the {Power} of {Partnerships} for {Data} {Science} in {Africa}},\n\tvolume = {24},\n\tissn = {1683-1470},\n\turl = {http://datascience.codata.org/articles/10.5334/dsj-2025-032/},\n\tdoi = {10.5334/dsj-2025-032},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Data Science Journal},\n\tauthor = {Agamah, Francis E. and Mistry, Amit and Muzambi, Tino and Dankyi, Gifty and Povlich, Laura and Skelton, Michelle},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {32},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Africa is an Essential Partner in the Research and Development of an HIV Vaccine.\n \n \n \n \n\n\n \n Gray, G.; Williamson, C.; Bekker, L.; Daniels, B.; Smidt, W.; Garrett, N.; Kityo Mutuluuza, C.; Mwesigwa, B.; Stranix-Chibanda, L.; Akimbu, A.; Obuku, A.; Johnson, T.; Naluyima, P.; Sawe, F.; Burgers, W.; Ntiginya, N.; Morar, N.; Takalani, A.; Hendricks, S.; Woeber, K.; Abrahams, F.; Tholanah, M.; Mugamba, S.; Mulder, M.; and Moore, P.\n\n\n \n\n\n\n Current HIV Research, 23(6): 482–493. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Africa$ Paper\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{gray_africa_2025,\n\ttitle = {Africa is an {Essential} {Partner} in the {Research} and {Development} of an {HIV} {Vaccine}},\n\tvolume = {23},\n\tissn = {1570162X},\n\turl = {https://www.eurekaselect.com/245756/article},\n\tdoi = {10.2174/011570162X361496250627004203},\n\tabstract = {Despite significant advances in HIV antiretroviral treatment, and proven efficacy of HIV prevention \noptions, an effective and affordable HIV vaccine is still necessary for the elimination of HIV, particularly \nin Africa. Furthermore, viral and host factors unique to the African continent provide a strong scientific rationale \nfor local vaccine discovery efforts. Several key challenges hamper Africa's vaccine research and production \ncapabilities. These include inadequate funding for African-led research, equipment and infrastructure challenges, \nlack of preclinical evaluation capacity, limited manufacturing facilities for clinical-grade vaccines, and \na shortage of scientists with specialized laboratory, bioinformatics and biostatistics training. A recently established \nAfrican-led consortium seeks to strengthen African HIV vaccine contributions by providing support, \ntraining and funding to address these gaps by strengthening discovery research and conducting early phase \nclinical trials of existing and novel Africa-derived vaccine candidates while strengthening African manufacturing \ninfrastructure and capacity. Constant and robust community and stakeholder engagement will be key to ensuring \nthe success of the consortiums’ efforts in providing sustainable vaccine development, manufacturing \nand clinical testing in Africa. Given the magnitude of the HIV burden in Africa, with largely undescribed viral \nand host diversity, it is vital that HIV vaccine discovery evolves to include the underutilized scientific expertise \nand capacity on the African continent. Recent interruptions in the funding of consortia in Africa threaten \nthis type of progress and can derail progress in vaccine discovery.},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {Current HIV Research},\n\tauthor = {Gray, Glenda and Williamson, Carolyn and Bekker, Linda-Gail and Daniels, Brodie and Smidt, Werner and Garrett, Nigel and Kityo Mutuluuza, Cissy and Mwesigwa, Betty and Stranix-Chibanda, Lynda and Akimbu, Alash'le and Obuku, Andrew and Johnson, Tian and Naluyima, Prossy and Sawe, Fredrick and Burgers, Wendy and Ntiginya, Nyanda and Morar, Neetha and Takalani, Azwidihwi and Hendricks, Simone and Woeber, Kubashni and Abrahams, Fatima and Tholanah, Martha and Mugamba, Stephen and Mulder, Michelle and Moore, Penny},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {482--493},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The next generation of drug resistant tuberculosis drug design.\n \n \n \n \n\n\n \n Singh, V.\n\n\n \n\n\n\n Future Medicinal Chemistry, 17(4): 385–387. February 2025.\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{singh_next_2025,\n\ttitle = {The next generation of drug resistant tuberculosis drug design},\n\tvolume = {17},\n\tissn = {1756-8919, 1756-8927},\n\turl = {https://www.tandfonline.com/doi/full/10.1080/17568919.2025.2453406},\n\tdoi = {10.1080/17568919.2025.2453406},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-28},\n\tjournal = {Future Medicinal Chemistry},\n\tauthor = {Singh, Vinayak},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {385--387},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Eight-year tuberculosis epidemic trends in the Republic of Congo, a high TB burden country: progress and gaps towards end-TB targets.\n \n \n \n \n\n\n \n Mouzinga, F. H.; Elion Assiana, D. O.; Dello, M. N. M.; Ngouama, B. B.; Okemba Okombi, F. H.; Akiera, B. A.; Grobusch, M. P; Mouanga, A. M.; Elenga, V. A.; Nguimbi, E.; and Ntoumi, F.\n\n\n \n\n\n\n BMJ Global Health, 10(12): e019877. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Eight-year$ Paper\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{mouzinga_eight-year_2025,\n\ttitle = {Eight-year tuberculosis epidemic trends in the {Republic} of {Congo}, a high {TB} burden country: progress and gaps towards end-{TB} targets},\n\tvolume = {10},\n\tissn = {2059-7908},\n\tshorttitle = {Eight-year tuberculosis epidemic trends in the {Republic} of {Congo}, a high {TB} burden country},\n\turl = {https://gh.bmj.com/lookup/doi/10.1136/bmjgh-2025-019877},\n\tdoi = {10.1136/bmjgh-2025-019877},\n\tabstract = {Background \n              Evaluating progress towards WHO End Tuberculosis Strategy goals is crucial for high burden countries like the Republic of Congo. This study analysed trends in tuberculosis (TB) incidence, treatment, care quality and operational research activities from 2016 to 2023 to assess the country’s control efforts. \n             \n             \n              Methods \n              An 8-year retrospective study of TB incidence/mortality trends was performed using a Joint Point Analysis V.5.2.0. We extracted annual national and WHO TB programme data for the period under review. \n             \n             \n              Results \n              From 2016 to 2023, the TB incidence rate decreased by 2.6\\% (annual percentage change (APC)=−0.33, 95\\% CI− 0.5 to −0.005; p{\\textless}0.05). The proportion of bacteriologically confirmed cases significantly increased (APC=4.2, 95\\% CI 0.9 to 7.7; p{\\textless}0.001), while treatment coverage rose by 22\\% (APC=2.81, 95\\% CI 1.1 to 4.5; p{\\textless}0.05). The proportion of notified patients with TB tested for HIV significantly increased (APC=25, 95\\% CI 2.6 to 52.63; p{\\textless}0.05), but the rate of patients with TB testing HIV positive decreased significantly (APC=−13.9, 95\\% CI −23.9 to −2.6; p{\\textless}0.05). The proportion of unsuccessful treatment outcomes showed a non-significant decline, with an APC of 4.90\\% (95\\% CI −11.7\\% to 2.3\\%; p=0.1), while TB-related deaths increased non-significantly, with an APC of 3.76\\% (95\\% CI −1.3\\% to 9.2\\%; p=0.12). Patients with TB/HIV on ART increased by 51\\% (APC=6.4, 95\\% CI −23.9 to −2.6; p{\\textless}0.05). No operational research activity has been carried out throughout the review period. \n             \n             \n              Conclusion \n              The observed progress was insufficient, as the Republic of Congo failed to meet the 20\\% TB incidence reduction target for 2020 and is unlikely to achieve the 50\\% reduction goal for 2025. More investment in case detection, diagnosis, treatment quality and the implementation of operational research activities is needed to achieve global goals.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2026-05-28},\n\tjournal = {BMJ Global Health},\n\tauthor = {Mouzinga, Freisnel Hermeland and Elion Assiana, Darrel Ornelle and Dello, Mita Naomie Merveille and Ngouama, Breli Bonheur and Okemba Okombi, Franck Hardain and Akiera, Baurel Arnaud and Grobusch, Martin P and Mouanga, Alain Maxime and Elenga, Viny Andzi and Nguimbi, Etienne and Ntoumi, Francine},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e019877},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Developmental challenges in infants who are HIV-exposed uninfected.\n \n \n \n \n\n\n \n Ntuli, L.; Mtshali, A.; Mzobe, G.; Pillay, N.; Happel, A.; and Ngcapu, S.\n\n\n \n\n\n\n Brain, Behavior, and Immunity, 130: 106078. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Developmental$ Paper\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{ntuli_developmental_2025,\n\ttitle = {Developmental challenges in infants who are {HIV}-exposed uninfected},\n\tvolume = {130},\n\tissn = {08891591},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0889159125003137},\n\tdoi = {10.1016/j.bbi.2025.106078},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Brain, Behavior, and Immunity},\n\tauthor = {Ntuli, Lungelo and Mtshali, Andile and Mzobe, Gugulethu and Pillay, Nashlin and Happel, Anna-Ursula and Ngcapu, Sinaye},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {106078},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Carrier-Free Peptide–Daunorubicin–Small Interfering RNA Nanoassembly for Targeted Therapy of Acute Myeloid Leukemia.\n \n \n \n \n\n\n \n Yang, H.; Yu, X.; Guo, Z.; Shi, S.; Wang, J.; Guo, S.; Hu, B.; Chai, M.; Wang, Z.; Barth, S.; Fan, K.; He, H.; Zhang, M.; and Huang, Y.\n\n\n \n\n\n\n Cyborg and Bionic Systems, 6: 0436. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Carrier-Free$ Paper\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{yang_carrier-free_2025,\n\ttitle = {Carrier-{Free} {Peptide}–{Daunorubicin}–{Small} {Interfering} {RNA} {Nanoassembly} for {Targeted} {Therapy} of {Acute} {Myeloid} {Leukemia}},\n\tvolume = {6},\n\tissn = {2692-7632},\n\turl = {https://spj.science.org/doi/10.34133/cbsystems.0436},\n\tdoi = {10.34133/cbsystems.0436},\n\tabstract = {Acute myeloid leukemia (AML) continues to represent a substantial unmet therapeutic need in clinical practice. In recent years, peptide–drug conjugates and small interfering RNA (siRNA) drugs have gained considerable attention due to their impressive clinical progress in treating various diseases. In this study, we designed a carrier-free “3-in-1” peptide–daunorubicin–siRNA (PDR) nanoassembly, which combines a cell-penetrating and tumor-suppressing peptide, a daunorubicin (DNR) prodrug, and siRNA targeting the LILRB4 gene. After optimizing the molar ratio among peptide, DNR prodrug, and siRNA, we identified the most potent PDR formulation, which exhibited excellent intracellular uptake efficiency, primarily through caveolin-mediated endocytosis, in THP-1 cells. The pH-responsive bond in the DNR prodrug facilitated the endosomal escape of siRNA, leading to significant gene repression of LILRB4. Additionally, the tumor-suppressing peptide p16 \n              MIS \n              effectively inhibited the transition of cells from the S phase to the G2/M phase and induced apoptosis. In a leukemia mouse model, PDR efficiently suppressed leukemia cell invasion, prolonged survival, and reduced leukemia cell infiltration in the bone marrow. Notably, silencing LILRB4 not only promoted T cell maturation in spleen and lymph nodes but also enhanced T cell infiltration in tumor tissues. This study offered a highly promising therapeutic strategy for AML and other diseases.},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Cyborg and Bionic Systems},\n\tauthor = {Yang, Haiyin and Yu, Xi and Guo, Zhitong and Shi, Songxuan and Wang, Jie and Guo, Shuai and Hu, Bo and Chai, Meihong and Wang, Zhuoran and Barth, Stefan and Fan, Kelong and He, Huining and Zhang, Mengjie and Huang, Yuanyu},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {0436},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Autoantibodies to interferon alpha, nuclear antigens, cardiolipin, and beta 2 glycoprotein 1 in a Ugandan cohort and their relation to SARS-CoV-2 infection.\n \n \n \n \n\n\n \n Epstein-Shuman, A.; Zhu, X.; Hunt, J. H.; Fernandez, R. E.; Rozek, G. M.; Redd, A. D.; Gotthold, Z. A.; Quiros, G.; Galiwango, R. M.; Kigozi, G.; Caturegli, P.; Ssekubugu, R.; Grabowski, M. K.; Chang, L. W.; Reynolds, S. J.; and Laeyendecker, O.\n\n\n \n\n\n\n Journal of Infection and Public Health, 18(6): 102722. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Autoantibodies$ Paper\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{epstein-shuman_autoantibodies_2025,\n\ttitle = {Autoantibodies to interferon alpha, nuclear antigens, cardiolipin, and beta 2 glycoprotein 1 in a {Ugandan} cohort and their relation to {SARS}-{CoV}-2 infection},\n\tvolume = {18},\n\tissn = {18760341},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1876034125000711},\n\tdoi = {10.1016/j.jiph.2025.102722},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Infection and Public Health},\n\tauthor = {Epstein-Shuman, Adam and Zhu, Xianming and Hunt, Joanne H. and Fernandez, Reinaldo E. and Rozek, Gracie M. and Redd, Andrew D. and Gotthold, Zoe A. and Quiros, Gabriel and Galiwango, Ronald M. and Kigozi, Godfrey and Caturegli, Patrizio and Ssekubugu, Robert and Grabowski, Mary K. and Chang, Larry W. and Reynolds, Steven J. and Laeyendecker, Oliver},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {102722},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Third exposure to COVID-19 infection or vaccination differentially impacts T cell responses.\n \n \n \n \n\n\n \n Ahimbisibwe, G.; Greenwood, D.; Wilkinson, K. A.; Gahir, J.; Townsley, H.; Miah, M.; Bawumia, P.; Chaloner, C.; Levi, D.; Hobson, P.; Riddell, A.; Hobbs, A.; Dowgier, G.; Penn, R.; Sanderson, T.; Stevenson-Leggett, P.; Daley, O.; Bazire, J.; Harvey, R.; Fowler, A. S.; Smith, C.; Miranda, M.; O’Reilly, N.; Warchal, S.; Ambrose, K.; Strange, A.; Kelly, G.; Kjar, S.; Williams, B.; Libri, V.; Gamblin, S.; Gandhi, S.; Swanton, C.; Bauer, D. L.; Wilkinson, R. J.; Carr, E. J.; and Wall, E. C.\n\n\n \n\n\n\n Journal of Infection, 91(3): 106598. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Third$ Paper\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{ahimbisibwe_third_2025,\n\ttitle = {Third exposure to {COVID}-19 infection or vaccination differentially impacts {T} cell responses},\n\tvolume = {91},\n\tissn = {01634453},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0163445325001987},\n\tdoi = {10.1016/j.jinf.2025.106598},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Infection},\n\tauthor = {Ahimbisibwe, Gift and Greenwood, David and Wilkinson, Katalin Andrea and Gahir, Joshua and Townsley, Hermaleigh and Miah, Murad and Bawumia, Philip and Chaloner, Charlotte and Levi, Dina and Hobson, Philip and Riddell, Andy and Hobbs, Agnieszka and Dowgier, Giulia and Penn, Rebecca and Sanderson, Theo and Stevenson-Leggett, Phoebe and Daley, Odiesia and Bazire, James and Harvey, Ruth and Fowler, Ashley S. and Smith, Callie and Miranda, Mauro and O’Reilly, Nicola and Warchal, Scott and Ambrose, Karen and Strange, Amy and Kelly, Gavin and Kjar, Svend and Williams, Bryan and Libri, Vincenzo and Gamblin, Steve and Gandhi, Sonia and Swanton, Charles and Bauer, David Lv and Wilkinson, Robert John and Carr, Edward J. and Wall, Emma C.},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {106598},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Enabling data-driven decision-making for innovative health care and delivery in Africa.\n \n \n \n \n\n\n \n Agamah, F. E.; Anyanful, A.; Ryabinina, O.; Twum, J.; Tunga, M.; Skelton, M.; Bope, C. D.; Chimusa, E. R.; and Thomford, N. E.\n\n\n \n\n\n\n npj Health Systems, 2(1): 48. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Enabling$ Paper\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{agamah_enabling_2025,\n\ttitle = {Enabling data-driven decision-making for innovative health care and delivery in {Africa}},\n\tvolume = {2},\n\tissn = {3005-1959},\n\turl = {https://www.nature.com/articles/s44401-025-00047-y},\n\tdoi = {10.1038/s44401-025-00047-y},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {npj Health Systems},\n\tauthor = {Agamah, Francis E. and Anyanful, Akwasi and Ryabinina, Oksana and Twum, Joel and Tunga, Mahadia and Skelton, Michelle and Bope, Christian D. and Chimusa, Emile R. and Thomford, Nicholas E.},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {48},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Factors influencing the efficacy of Bacille Calmette-Guérin (BCG) vaccine.\n \n \n \n \n\n\n \n Bukula, L.; Chengalroyen, M. D.; Omollo, C.; and Moseki, R. M.\n\n\n \n\n\n\n The Microbe, 6: 100230. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Factors$ Paper\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{bukula_factors_2025,\n\ttitle = {Factors influencing the efficacy of {Bacille} {Calmette}-{Guérin} ({BCG}) vaccine},\n\tvolume = {6},\n\tissn = {29501946},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2950194624001973},\n\tdoi = {10.1016/j.microb.2024.100230},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {The Microbe},\n\tauthor = {Bukula, Lwandile and Chengalroyen, Melissa D. and Omollo, Charles and Moseki, Raymond M.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {100230},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Optimization of 2,8-Diaryl-1,5-naphthyridines as Plasmodium falciparum Phosphatidylinositol 4-Kinase Inhibitors with Improved ADME Profiles and In Vivo Efficacy.\n \n \n \n \n\n\n \n Dziwornu, G. A.; Seanego, D.; Fienberg, S.; Sypu, V. S.; Salomane, N.; Krugmann, L.; Taylor, D.; Masike, K.; Njoroge, M.; Boonyalai, N.; Lee, M. C. S.; Godoy, L. C.; Pasaje, C. F.; Niles, J. C.; Basarab, G. S.; Coulson, L. B.; Ghorpade, S. R.; and Chibale, K.\n\n\n \n\n\n\n Journal of Medicinal Chemistry, 68(20): 21878–21891. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Optimization$ Paper\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_optimization_2025,\n\ttitle = {Optimization of 2,8-{Diaryl}-1,5-naphthyridines as \\textit{{Plasmodium} falciparum} {Phosphatidylinositol} 4-{Kinase} {Inhibitors} with {Improved} {ADME} {Profiles} and {In} {Vivo} {Efficacy}},\n\tvolume = {68},\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.5c02248},\n\tdoi = {10.1021/acs.jmedchem.5c02248},\n\tlanguage = {en},\n\tnumber = {20},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Medicinal Chemistry},\n\tauthor = {Dziwornu, Godwin A. and Seanego, Donald and Fienberg, Stephen and Sypu, Venkata S. and Salomane, Nicolaas and Krugmann, Liezl and Taylor, Dale and Masike, Keabetswe and Njoroge, Mathew and Boonyalai, Nonlawat and Lee, Marcus C. S. and Godoy, Luiz C. and Pasaje, Charisse Flerida and Niles, Jacquin C. and Basarab, Gregory S. and Coulson, Lauren B. and Ghorpade, Sandeep R. and Chibale, Kelly},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {21878--21891},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Travel-associated international spread of Oropouche virus beyond the Amazon.\n \n \n \n \n\n\n \n De Melo Iani, F. C.; Pereira, F. M.; De Oliveira, E. C.; Rodrigues, J. T. N.; Machado, M. H.; Fonseca, V.; Adelino, T. E. R.; Guimarães, N. R.; Tomé, L. M. R.; Gómez, M. K. A.; Nardy, V. B.; Ribeiro, A. A.; Rosewell, A.; Ferreira, Á. G. A; Silva De Mello, A. L. E; Fernandes, B. M. M.; De Albuquerque, C. F. C.; Dos Santos Pereira, D.; Pimentel, E. C.; Lima, F. G. M.; Silva, F. V. M.; De Carvalho Pereira, G.; Tegally, H.; Almeida, J. D. P. C.; Moreno, K. M. F.; Vasconcelos, K. R.; Santos, L. C.; Silva, L. C. M.; Frutuoso, L. C V; Lamounier, L. O.; Costa, M. A.; De Oliveira, M. S.; Dos Anjos, M. P. D.; Ciccozzi, M.; Lima, M. T.; Pereira, M. A.; Rocha, M. L. C.; De Souza Da Silva, P. E.; Rabinowitz, P. M; De Almeida, P. S.; Lessells, R.; Gazzinelli, R. T; Da Cunha, R. V.; Gonçalves, S.; Dos Santos, S. C. F.; De Alcântara Belettini, S. A.; Pedroso, S. H. S. P.; Araújo, S. I. R.; Da Silva, S. F.; Croda, J.; Maciel, E.; Van Voorhis, W.; Martin, D. P; Holmes, E. C; De Oliveira, T.; Lourenço, J.; Alcantara, L. C. J.; and Giovanetti, M.\n\n\n \n\n\n\n Journal of Travel Medicine, 32(3): taaf018. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Travel-associated$ 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 abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{de_melo_iani_travel-associated_2025,\n\ttitle = {Travel-associated international spread of {Oropouche} virus beyond the {Amazon}},\n\tvolume = {32},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1195-1982, 1708-8305},\n\turl = {https://academic.oup.com/jtm/article/doi/10.1093/jtm/taaf018/8046862},\n\tdoi = {10.1093/jtm/taaf018},\n\tabstract = {Abstract \n            Oropouche virus (OROV), first detected in Trinidad and Tobago in 1955, was historically confined to the Brazilian Amazon Basin. However, since late 2022, an increasing number of OROV cases have been reported across various regions of Brazil as well as in urban centers in Bolivia, Ecuador, Guyana, Colombia, Cuba, Panama, and Peru. In collaboration with Central Public Health Laboratories across Brazil, we integrated epidemiological metadata with genomic analyses from recent cases, generating 133 whole-genome sequences covering the virus’s three genomic segments (L, M, and S). These include the first genomes from regions outside the Amazon and from the first recorded fatal cases. Phylogenetic analyses show that the 2024 OROV genomes form a monophyletic group with sequences from the Amazon Basin sampled since 2022, revealing a rapid north-to-south viral movement into historically non-endemic areas. We identified 21 reassortment events, though it remains unclear whether these genomic changes have facilitated viral adaptation to local ecological conditions or contributed to phenotypic traits of public health significance. Our findings demonstrate how OROV has evolved through reassortment and spread rapidly across multiple states in Brazil, leading to the largest outbreak ever recorded outside the Amazon and the first confirmed fatalities. Additionally, by analysing travel-related cases, we provide the first insights into the international spread of OROV beyond Brazil, further highlighting the role of human mobility in its dissemination. The virus’s recent rapid geographic expansion and the emergence of severe cases emphasize the urgent need for enhanced surveillance across the Americas. In the absence of significant human population changes over the past two years, factors such as viral adaptation, deforestation, and climate shifts—either individually or in combination—may have facilitated the spread of OROV beyond the Amazon Basin through both local and travel-associated transmission.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Travel Medicine},\n\tauthor = {De Melo Iani, Felipe Campos and Pereira, Felicidade Mota and De Oliveira, Elaine Cristina and Rodrigues, Janete Taynã Nascimento and Machado, Mariza Hoffmann and Fonseca, Vagner and Adelino, Talita Emile Ribeiro and Guimarães, Natália Rocha and Tomé, Luiz Marcelo Ribeiro and Gómez, Marcela Kelly Astete and Nardy, Vanessa Brandão and Ribeiro, Adriana Aparecida and Rosewell, Alexander and Ferreira, Álvaro Gil A and Silva De Mello, Arabela Leal E and Fernandes, Brenda Machado Moura and De Albuquerque, Carlos Frederico Campelo and Dos Santos Pereira, Dejanira and Pimentel, Eline Carvalho and Lima, Fábio Guilherme Mesquita and Silva, Fernanda Viana Moreira and De Carvalho Pereira, Glauco and Tegally, Houriiyah and Almeida, Júlia Deffune Profeta Cidin and Moreno, Keldenn Melo Farias and Vasconcelos, Klaucia Rodrigues and Santos, Leandro Cavalcante and Silva, Lívia Cristina Machado and Frutuoso, Livia C V and Lamounier, Ludmila Oliveira and Costa, Mariana Araújo and De Oliveira, Marília Santini and Dos Anjos, Marlei Pickler Dediasi and Ciccozzi, Massimo and Lima, Maurício Teixeira and Pereira, Maira Alves and Rocha, Marília Lima Cruz and De Souza Da Silva, Paulo Eduardo and Rabinowitz, Peter M and De Almeida, Priscila Souza and Lessells, Richard and Gazzinelli, Ricardo T and Da Cunha, Rivaldo Venâncio and Gonçalves, Sabrina and Dos Santos, Sara Cândida Ferreira and De Alcântara Belettini, Senele Ana and Pedroso, Silvia Helena Sousa Pietra and Araújo, Sofia Isabel Rótulo and Da Silva, Stephanni Figueiredo and Croda, Julio and Maciel, Ethel and Van Voorhis, Wes and Martin, Darren P and Holmes, Edward C and De Oliveira, Tulio and Lourenço, José and Alcantara, Luiz Carlos Junior and Giovanetti, Marta},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {taaf018},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Oropouche virus (OROV), first detected in Trinidad and Tobago in 1955, was historically confined to the Brazilian Amazon Basin. However, since late 2022, an increasing number of OROV cases have been reported across various regions of Brazil as well as in urban centers in Bolivia, Ecuador, Guyana, Colombia, Cuba, Panama, and Peru. In collaboration with Central Public Health Laboratories across Brazil, we integrated epidemiological metadata with genomic analyses from recent cases, generating 133 whole-genome sequences covering the virus’s three genomic segments (L, M, and S). These include the first genomes from regions outside the Amazon and from the first recorded fatal cases. Phylogenetic analyses show that the 2024 OROV genomes form a monophyletic group with sequences from the Amazon Basin sampled since 2022, revealing a rapid north-to-south viral movement into historically non-endemic areas. We identified 21 reassortment events, though it remains unclear whether these genomic changes have facilitated viral adaptation to local ecological conditions or contributed to phenotypic traits of public health significance. Our findings demonstrate how OROV has evolved through reassortment and spread rapidly across multiple states in Brazil, leading to the largest outbreak ever recorded outside the Amazon and the first confirmed fatalities. Additionally, by analysing travel-related cases, we provide the first insights into the international spread of OROV beyond Brazil, further highlighting the role of human mobility in its dissemination. The virus’s recent rapid geographic expansion and the emergence of severe cases emphasize the urgent need for enhanced surveillance across the Americas. In the absence of significant human population changes over the past two years, factors such as viral adaptation, deforestation, and climate shifts—either individually or in combination—may have facilitated the spread of OROV beyond the Amazon Basin through both local and travel-associated transmission.\n

\n\n\n

\n \n\n \n \n \n \n \n \n TB elimination in Southern Africa: overview and critical reflection.\n \n \n \n \n\n\n \n Boffa, J.; Vambe, D.; Khosa, C.; José, B.; Ndjeka, N.; Nkomo, T.; Kay, A.; Mandalakas, A.; Mvusi, L.; Omar, S.; Thi, S.; Velen, K.; Charalambous, S.; and Rangaka, M.\n\n\n \n\n\n\n IJTLD Open, 2(7): 381–387. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"TB$ Paper\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{boffa_tb_2025,\n\ttitle = {{TB} elimination in {Southern} {Africa}: overview and critical reflection},\n\tvolume = {2},\n\tissn = {3005-7590},\n\tshorttitle = {{TB} elimination in {Southern} {Africa}},\n\turl = {https://journals.theunion.org/lookup/doi/10.5588/ijtldopen.25.0050},\n\tdoi = {10.5588/ijtldopen.25.0050},\n\tabstract = {SUMMARY \n            Despite significant progress, TB remains a major public health challenge in Southern Africa. We highlight the key initiatives in Eswatini, Mozambique and South Africa, which have implemented various interventions, including systematic TB screening, TB preventive treatment, targeted next-generation sequencing, targeted universal testing, and shorter drug-resistant and paediatric TB regimens. We also identify the key challenges, such as inconsistent drug access, increasing drug resistance and limited healthcare capacity, which continue to affect progress. Health systems must also balance TB care with broader healthcare priorities, and the integration of TB care into existing services requires further investment in outreach, treatment support and training. Identifying and treating missing people with TB, diagnosing TB in children, and improving treatment adherence remain critical areas requiring enhanced support and resources. While new diagnostic tools and treatments offer promise, their high costs and labour demands present barriers to routine implementation. Successful TB elimination will depend on simple, low-cost prevention, testing and treatment options, tailored to each country’s specific needs. All of which will require sustained political commitment, innovation and strategic investments in health system strengthening and community-based care.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-28},\n\tjournal = {IJTLD Open},\n\tauthor = {Boffa, J. and Vambe, D. and Khosa, C. and José, B. and Ndjeka, N. and Nkomo, T. and Kay, A.W. and Mandalakas, A.M. and Mvusi, L. and Omar, S.V. and Thi, S. and Velen, K. and Charalambous, S. and Rangaka, M.X.},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {381--387},\n}\n\n\n\n

\n

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

\n \n\n \n \n \n \n \n \n Nasopharyngeal carriage of Staphylococcus aureus in a rural population, Sierra Leone.\n \n \n \n \n\n\n \n Kleine, L. M.; Kanu, E. M.; Grebe, T.; Sesay, D. M.; Loismann, H.; Sesay, M.; Theiler, T.; Rudolf, V.; Mellmann, A.; Kalkman, L. C.; Grobusch, M. P.; and Schaumburg, F.\n\n\n \n\n\n\n International Journal of Medical Microbiology, 318: 151643. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Nasopharyngeal$ Paper\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{kleine_nasopharyngeal_2025,\n\ttitle = {Nasopharyngeal carriage of {Staphylococcus} aureus in a rural population, {Sierra} {Leone}},\n\tvolume = {318},\n\tissn = {14384221},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S143842212400047X},\n\tdoi = {10.1016/j.ijmm.2024.151643},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {International Journal of Medical Microbiology},\n\tauthor = {Kleine, Lisa Maria and Kanu, Emmanuel Marx and Grebe, Tobias and Sesay, Desmond Mohamed and Loismann, Henning and Sesay, Maxwell and Theiler, Tom and Rudolf, Viktoria and Mellmann, Alexander and Kalkman, Laura C. and Grobusch, Martin P. and Schaumburg, Frieder},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {151643},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n TBtypeR: Sensitive detection and sublineage classification of Mycobacterium tuberculosis complex mixed-strain infections.\n \n \n \n \n\n\n \n Munro, J. E.; Coussens, A. K.; and Bahlo, M.\n\n\n \n\n\n\n Communications Biology, 8(1): 260. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"TBtypeR:$ Paper\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{munro_tbtyper_2025,\n\ttitle = {{TBtypeR}: {Sensitive} detection and sublineage classification of {Mycobacterium} tuberculosis complex mixed-strain infections},\n\tvolume = {8},\n\tissn = {2399-3642},\n\tshorttitle = {{TBtypeR}},\n\turl = {https://www.nature.com/articles/s42003-025-07705-9},\n\tdoi = {10.1038/s42003-025-07705-9},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Communications Biology},\n\tauthor = {Munro, Jacob E. and Coussens, Anna K. and Bahlo, Melanie},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {260},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Antimalarial Drug Repurposing of Epirubicin and Pelitinib in Combination with Artemether and Lumefantrine.\n \n \n \n \n\n\n \n Ochora, D. O.; Mogire, R. M.; Murithi, B. M.; Abdi, F.; Ondari, E. N.; Masai, R. J.; Mwakio, E.; Cheruyiot, A.; Yenesew, A.; and Akala, H. M.\n\n\n \n\n\n\n Pharmaceuticals, 18(7): 956. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Antimalarial$ Paper\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{ochora_antimalarial_2025,\n\ttitle = {Antimalarial {Drug} {Repurposing} of {Epirubicin} and {Pelitinib} in {Combination} with {Artemether} and {Lumefantrine}},\n\tvolume = {18},\n\tissn = {1424-8247},\n\turl = {https://www.mdpi.com/1424-8247/18/7/956},\n\tdoi = {10.3390/ph18070956},\n\tabstract = {Background: Drug therapy remains the principal management strategy for malaria but is increasingly challenged by the emergence of drug-resistant malaria parasites. The need for new antimalarial drugs is urgent, yet drug discovery and development are hindered by high costs, long durations, and safety concerns that prevent approval. The current study aimed to determine antiplasmodial activities of approved drugs in combination with artemether (ART) and lumefantrine (LU). Methods: Using the SYBR Green I assay test, this study investigated the efficacy of epirubicin (EPI) and pelitinib (PEL) combined with ART and LU at fixed drug–drug ratios (4:1, 3:1, 1:1, 1:2, 1:3 and 1:4) and volume/volume. These combinations, as well as single drug treatments, were tested against cultured strains of Plasmodium falciparum (W2, DD2, D6, 3D7 and F32-ART) and fresh and cultured clinical isolates. The fifty percent inhibition concentration (IC50) and a mean sum of fifty percent fractional inhibition concentration (FIC50) were determined. Results: Synergism was observed when EPI was combined with both ART and LU across all fixed ratios with a mean of mean FIC50 values of {\\textless}0.6. The combination of LU and EPI against the 3D7 strain demonstrated the highest efficacy with a synergism FIC50 value of 0.18. Most combinations of PEL with ART and LU showed antagonism (FIC50 {\\textgreater} 1) when tested against strains of P. falciparum and clinical isolates. Conclusions: This study underscores the utility of alternative drug discovery and development strategies to bypass cost, time, and safety barriers, thereby enriching the antimalarial drug pipeline and accelerating the transition from lab to market.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-28},\n\tjournal = {Pharmaceuticals},\n\tauthor = {Ochora, Douglas O. and Mogire, Reagan M. and Murithi, Bernard M. and Abdi, Farid and Ondari, Erick N. and Masai, Rael J. and Mwakio, Edwin and Cheruyiot, Agnes and Yenesew, Abiy and Akala, Hoseah M.},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {956},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n SNAP‐Tag–Based Recombinant Photoimmunotherapeutic Agents for the Selective Detection and Killing of Light‐Accessible Melanotransferrin‐Expressing Melanoma and Triple‐Negative Breast Cancer.\n \n \n \n \n\n\n \n Magagoum, S. H.; Biteghe, F. A. N.; Siwe, G. T.; Lang, D.; Lekena, N.; and Barth, S.\n\n\n \n\n\n\n Cancer Medicine, 14(9): e70912. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"SNAP‐Tag–Based$ 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

\n

@article{magagoum_snaptagbased_2025,\n\ttitle = {{SNAP}‐{Tag}–{Based} {Recombinant} {Photoimmunotherapeutic} {Agents} for the {Selective} {Detection} and {Killing} of {Light}‐{Accessible} {Melanotransferrin}‐{Expressing} {Melanoma} and {Triple}‐{Negative} {Breast} {Cancer}},\n\tvolume = {14},\n\tissn = {2045-7634, 2045-7634},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/cam4.70912},\n\tdoi = {10.1002/cam4.70912},\n\tabstract = {ABSTRACT \n             \n              Background \n              Melanoma and triple negative breast cancer (TNBC) represent the most aggressive skin and breast cancer subtypes and are associated with poor diagnostic and limited therapeutic options leading to poor prognosis. Melanotransferrin/p97 (MTf), initially identified as a tumor‐associated antigen (TAA) in melanoma, is overexpressed in various solid tumors, including TNBC. Beyond its high differential expression and dreadful tumorigenic impact, MTf is also associated with chemoresistance development, and its inhibition significantly hampers tumor progression, making MTf a promising target for effective targeted therapies. Near‐infrared photoimmunotherapy (NIR‐PIT) is an approach that combines the precision of antibodies directed against specific TAA with the phototoxic effects of a light‐sensitive photosensitizer (IR700), activated by near‐infrared (NIR) light irradiation. This study aimed to generate a novel photoimmunoconjugate to specifically destroy MTf‐positive melanoma and TNBC cells in vitro following NIR light irradiation. \n             \n             \n              Methods \n              A single‐chain variable fragment (scFv) assembled from anti‐MTf antibody L49 was recombinantly fused with the SNAP‐tag protein (L49(scFv)‐SNAP), capable of irreversible and autocatalytic conjugation to any O(6)‐benzylguanine (BG) substrate in a 1:1 stoichiometry. Purified full‐length SNAP‐tag–based fusion protein (L49(scFv)‐SNAP‐tag) was either conjugated to a BG‐modified fluorescent imaging agent (Alexa 488) to specifically assess its selective binding to MTf‐expressing cell lines via confocal imaging and flow cytometry or to a BG‐modified light‐sensitive photosensitizer (IR700) to evaluate its phototoxic properties using an XTT cell viability assay. \n             \n             \n              Results \n               \n                The selective binding and internalization of L49(scFv)‐SNAP‐Alexa 488 towards MTf‐positive melanoma and TNBC cell lines were successfully demonstrated with MTF expression percentages ranging from 52.8 to 83.1. Once confirmed, dose‐dependent phototoxicity of L49(scFv)‐SNAP‐IR700 was achieved on illuminated MTf‐positive cell lines showing IC \n                50 \n                values in the nanomolar range (2.20–5.24 nM). \n               \n             \n             \n              Conclusion \n              This study highlights the therapeutic potential of MTf as a promising target for the diagnosis as well as selective and efficient elimination of NIR‐light‐accessible melanoma and TNBC by NIR‐PIT.},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-28},\n\tjournal = {Cancer Medicine},\n\tauthor = {Magagoum, Suzanne Hippolite and Biteghe, Fleury Augustin Nsole and Siwe, Gael Tchokomeni and Lang, Dirk and Lekena, Nkhasi and Barth, Stefan},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {e70912},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Background Melanoma and triple negative breast cancer (TNBC) represent the most aggressive skin and breast cancer subtypes and are associated with poor diagnostic and limited therapeutic options leading to poor prognosis. Melanotransferrin/p97 (MTf), initially identified as a tumor‐associated antigen (TAA) in melanoma, is overexpressed in various solid tumors, including TNBC. Beyond its high differential expression and dreadful tumorigenic impact, MTf is also associated with chemoresistance development, and its inhibition significantly hampers tumor progression, making MTf a promising target for effective targeted therapies. Near‐infrared photoimmunotherapy (NIR‐PIT) is an approach that combines the precision of antibodies directed against specific TAA with the phototoxic effects of a light‐sensitive photosensitizer (IR700), activated by near‐infrared (NIR) light irradiation. This study aimed to generate a novel photoimmunoconjugate to specifically destroy MTf‐positive melanoma and TNBC cells in vitro following NIR light irradiation. Methods A single‐chain variable fragment (scFv) assembled from anti‐MTf antibody L49 was recombinantly fused with the SNAP‐tag protein (L49(scFv)‐SNAP), capable of irreversible and autocatalytic conjugation to any O(6)‐benzylguanine (BG) substrate in a 1:1 stoichiometry. Purified full‐length SNAP‐tag–based fusion protein (L49(scFv)‐SNAP‐tag) was either conjugated to a BG‐modified fluorescent imaging agent (Alexa 488) to specifically assess its selective binding to MTf‐expressing cell lines via confocal imaging and flow cytometry or to a BG‐modified light‐sensitive photosensitizer (IR700) to evaluate its phototoxic properties using an XTT cell viability assay. Results The selective binding and internalization of L49(scFv)‐SNAP‐Alexa 488 towards MTf‐positive melanoma and TNBC cell lines were successfully demonstrated with MTF expression percentages ranging from 52.8 to 83.1. Once confirmed, dose‐dependent phototoxicity of L49(scFv)‐SNAP‐IR700 was achieved on illuminated MTf‐positive cell lines showing IC 50 values in the nanomolar range (2.20–5.24 nM). Conclusion This study highlights the therapeutic potential of MTf as a promising target for the diagnosis as well as selective and efficient elimination of NIR‐light‐accessible melanoma and TNBC by NIR‐PIT.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Somatic whole exome sequencing of colorectal carcinoma in young patients from sub‐Saharan Africa reveals novel insights.\n \n \n \n \n\n\n \n Aldera, A. P.; Owusu, D.; Biral, L.; Pillay, K.; Boutall, A.; Dave, S.; and Ramesar, R.\n\n\n \n\n\n\n The Journal of Pathology: Clinical Research, 11(5): e70048. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Somatic$ Paper\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{aldera_somatic_2025,\n\ttitle = {Somatic whole exome sequencing of colorectal carcinoma in young patients from sub‐{Saharan} {Africa} reveals novel insights},\n\tvolume = {11},\n\tissn = {2056-4538, 2056-4538},\n\turl = {https://pathsocjournals.onlinelibrary.wiley.com/doi/10.1002/2056-4538.70048},\n\tdoi = {10.1002/2056-4538.70048},\n\tabstract = {Abstract \n             \n              Colorectal carcinoma (CRC) is a frequent cause of morbidity and mortality in sub‐Saharan Africa. The incidence of early‐onset, microsatellite stable (MSS) CRC is on the rise, and the tumour biology of these lesions is poorly categorised. Preliminary data from one centre in Nigeria found differences in the frequencies of mutations in driver genes and altered signalling pathways. We sought to investigate potential alternative driver genes and signalling pathways by whole exome sequencing. Eighty‐three cases passed quality control filters and were included in the analysis (77 MSS, 4 microsatellite instability‐high, and 2 \n              POLE \n              mutant). \n              APC \n              , \n              TP53 \n              , and \n              KRAS \n              were among the most frequently mutated driver genes, although at a lower frequency than expected. \n              BRAF \n              V600E mutations were absent in our cohort. Although there were differences in the frequencies of mutations in the major driver genes, the frequencies of oncogenic pathway alterations were found to be similar. \n              FAT4 \n              (26\\%) and \n              TET2 \n              (15\\%) emerged as important mutated driver genes and potential therapeutic targets for further investigation. We have highlighted distinct differences in driver gene mutations in our cohort of young CRC from sub‐Saharan Africa and have identified \n              FAT4 \n              and \n              TET2 \n              as potential drivers that are more common and are potential therapeutic targets.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {The Journal of Pathology: Clinical Research},\n\tauthor = {Aldera, Alessandro Pietro and Owusu, Dennis and Biral, Leonardo and Pillay, Komala and Boutall, Adam and Dave, Sandeep and Ramesar, Raj},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {e70048},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A cluster of Burkholderia contaminans bloodstream infections in a rural hospital in Sierra Leone.\n \n \n \n \n\n\n \n Olaru, I. D.; Kalkman, L. C.; Kanu, E. M.; Kargbo, I. M.; Böing, C.; Bletz, S.; Grobusch, M. P.; and Schaumburg, F.\n\n\n \n\n\n\n Infection Control & Hospital Epidemiology, 46(6): 656–657. June 2025.\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{olaru_cluster_2025,\n\ttitle = {A cluster of {Burkholderia} contaminans bloodstream infections in a rural hospital in {Sierra} {Leone}},\n\tvolume = {46},\n\tissn = {0899-823X, 1559-6834},\n\turl = {https://www.cambridge.org/core/product/identifier/S0899823X25000637/type/journal_article},\n\tdoi = {10.1017/ice.2025.63},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-28},\n\tjournal = {Infection Control \\& Hospital Epidemiology},\n\tauthor = {Olaru, Ioana Diana and Kalkman, Laura C. and Kanu, Emmanuel Marx and Kargbo, Islam Mohamed and Böing, Christian and Bletz, Stefan and Grobusch, Martin P. and Schaumburg, Frieder},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {656--657},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Short-Term CD4+ Cell Count Declines During Antiretroviral Therapy Interruptions: A Focused Review.\n \n \n \n \n\n\n \n Moolla, H.; Meintjes, G.; Davies, M.; Kassanjee, R.; De Waal, R.; and Johnson, L. F.\n\n\n \n\n\n\n JAIDS Journal of Acquired Immune Deficiency Syndromes, 100(3): e11–e13. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Short-Term$ Paper\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{moolla_short-term_2025,\n\ttitle = {Short-{Term} {CD4}+ {Cell} {Count} {Declines} {During} {Antiretroviral} {Therapy} {Interruptions}: {A} {Focused} {Review}},\n\tvolume = {100},\n\tissn = {1525-4135, 1944-7884},\n\tshorttitle = {Short-{Term} {CD4}+ {Cell} {Count} {Declines} {During} {Antiretroviral} {Therapy} {Interruptions}},\n\turl = {https://journals.lww.com/10.1097/QAI.0000000000003748},\n\tdoi = {10.1097/QAI.0000000000003748},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},\n\tauthor = {Moolla, Haroon and Meintjes, Graeme and Davies, Mary-Ann and Kassanjee, Reshma and De Waal, Renee and Johnson, Leigh F.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {e11--e13},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Phage Therapy for Mycobacteria: Overcoming Challenges, Unleashing Potential.\n \n \n \n \n\n\n \n Opperman, C. J.; and Brink, A. J.\n\n\n \n\n\n\n Infectious Disease Reports, 17(2): 24. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Phage$ Paper\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{opperman_phage_2025,\n\ttitle = {Phage {Therapy} for {Mycobacteria}: {Overcoming} {Challenges}, {Unleashing} {Potential}},\n\tvolume = {17},\n\tissn = {2036-7449},\n\tshorttitle = {Phage {Therapy} for {Mycobacteria}},\n\turl = {https://www.mdpi.com/2036-7449/17/2/24},\n\tdoi = {10.3390/idr17020024},\n\tabstract = {Bacteriophage (phage) therapy is emerging as a promising alternative to traditional antibiotics for treating drug-resistant mycobacterial infections, including Mycobacterium tuberculosis complex (MTBC) and non-tuberculous mycobacteria (NTM) [...]},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {Infectious Disease Reports},\n\tauthor = {Opperman, Christoffel Johannes and Brink, Adrian J.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {24},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Randomized trial of multi-strain Lactobacillus crispatus vaginal live biotherapeutic products after antibiotic therapy for bacterial vaginosis: study protocol for VIBRANT (vaginal lIve biotherapeutic RANdomized trial).\n \n \n \n \n\n\n \n Chetty, C.; Mafunda, N.; Happel, A.; Khan, A.; Cooley Demidkina, B.; Yende-Zuma, N.; Saidi, Y.; Mahabeer Polliah, A.; Lewis, L.; Osman, F.; Radebe, P.; Passmore, J. S.; Kwon, D.; Ravel, J.; Ngcapu, S.; Liebenberg, L.; Symul, L.; Holmes, S.; Mitchell, C. M.; and Potloane, D.\n\n\n \n\n\n\n Contemporary Clinical Trials Communications, 48: 101554. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Randomized$ Paper\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{chetty_randomized_2025,\n\ttitle = {Randomized trial of multi-strain {Lactobacillus} crispatus vaginal live biotherapeutic products after antibiotic therapy for bacterial vaginosis: study protocol for {VIBRANT} (vaginal {lIve} biotherapeutic {RANdomized} trial)},\n\tvolume = {48},\n\tissn = {24518654},\n\tshorttitle = {Randomized trial of multi-strain {Lactobacillus} crispatus vaginal live biotherapeutic products after antibiotic therapy for bacterial vaginosis},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2451865425001280},\n\tdoi = {10.1016/j.conctc.2025.101554},\n\tlanguage = {en},\n\turldate = {2026-05-28},\n\tjournal = {Contemporary Clinical Trials Communications},\n\tauthor = {Chetty, Callin and Mafunda, Nomfuneko and Happel, Anna-Ursula and Khan, Anam and Cooley Demidkina, Briah and Yende-Zuma, Nonhlanhla and Saidi, Yusra and Mahabeer Polliah, Asthu and Lewis, Lara and Osman, Farzana and Radebe, Precious and Passmore, Jo-Ann S. and Kwon, Doug and Ravel, Jacques and Ngcapu, Sinaye and Liebenberg, Lenine and Symul, Laura and Holmes, Susan and Mitchell, Caroline M. and Potloane, Disebo},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {101554},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Ciprofloxacin Inhibits Angiotensin I-Converting Enzyme (ACE) Activity by Binding at the Exosite, Distal to the Catalytic Pocket.\n \n \n \n \n\n\n \n Gregory, K. S.; Ramasamy, V.; Sturrock, E. D.; and Acharya, K. R.\n\n\n \n\n\n\n ACS Bio & Med Chem Au, 5(5): 852–859. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Ciprofloxacin$ Paper\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{gregory_ciprofloxacin_2025,\n\ttitle = {Ciprofloxacin {Inhibits} {Angiotensin} {I}-{Converting} {Enzyme} ({ACE}) {Activity} by {Binding} at the {Exosite}, {Distal} to the {Catalytic} {Pocket}},\n\tvolume = {5},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2694-2437, 2694-2437},\n\turl = {https://pubs.acs.org/doi/10.1021/acsbiomedchemau.5c00089},\n\tdoi = {10.1021/acsbiomedchemau.5c00089},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {ACS Bio \\& Med Chem Au},\n\tauthor = {Gregory, Kyle S. and Ramasamy, Vinasha and Sturrock, Edward D. and Acharya, K. Ravi},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {852--859},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Whole Exome Sequencing Helps Diagnose Familial Anophthalmia in Zimbabwe: A Call from the Field to Fund Clinical Genomics for Planetary Health.\n \n \n \n \n\n\n \n Mabizela, N.; Soko, N. D.; Mudawarima, L. R.; Shamu, S.; and Dandara, C.\n\n\n \n\n\n\n OMICS: A Journal of Integrative Biology, 29(5): 183–190. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Whole$ Paper\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{mabizela_whole_2025,\n\ttitle = {Whole {Exome} {Sequencing} {Helps} {Diagnose} {Familial} {Anophthalmia} in {Zimbabwe}: {A} {Call} from the {Field} to {Fund} {Clinical} {Genomics} for {Planetary} {Health}},\n\tvolume = {29},\n\tissn = {1536-2310, 1557-8100},\n\tshorttitle = {Whole {Exome} {Sequencing} {Helps} {Diagnose} {Familial} {Anophthalmia} in {Zimbabwe}},\n\turl = {https://journals.sagepub.com/doi/full/10.1089/omi.2024.0199},\n\tdoi = {10.1089/omi.2024.0199},\n\tabstract = {Anophthalmia is the most severe ocular malformation inherited in an autosomal, X-linked, recessive, or dominant form. We report here the use of whole exome sequencing (WES) to help the clinical diagnosis of familial anophthalmia in Harare, Zimbabwe. A mother presented her two sons, who are half-brothers, at the Eye, Ear, Nose, and Throat Institute, Ophthalmology Unit in Harare, Zimbabwe. Upon clinical examination, half-brothers were diagnosed with clinical bilateral anophthalmia. The mother requested a genetic diagnosis for her two sons. To segregate the phenotype with genotype, whole blood was collected from two half-brothers, their mother, maternal aunt, and maternal uncle to the half-brothers, and an unrelated healthy control. Genetic characterization was done, first, through a candidate gene approach screening of putative genes \n              SOX2 \n              , \n              OTX2 \n              , \n              VSX2 \n              , \n              PAX6, \n              and \n              RAX. \n              When no causative variants were identified, the next step employed WES. Variants in 80 genes associated with anophthalmia were prioritized and subjected to pathogenicity testing. One pathogenic variant, \n              BCOR \n              c.254C{\\textgreater}T (rs121434618, p. Pro85Leu), segregated with the mother and her two sons. The present clinical genomics study of a family and a healthy control sample underscores WES as a valuable tool that can help clinical diagnosis of anophthalmia in the Zimbabwean clinical setting. In this article, we also offer a reasoned discussion and call from the field, to fund clinical genomics and omics research and development in planetary health, especially in the current era of uncertainties in international aid and funding of innovative technologies. The findings reported herein encourage further research on the clinical utility of WES as a diagnostic tool in Africa and around the world as well, given that the candidate gene approach might miss the important genes or variants of relevance to disease pathophysiology.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {OMICS: A Journal of Integrative Biology},\n\tauthor = {Mabizela, Nosipho and Soko, Nyarai D. and Mudawarima, Louisa R.C. and Shamu, Sharai and Dandara, Collet},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {183--190},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n One RNA-binding protein, many decisions: integrating the transcript life cycle into neuronal regulation.\n \n \n \n \n\n\n \n Doxakis, E.; Xue, Y. C.; and Savulescu, A. F.\n\n\n \n\n\n\n Frontiers in Molecular Neuroscience, 18: 1716825. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"One$ Paper\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{doxakis_one_2025,\n\ttitle = {One {RNA}-binding protein, many decisions: integrating the transcript life cycle into neuronal regulation},\n\tvolume = {18},\n\tissn = {1662-5099},\n\tshorttitle = {One {RNA}-binding protein, many decisions},\n\turl = {https://www.frontiersin.org/articles/10.3389/fnmol.2025.1716825/full},\n\tdoi = {10.3389/fnmol.2025.1716825},\n\turldate = {2026-05-28},\n\tjournal = {Frontiers in Molecular Neuroscience},\n\tauthor = {Doxakis, Epaminondas and Xue, Yuan Chao and Savulescu, Anca F.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {1716825},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Responsible governance of genomics data and biospecimens in the context of broad consent: experiences of a pioneering access committee in Africa.\n \n \n \n \n\n\n \n Rebai, A.; Abayomi, A.; Andanda, P; Kerr, R; Herbst, K.; Mabuka, J; Wamuyu, R; Bukini, D.; and Dandara, C\n\n\n \n\n\n\n BMJ Global Health, 10(2): e016026. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Responsible$ Paper\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{rebai_responsible_2025,\n\ttitle = {Responsible governance of genomics data and biospecimens in the context of broad consent: experiences of a pioneering access committee in {Africa}},\n\tvolume = {10},\n\tissn = {2059-7908},\n\tshorttitle = {Responsible governance of genomics data and biospecimens in the context of broad consent},\n\turl = {https://gh.bmj.com/lookup/doi/10.1136/bmjgh-2024-016026},\n\tdoi = {10.1136/bmjgh-2024-016026},\n\tabstract = {International collaboration in genomic research is gaining momentum in African countries and is often supported by external funding. Over the last decade, there has been an increased interest in African genomic data. The contribution of this rich data resource in understanding diseases predominant in both African and global populations has been limited to date. There has been some non-governmental funding dedicated to the advancement of genomic research and innovation by African-based and African-led research groups, but the impact of these initiatives is hard to quantify. However, there is now an opportunity for the global research community to leverage decades of genomic data and biospecimens originating from African populations. The experience we describe in this paper is of an access governance framework established under the Human, Heredity, and Health in Africa (H3A) consortium, given the task of managing wider access to the data and biospecimen resources collected via its various projects. The function of the Data and Biospecimen Access Committee (DBAC) is to facilitate the advancement of medicine and health while fostering the development of bioinformatics capabilities at Africa-based institutions or regional hubs. Our collective experiences and lessons learnt as a committee provide examples of nuanced considerations when evaluating access to African data. The committee was semi-autonomous in its establishment and had independence in decision-making. The DBAC continually advocates for the responsible use of genomic data and biospecimens that were obtained from African research participants, under broad consent, by primary researchers who no longer have oversight over the future use of these resources.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {BMJ Global Health},\n\tauthor = {Rebai, Ahmed and Abayomi, Akin and Andanda, P and Kerr, R and Herbst, Kobus and Mabuka, J and Wamuyu, R and Bukini, Daima and Dandara, C},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {e016026},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Intra-host SARS-CoV-2 diversity in immunocompromised people living with HIV provides insight into the evolutionary trajectory of SARS-CoV-2.\n \n \n \n \n\n\n \n Joseph, R.; Marais, G.; Iranzadeh, I.; Alisoltani, A.; Hardie, D.; Davies, M.; Heekes, A.; Chetty, N.; Timmerman, V.; Hsiao, N.; and Williamson, C.\n\n\n \n\n\n\n Journal of Virology, 99(10): e00780–25. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Intra-host$ Paper\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_intra-host_2025,\n\ttitle = {Intra-host {SARS}-{CoV}-2 diversity in immunocompromised people living with {HIV} provides insight into the evolutionary trajectory of {SARS}-{CoV}-2},\n\tvolume = {99},\n\tissn = {0022-538X, 1098-5514},\n\turl = {https://journals.asm.org/doi/10.1128/jvi.00780-25},\n\tdoi = {10.1128/jvi.00780-25},\n\tabstract = {ABSTRACT \n             \n               \n              Ongoing viral evolution in immunocompromised individuals with persistent infection may facilitate the evolution of SARS-CoV-2 and emergence of variants of concern (VOC). This study was conducted in the Western Cape Province of South Africa where the HIV prevalence is around 8\\%, with limited information on the frequency of persistent SARS-CoV-2 infection, the pattern of evolution in these individuals, and if these variants contribute to the diversity of circulating viruses. This study investigated 75 individuals with two or more SARS-CoV-2 diagnoses at least one month apart. Of the 75, 13 were people living with Human Immunodeficiency Virus (PLWH) of which three were immunocompromised, 23 were HIV-negative, and the status of the remaining 39 was unknown. SARS-CoV-2 full-length genome sequence analysis identified 72 as reinfections with a distinct variant and 3 as persistent infections with B.1.1 (20B), B.1.1.459 (20B), and B.1.351 (20H) for 7, 4, and 3 months, respectively. All persistent infections were in severely immunocompromised PLWH with CD4+ T cell count below 30 cells/µL. We identified the emergence of uncommon mutations (global prevalence {\\textless}0.01\\%) in SARS-CoV-2, together with permanent and/or transient non-lineage defining mutations with immune escape potential particularly in Spike (141-144del; 241-244del; D215G; E484K; Q498R; P681R; A701V). Some of these mutations were found in later VOCs including Omicron lineages (L18F; 141-144del; D215G; E484K; Q498R; P681R; A701V). Longitudinal viral sequences from these persistent infections provided insights into the evolutionary trajectory of SARS-CoV-2 and are suggestive of convergent evolution and host adaptation. \n             \n             \n              IMPORTANCE \n              Unlike other respiratory viruses, SARS-CoV-2 has not yet established a seasonal pattern. Thus, resurgence and the emergence of novel variants including VOCs remain a concern. Ongoing SARS-CoV-2 replication in immunocompromised individuals may serve as reservoirs that could facilitate the emergence of mutations conferring transient and/or long-lasting immune escape potential and seed future outbreaks. Two of the five variants, Beta variant and Omicron variant, were first described in Southern Africa—a region with one of the highest rates of HIV infection globally. Targeted genomic surveillance in immunocompromised individuals including PLWH will provide insight into the evolutionary trajectory of SARS-CoV-2 and inform vaccine design that may help to circumvent resurgence. \n             \n          ,  \n            Unlike other respiratory viruses, SARS-CoV-2 has not yet established a seasonal pattern. Thus, resurgence and the emergence of novel variants including VOCs remain a concern. Ongoing SARS-CoV-2 replication in immunocompromised individuals may serve as reservoirs that could facilitate the emergence of mutations conferring transient and/or long-lasting immune escape potential and seed future outbreaks. Two of the five variants, Beta variant and Omicron variant, were first described in Southern Africa—a region with one of the highest rates of HIV infection globally. Targeted genomic surveillance in immunocompromised individuals including PLWH will provide insight into the evolutionary trajectory of SARS-CoV-2 and inform vaccine design that may help to circumvent resurgence.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Virology},\n\tauthor = {Joseph, R. and Marais, G. and Iranzadeh, I. and Alisoltani, A. and Hardie, D. and Davies, M.-A. and Heekes, A. and Chetty, N. and Timmerman, V. and Hsiao, N.-Y. and Williamson, C.},\n\teditor = {Liu, Shan-Lu},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {e00780--25},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Ongoing viral evolution in immunocompromised individuals with persistent infection may facilitate the evolution of SARS-CoV-2 and emergence of variants of concern (VOC). This study was conducted in the Western Cape Province of South Africa where the HIV prevalence is around 8%, with limited information on the frequency of persistent SARS-CoV-2 infection, the pattern of evolution in these individuals, and if these variants contribute to the diversity of circulating viruses. This study investigated 75 individuals with two or more SARS-CoV-2 diagnoses at least one month apart. Of the 75, 13 were people living with Human Immunodeficiency Virus (PLWH) of which three were immunocompromised, 23 were HIV-negative, and the status of the remaining 39 was unknown. SARS-CoV-2 full-length genome sequence analysis identified 72 as reinfections with a distinct variant and 3 as persistent infections with B.1.1 (20B), B.1.1.459 (20B), and B.1.351 (20H) for 7, 4, and 3 months, respectively. All persistent infections were in severely immunocompromised PLWH with CD4+ T cell count below 30 cells/µL. We identified the emergence of uncommon mutations (global prevalence \\textless0.01%) in SARS-CoV-2, together with permanent and/or transient non-lineage defining mutations with immune escape potential particularly in Spike (141-144del; 241-244del; D215G; E484K; Q498R; P681R; A701V). Some of these mutations were found in later VOCs including Omicron lineages (L18F; 141-144del; D215G; E484K; Q498R; P681R; A701V). Longitudinal viral sequences from these persistent infections provided insights into the evolutionary trajectory of SARS-CoV-2 and are suggestive of convergent evolution and host adaptation. IMPORTANCE Unlike other respiratory viruses, SARS-CoV-2 has not yet established a seasonal pattern. Thus, resurgence and the emergence of novel variants including VOCs remain a concern. Ongoing SARS-CoV-2 replication in immunocompromised individuals may serve as reservoirs that could facilitate the emergence of mutations conferring transient and/or long-lasting immune escape potential and seed future outbreaks. Two of the five variants, Beta variant and Omicron variant, were first described in Southern Africa—a region with one of the highest rates of HIV infection globally. Targeted genomic surveillance in immunocompromised individuals including PLWH will provide insight into the evolutionary trajectory of SARS-CoV-2 and inform vaccine design that may help to circumvent resurgence. , Unlike other respiratory viruses, SARS-CoV-2 has not yet established a seasonal pattern. Thus, resurgence and the emergence of novel variants including VOCs remain a concern. Ongoing SARS-CoV-2 replication in immunocompromised individuals may serve as reservoirs that could facilitate the emergence of mutations conferring transient and/or long-lasting immune escape potential and seed future outbreaks. Two of the five variants, Beta variant and Omicron variant, were first described in Southern Africa—a region with one of the highest rates of HIV infection globally. Targeted genomic surveillance in immunocompromised individuals including PLWH will provide insight into the evolutionary trajectory of SARS-CoV-2 and inform vaccine design that may help to circumvent resurgence.\n

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\n \n\n \n \n \n \n \n \n The RecA-NT homology motif in ImuB mediates the interaction with ImuA′, which is essential for DNA damage–induced mutagenesis.\n \n \n \n \n\n\n \n Santos, J. A.; Timinskas, K.; Ramudzuli, A. A.; Lamers, M. H.; Venclovas, Č.; Warner, D. F.; and Gessner, S. J.\n\n\n \n\n\n\n Journal of Biological Chemistry, 301(2): 108108. February 2025.\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{santos_reca-nt_2025,\n\ttitle = {The {RecA}-{NT} homology motif in {ImuB} mediates the interaction with {ImuA}′, which is essential for {DNA} damage–induced mutagenesis},\n\tvolume = {301},\n\tissn = {00219258},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0021925824026103},\n\tdoi = {10.1016/j.jbc.2024.108108},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Biological Chemistry},\n\tauthor = {Santos, Joana A. and Timinskas, Kęstutis and Ramudzuli, Atondaho A. and Lamers, Meindert H. and Venclovas, Česlovas and Warner, Digby F. and Gessner, Sophia J.},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {108108},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n endTB-Q results in the face of rising bedaquiline resistance.\n \n \n \n \n\n\n \n Heinrich, N.; Ndjeka, N.; Khosa, C.; Howell, P.; Kranzer, K.; Vambe, D.; Wasserman, S.; and Hoelscher, M.\n\n\n \n\n\n\n The Lancet Respiratory Medicine, 13(9): 773–775. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"endTB-Q$ Paper\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{heinrich_endtb-q_2025,\n\ttitle = {{endTB}-{Q} results in the face of rising bedaquiline resistance},\n\tvolume = {13},\n\tissn = {22132600},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2213260025002462},\n\tdoi = {10.1016/S2213-2600(25)00246-2},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-28},\n\tjournal = {The Lancet Respiratory Medicine},\n\tauthor = {Heinrich, Norbert and Ndjeka, Norbert and Khosa, Celso and Howell, Pauline and Kranzer, Katharina and Vambe, Debra and Wasserman, Sean and Hoelscher, Michael},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {773--775},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Design of Novel Mercapto-3-phenylpropanoyl Dipeptides as Dual Angiotensin-Converting Enzyme C–Domain-Selective/Neprilysin Inhibitors.\n \n \n \n \n\n\n \n Cozier, G. E.; Coulson, L. B.; Eyermann, C. J.; Basarab, G. S.; Schwager, S. L.; Chibale, K.; Sturrock, E. D.; and Acharya, K. R.\n\n\n \n\n\n\n Journal of Medicinal Chemistry, 68(7): 7720–7736. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Design$ Paper\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{cozier_design_2025,\n\ttitle = {Design of {Novel} {Mercapto}-3-phenylpropanoyl {Dipeptides} as {Dual} {Angiotensin}-{Converting} {Enzyme} {C}–{Domain}-{Selective}/{Neprilysin} {Inhibitors}},\n\tvolume = {68},\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.5c00329},\n\tdoi = {10.1021/acs.jmedchem.5c00329},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Medicinal Chemistry},\n\tauthor = {Cozier, Gyles E. and Coulson, Lauren B. and Eyermann, Charles J. and Basarab, Gregory S. and Schwager, Sylva L. and Chibale, Kelly and Sturrock, Edward D. and Acharya, K. Ravi},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {7720--7736},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The persistent pool of HIV-1-infected cells is formed episodically during untreated infection.\n \n \n \n \n\n\n \n Council, O. D.; Tyers, L.; Moeser, M.; Sondgeroth, A.; Spielvogel, E.; Richardson, B. D.; Doolabh, D.; Zhou, S.; Emery, A.; Archin, N. M.; Shook-Sa, B.; Margolis, D. M.; Abdool Karim, S. S.; Kosakovsky Pond, S.; Garrett, N.; Abrahams, M.; Joseph, S. B.; Williamson, C.; and Swanstrom, R.\n\n\n \n\n\n\n Journal of Virology, 99(2): e00979–24. February 2025.\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{council_persistent_2025,\n\ttitle = {The persistent pool of {HIV}-1-infected cells is formed episodically during untreated infection},\n\tvolume = {99},\n\tissn = {0022-538X, 1098-5514},\n\turl = {https://journals.asm.org/doi/10.1128/jvi.00979-24},\n\tdoi = {10.1128/jvi.00979-24},\n\tabstract = {ABSTRACT \n             \n               \n              Previous studies have shown that the majority of long-lived cells harboring persistent HIV-1 proviral genomes originates from viruses circulating in the year prior to antiretroviral therapy (ART) initiation, but a smaller proportion originates from viruses circulating much earlier in untreated infection. These observations suggest that discrete biological factors influence the entry and persistence of viruses into the persistent proviral pool, and there may be periods earlier in untreated infection with increased seeding. Therefore, we examined the timing of formation of the long-lived pool of infected cells that persists during ART in seven women (after a median of 5.1 years of suppressive ART) by comparing the phylogenetic distance between unique 3′ half genome on-ART proviral sequences and longitudinally sampled pre-ART viral RNA sequences, focusing on the period {\\textgreater}1 year prior to ART initiation (i.e., the “early” proviral pool). We constructed models of continuous entry into the persistent proviral pool prior to ART initiation and analyzed the fit of our experimentally derived data to these models. We found that the pattern of persistent proviral pool formation in five of seven participants is incongruent with a model of continuous entry, implying that persistent proviral pool formation can occur episodically during untreated infection. Notably, increased entry into the persistent proviral pool was not universally observed during acute infection, and the timing of enhanced early entry differed across the participants. \n               \n                IMPORTANCE \n                Cells harboring HIV-1 proviruses that persist on antiretroviral therapy (ART) constitute the main barrier to an HIV-1 cure. Recent work has elucidated that the majority of persisting proviruses harbor HIV-1 variants circulating near the time of ART initiation, whether the proviruses are intact or defective, though a portion forms earlier in untreated infection. We examined the formation of the “early-forming” persistent proviral pool and found that in 5/7 participants, persistent proviral pool formation was episodic, rather than continuous, suggesting that there are host/biological factors that periodically enhance the formation of the persistent proviral pool. Further characterization of these factors will aid in the development of methods to abrogate their effect, thereby reducing the size of the persistent proviral pool. \n               \n             \n          ,  \n            Cells harboring HIV-1 proviruses that persist on antiretroviral therapy (ART) constitute the main barrier to an HIV-1 cure. Recent work has elucidated that the majority of persisting proviruses harbor HIV-1 variants circulating near the time of ART initiation, whether the proviruses are intact or defective, though a portion forms earlier in untreated infection. We examined the formation of the “early-forming” persistent proviral pool and found that in 5/7 participants, persistent proviral pool formation was episodic, rather than continuous, suggesting that there are host/biological factors that periodically enhance the formation of the persistent proviral pool. Further characterization of these factors will aid in the development of methods to abrogate their effect, thereby reducing the size of the persistent proviral pool.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {Journal of Virology},\n\tauthor = {Council, Olivia D. and Tyers, Lynn and Moeser, Matthew and Sondgeroth, Amy and Spielvogel, Ean and Richardson, Brian D. and Doolabh, Deelan and Zhou, Shuntai and Emery, Ann and Archin, Nancie M. and Shook-Sa, Bonnie and Margolis, David M. and Abdool Karim, Salim S. and Kosakovsky Pond, Sergei and Garrett, Nigel and Abrahams, Melissa-Rose and Joseph, Sarah B. and Williamson, Carolyn and Swanstrom, Ronald},\n\teditor = {Liu, Shan-Lu},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {e00979--24},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Previous studies have shown that the majority of long-lived cells harboring persistent HIV-1 proviral genomes originates from viruses circulating in the year prior to antiretroviral therapy (ART) initiation, but a smaller proportion originates from viruses circulating much earlier in untreated infection. These observations suggest that discrete biological factors influence the entry and persistence of viruses into the persistent proviral pool, and there may be periods earlier in untreated infection with increased seeding. Therefore, we examined the timing of formation of the long-lived pool of infected cells that persists during ART in seven women (after a median of 5.1 years of suppressive ART) by comparing the phylogenetic distance between unique 3′ half genome on-ART proviral sequences and longitudinally sampled pre-ART viral RNA sequences, focusing on the period \\textgreater1 year prior to ART initiation (i.e., the “early” proviral pool). We constructed models of continuous entry into the persistent proviral pool prior to ART initiation and analyzed the fit of our experimentally derived data to these models. We found that the pattern of persistent proviral pool formation in five of seven participants is incongruent with a model of continuous entry, implying that persistent proviral pool formation can occur episodically during untreated infection. Notably, increased entry into the persistent proviral pool was not universally observed during acute infection, and the timing of enhanced early entry differed across the participants. IMPORTANCE Cells harboring HIV-1 proviruses that persist on antiretroviral therapy (ART) constitute the main barrier to an HIV-1 cure. Recent work has elucidated that the majority of persisting proviruses harbor HIV-1 variants circulating near the time of ART initiation, whether the proviruses are intact or defective, though a portion forms earlier in untreated infection. We examined the formation of the “early-forming” persistent proviral pool and found that in 5/7 participants, persistent proviral pool formation was episodic, rather than continuous, suggesting that there are host/biological factors that periodically enhance the formation of the persistent proviral pool. Further characterization of these factors will aid in the development of methods to abrogate their effect, thereby reducing the size of the persistent proviral pool. , Cells harboring HIV-1 proviruses that persist on antiretroviral therapy (ART) constitute the main barrier to an HIV-1 cure. Recent work has elucidated that the majority of persisting proviruses harbor HIV-1 variants circulating near the time of ART initiation, whether the proviruses are intact or defective, though a portion forms earlier in untreated infection. We examined the formation of the “early-forming” persistent proviral pool and found that in 5/7 participants, persistent proviral pool formation was episodic, rather than continuous, suggesting that there are host/biological factors that periodically enhance the formation of the persistent proviral pool. Further characterization of these factors will aid in the development of methods to abrogate their effect, thereby reducing the size of the persistent proviral pool.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Enamel proteins reveal biological sex and genetic variability in southern African Paranthropus.\n \n \n \n \n\n\n \n Madupe, P. P.; Koenig, C.; Patramanis, I.; Rüther, P. L.; Hlazo, N.; Mackie, M.; Tawane, M.; Krueger, J.; Taurozzi, A. J.; Troché, G.; Kibii, J.; Pickering, R.; Dickinson, M. R.; Sahle, Y.; Kgotleng, D.; Musiba, C.; Manthi, F.; Bell, L.; DuPlessis, M.; Gilbert, C.; Zipfel, B.; Kuderna, L. F. K.; Lizano, E.; Welker, F.; Kyriakidou, P.; Cox, J.; Mollereau, C.; Tokarski, C.; Blackburn, J.; Ramos-Madrigal, J.; Marques-Bonet, T.; Penkman, K.; Zanolli, C.; Schroeder, L.; Racimo, F.; Olsen, J. V.; Ackermann, R. R.; and Cappellini, E.\n\n\n \n\n\n\n Science, 388(6750): 969–973. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Enamel$ Paper\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{madupe_enamel_2025,\n\ttitle = {Enamel proteins reveal biological sex and genetic variability in southern {African} \\textit{{Paranthropus}}},\n\tvolume = {388},\n\tissn = {0036-8075, 1095-9203},\n\turl = {https://www.science.org/doi/10.1126/science.adt9539},\n\tdoi = {10.1126/science.adt9539},\n\tabstract = {Paranthropus robustus \n              is a morphologically well-documented Early Pleistocene hominin species from southern Africa with no genetic evidence reported so far. In this work, we describe the mass spectrometric sequencing of enamel peptides from four {\\textasciitilde}2 million–year-old dental specimens attributed morphologically to \n              P. robustus \n              from the site of Swartkrans in South Africa. The identification of AMELY-specific peptides enabled us to assign two specimens to male individuals, whereas semiquantitative mass spectrometric data analysis attributed the other two to females. A single amino acid polymorphism and the enamel-dentine junction shape variation indicated potential subgroups present within southern African \n              Paranthropus \n              . This study demonstrates how palaeoproteomics can help distinguish sexual dimorphism from other sources of variation in African Early Pleistocene hominins. \n             \n          ,  \n            Editor’s summary \n             \n              It is now well known that the early hominin fauna was species rich, with many overlapping lineages existing in the African Pleistocene. However, our knowledge of diversity within many of these lineages has been limited because current ancient DNA technologies have not been able to reveal genetic sequences older than around 0.2 million years. Madupe \n              et al \n              . examined protein sequences from approximately 2-million-year-old \n              Paranthropus robustus \n              teeth that were particularly well preserved. Using proteomics approaches, the authors were able to assign the individual teeth to sex and to identify patterns of diversity suggesting the existence of multiple populations. —Sacha Vignieri},\n\tlanguage = {en},\n\tnumber = {6750},\n\turldate = {2026-05-28},\n\tjournal = {Science},\n\tauthor = {Madupe, Palesa P. and Koenig, Claire and Patramanis, Ioannis and Rüther, Patrick L. and Hlazo, Nomawethu and Mackie, Meaghan and Tawane, Mirriam and Krueger, Johanna and Taurozzi, Alberto J. and Troché, Gaudry and Kibii, Job and Pickering, Robyn and Dickinson, Marc R. and Sahle, Yonatan and Kgotleng, Dipuo and Musiba, Charles and Manthi, Fredrick and Bell, Liam and DuPlessis, Michelle and Gilbert, Catherine and Zipfel, Bernhard and Kuderna, Lukas F. K. and Lizano, Esther and Welker, Frido and Kyriakidou, Pelagia and Cox, Jürgen and Mollereau, Catherine and Tokarski, Caroline and Blackburn, Jonathan and Ramos-Madrigal, Jazmín and Marques-Bonet, Tomas and Penkman, Kirsty and Zanolli, Clément and Schroeder, Lauren and Racimo, Fernando and Olsen, Jesper V. and Ackermann, Rebecca R. and Cappellini, Enrico},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {969--973},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Acute Plasmodium yoelii \\textlessspan style=\"font-variant:small-caps;\"\\textgreater17XNL\\textless/span\\textgreater Infection During \\textlessspan style=\"font-variant:small-caps;\"\\textgreaterBCG\\textless/span\\textgreater Vaccination Limits T Cell Responses and Mycobacterial Growth Inhibition.\n \n \n \n \n\n\n \n Tangie, E.; Pinpathomrat, N.; Tanner, R.; Hsu, N.; Spencer, A. J.; Jacobs, M.; Mcshane, H.; and Keeton, R.\n\n\n \n\n\n\n Immunology, 176(3): 373–384. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Acute$ Paper\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{tangie_acute_2025,\n\ttitle = {Acute \\textit{{Plasmodium} yoelii} {\\textless}span style="font-variant:small-caps;"{\\textgreater}{17XNL}{\\textless}/span{\\textgreater} {Infection} {During} {\\textless}span style="font-variant:small-caps;"{\\textgreater}{BCG}{\\textless}/span{\\textgreater} {Vaccination} {Limits} {T} {Cell} {Responses} and {Mycobacterial} {Growth} {Inhibition}},\n\tvolume = {176},\n\tissn = {0019-2805, 1365-2567},\n\tshorttitle = {Acute \\textit{{Plasmodium} yoelii} {\\textless}span style="font-variant},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/imm.70006},\n\tdoi = {10.1111/imm.70006},\n\tabstract = {ABSTRACT \n             \n              Tuberculosis and malaria overlap in many sub‐Saharan African countries where Bacillus Calmette Guérin (BCG) vaccination is routinely administered. The aim of this study was to determine whether the timing of BCG vaccination in relation to a malaria infection has implications for BCG vaccine efficacy. Mice were intradermally vaccinated with BCG either 4 weeks before infection with blood‐stage \n              Plasmodium yoelii 17XNL \n              , at 13 days post‐infection (during an acute blood‐stage malaria infection) or 21 days post‐infection (after clearance of \n              P. yoelii 17XNL \n              infection). Ex vivo control of mycobacterial growth by splenocytes was used as a surrogate of protective efficacy, and PPD‐specific T‐cell responses were quantified by flow cytometry. No differences in mycobacterial growth control were detected between BCG vaccinated mice and groups receiving vaccination prior to or after clearance of \n              P. yoelii 17XNL \n              infection. Poorer control of mycobacterial growth was observed following BCG vaccination administered during an acute malarial infection compared to BCG vaccination only or BCG vaccination after blood‐stage malaria infection, and mycobacterial growth negatively correlated with the magnitude of total cytokine production from PPD‐specific CD4 \n              + \n              T cells ( \n              p \n               {\\textless} 0.0001). Delayed BCG vaccination beyond the neonatal period may increase the risk of concurrent malarial infections with the potential to reduce BCG efficacy in children in malaria‐endemic areas.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-28},\n\tjournal = {Immunology},\n\tauthor = {Tangie, Emily and Pinpathomrat, Nawamin and Tanner, Rachel and Hsu, Nai‐Jen and Spencer, Alexandra J. and Jacobs, Muazzam and Mcshane, Helen and Keeton, Roanne},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {373--384},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Brief Report: Preferences and Acceptability in Methods of Tenofovir Diphosphate in Dried Blood Spots Collection and Feedback in a Cohort of PLWH in Cape Town South Africa.\n \n \n \n \n\n\n \n D’Avanzo, P. A.; Ferraris, C. M.; Pence-Moore, M.; Jennings, L.; Robbins, R. N.; Orrell, C.; and Remien, R. H.\n\n\n \n\n\n\n AIDS and Behavior, 29(5): 1562–1568. May 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{davanzo_brief_2025,\n\ttitle = {Brief {Report}: {Preferences} and {Acceptability} in {Methods} of {Tenofovir} {Diphosphate} in {Dried} {Blood} {Spots} {Collection} and {Feedback} in a {Cohort} of {PLWH} in {Cape} {Town} {South} {Africa}},\n\tvolume = {29},\n\tissn = {1090-7165, 1573-3254},\n\tshorttitle = {Brief {Report}},\n\turl = {https://link.springer.com/10.1007/s10461-025-04626-w},\n\tdoi = {10.1007/s10461-025-04626-w},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-28},\n\tjournal = {AIDS and Behavior},\n\tauthor = {D’Avanzo, Paul A. and Ferraris, Christopher M. and Pence-Moore, Melissa and Jennings, Lauren and Robbins, Reuben N. and Orrell, Catherine and Remien, Robert H.},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {1562--1568},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The role of the jasmonate signalling transcription factors MYC2/3/4 in circadian clock-mediated regulation of immunity in Arabidopsis.\n \n \n \n \n\n\n \n Joseph, R.; Odendaal, J. L.; Ingle, R. A.; and Roden, L. C.\n\n\n \n\n\n\n Philosophical Transactions of the Royal Society B: Biological Sciences, 380(1918): 20230338. January 2025.\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_role_2025,\n\ttitle = {The role of the jasmonate signalling transcription factors {MYC2}/3/4 in circadian clock-mediated regulation of immunity in {Arabidopsis}},\n\tvolume = {380},\n\tissn = {0962-8436, 1471-2970},\n\turl = {http://royalsocietypublishing.org/rstb/article/109600},\n\tdoi = {10.1098/rstb.2023.0338},\n\tabstract = {Plants are exposed to pathogens at specific, yet predictable times of the day–night cycle. In Arabidopsis, the circadian clock influences temporal differences in susceptibility to the necrotrophic pathogen \n              Botrytis cinerea \n              . The jasmonic acid (JA) pathway regulates immune responses against \n              B. cinerea \n              . The paralogous basic helix–loop–helix transcription factors MYC2, MYC3 and MYC4 are primary regulators of the JA pathway, but their role in regulating temporal variation in immunity is untested. This study aimed to investigate the roles of the MYC transcription factors in the temporal defence response to \n              B. cinerea \n              . We inoculated leaves from wild-type, \n              myc \n              single-, double- and triple-knockout mutants, and lines overexpressing \n              MYC2 \n              , \n              MYC3 \n              or \n              MYC4 \n              , with \n              B. cinerea \n              at two times of day in constant light, and compared lesion sizes. The presence of MYC2, MYC3 or MYC4 alone was sufficient to maintain temporal variation in susceptibility, but this was abolished in the \n              myc234 \n              triple-knockout mutant. Constitutive expression of \n              MYC2 \n              , \n              MYC3 \n              or \n              MYC4 \n              abolished time-of-day differences in susceptibility. The data suggest that MYC2, MYC3 and MYC4 function redundantly in regulating temporal defence responses against \n              B. cinerea \n              and are a point of convergence between the JA pathway and the circadian clock in Arabidopsis. \n             \n            This article is part of the Theo Murphy meeting issue ‘Circadian rhythms in infection and immunity’.},\n\tlanguage = {en},\n\tnumber = {1918},\n\turldate = {2026-05-28},\n\tjournal = {Philosophical Transactions of the Royal Society B: Biological Sciences},\n\tauthor = {Joseph, Rageema and Odendaal, Jessica L. and Ingle, Robert A. and Roden, Laura C.},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {20230338},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Genetic variability in HPV 33 and 35 E6 and E7 genes from South African and Mozambican women with different cervical cytology status.\n \n \n \n \n\n\n \n Maueia, C.; Murahwa, A. T.; Carulei, O.; Taku, O.; Mbulawa, Z.; Manjate, A.; Valey, Z. O.; Mussá, T.; and Williamson, A.\n\n\n \n\n\n\n Virology Journal, 22(1): 234. July 2025.\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

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@article{maueia_genetic_2025,\n\ttitle = {Genetic variability in {HPV} 33 and 35 {E6} and {E7} genes from {South} {African} and {Mozambican} women with different cervical cytology status},\n\tvolume = {22},\n\tissn = {1743-422X},\n\turl = {https://virologyj.biomedcentral.com/articles/10.1186/s12985-025-02851-2},\n\tdoi = {10.1186/s12985-025-02851-2},\n\tabstract = {Abstract \n             \n              Background \n              Among the high-risk human Papillomavirus (hr-HPV) genotypes related to cervical cancer (CC) cases, HPV16 and 18 are the most studied worldwide. However, several studies have identified HPV 33 and HPV 35 as some of the most common genotypes in sub-Saharan African regions. This study aims to investigate the genetic variability and lineages of HPV 33 and 35 based on the HPV E6 and E7 genes in isolates from South African and Mozambican women with different cervical cytology statuses. \n             \n             \n              Methods \n              The study analysed 26 HPV 33 and 46 HPV 35 DNA samples collected previously from South African and Mozambican women. The E6 and E7 genes were amplified by polymerase chain reaction (PCR) using genotype-specific primers. Sequences were mapped to the reference sequences using Qiagen CLC Genomics Workbench software and aligned with the HPV 33 and 35 lineages reference sequences. Single nucleotide polymorphisms (SNPs) in the E6 and E7 genes were identified, and the phylogenetic trees were generated. \n             \n             \n              Results \n              Of the 26 HPV 33-positive subjects, 62\\% (16/26) were from women with high-grade squamous intraepithelial lesions (HSILs). Phylogenetic analysis revealed that 38\\% (10/26) of the isolates clustered with European lineages. Specifically, 30\\% (8/26) of isolates clustered in the A1 sublineage, and 8\\% (2/26) in the A2 sublineage. The African 1 lineage (B1 sublineage) was identified in 19\\% (5/26) of the isolates. Notably, 42\\% (11/26) of the isolates did not cluster with any of the reference sequences under investigation, through E6 and E7 genes analysis. In the HPV 33 E6 gene, 80 SNPs were identified and 30 in the E7, frequently in the HSILs subjects. Of the 46 HPV35-positive subjects, 46\\% (21/46) were from women with HSILs, and 43\\% (20/46) of the isolates clustered with the European lineages. Specifically, 39\\% (18/46) clustered to the A1 sublineage, and 4\\% (2/46) clustered to the A2 sublineage. However, 4\\% (2/46) of the isolates did not cluster with any of the study sublineage. Seven SNPs were detected in the E6 region and two in the E7 region of the HPV 35 isolates. \n             \n             \n              Conclusion \n              The present study’s genetic analysis showed a higher prevalence of European HPV 33 and 35 variants. Fewer SNPs were found in the studied genes of HPV 35 isolates. The addition of HPV 35 to the HPV vaccines would result in improved cervical cancer prevention. The study findings contribute to a better understanding of the genetic diversity of the HPV circulating in Southern African women and may inform strategies for cervical cancer prevention, including the design of therapeutic vaccines for women in advanced cytological disease stages.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-28},\n\tjournal = {Virology Journal},\n\tauthor = {Maueia, Cremildo and Murahwa, Alltalents T. and Carulei, Olivia and Taku, Ongeziwe and Mbulawa, Zizipho and Manjate, Alice and Valey, Ziyaad Omar and Mussá, Tufária and Williamson, Anna-Lise},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {234},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Background Among the high-risk human Papillomavirus (hr-HPV) genotypes related to cervical cancer (CC) cases, HPV16 and 18 are the most studied worldwide. However, several studies have identified HPV 33 and HPV 35 as some of the most common genotypes in sub-Saharan African regions. This study aims to investigate the genetic variability and lineages of HPV 33 and 35 based on the HPV E6 and E7 genes in isolates from South African and Mozambican women with different cervical cytology statuses. Methods The study analysed 26 HPV 33 and 46 HPV 35 DNA samples collected previously from South African and Mozambican women. The E6 and E7 genes were amplified by polymerase chain reaction (PCR) using genotype-specific primers. Sequences were mapped to the reference sequences using Qiagen CLC Genomics Workbench software and aligned with the HPV 33 and 35 lineages reference sequences. Single nucleotide polymorphisms (SNPs) in the E6 and E7 genes were identified, and the phylogenetic trees were generated. Results Of the 26 HPV 33-positive subjects, 62% (16/26) were from women with high-grade squamous intraepithelial lesions (HSILs). Phylogenetic analysis revealed that 38% (10/26) of the isolates clustered with European lineages. Specifically, 30% (8/26) of isolates clustered in the A1 sublineage, and 8% (2/26) in the A2 sublineage. The African 1 lineage (B1 sublineage) was identified in 19% (5/26) of the isolates. Notably, 42% (11/26) of the isolates did not cluster with any of the reference sequences under investigation, through E6 and E7 genes analysis. In the HPV 33 E6 gene, 80 SNPs were identified and 30 in the E7, frequently in the HSILs subjects. Of the 46 HPV35-positive subjects, 46% (21/46) were from women with HSILs, and 43% (20/46) of the isolates clustered with the European lineages. Specifically, 39% (18/46) clustered to the A1 sublineage, and 4% (2/46) clustered to the A2 sublineage. However, 4% (2/46) of the isolates did not cluster with any of the study sublineage. Seven SNPs were detected in the E6 region and two in the E7 region of the HPV 35 isolates. Conclusion The present study’s genetic analysis showed a higher prevalence of European HPV 33 and 35 variants. Fewer SNPs were found in the studied genes of HPV 35 isolates. The addition of HPV 35 to the HPV vaccines would result in improved cervical cancer prevention. The study findings contribute to a better understanding of the genetic diversity of the HPV circulating in Southern African women and may inform strategies for cervical cancer prevention, including the design of therapeutic vaccines for women in advanced cytological disease stages.\n

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\n \n\n \n \n \n \n \n \n Linezolid for the treatment of drug-resistant tuberculosis.\n \n \n \n \n\n\n \n Lange, C.; Barry, C.; and Sotgiu, G.\n\n\n \n\n\n\n European Respiratory Journal, 66(2): 2500927. August 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{lange_linezolid_2025,\n\ttitle = {Linezolid for the treatment of drug-resistant tuberculosis},\n\tvolume = {66},\n\tissn = {0903-1936, 1399-3003},\n\turl = {https://publications.ersnet.org/lookup/doi/10.1183/13993003.00927-2025},\n\tdoi = {10.1183/13993003.00927-2025},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-28},\n\tjournal = {European Respiratory Journal},\n\tauthor = {Lange, Christoph and Barry, Clifton and Sotgiu, Giovanni},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {2500927},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Structural Biology Enabling Drug Discovery.\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, 68(22): 23641–23642. November 2025.\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

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@article{heppner_structural_2025,\n\ttitle = {Structural {Biology} {Enabling} {Drug} {Discovery}},\n\tvolume = {68},\n\tcopyright = {https://doi.org/10.15223/policy-001},\n\tissn = {0022-2623, 1520-4804},\n\turl = {https://pubs.acs.org/doi/10.1021/acs.jmedchem.5c03093},\n\tdoi = {10.1021/acs.jmedchem.5c03093},\n\tlanguage = {en},\n\tnumber = {22},\n\turldate = {2026-05-28},\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 = nov,\n\tyear = {2025},\n\tpages = {23641--23642},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Synthesis and characterisation of \\textlessspan style=\"font-variant:small-caps;\"\\textgreaterDOTA\\textless/span\\textgreater ‐kisspeptin‐10 as a potential gallium‐68/lutetium‐177 pan‐tumour radiopharmaceutical.\n \n \n \n \n\n\n \n Kleynhans, J.; Reeve, R.; Driver, C. H. S.; Marjanovic‐Painter, B.; Sathekge, M.; Zeevaart, J. R.; Ebenhan, T.; and Millar, R. P.\n\n\n \n\n\n\n Journal of Neuroendocrinology, 37(3): e13487. March 2025.\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{kleynhans_synthesis_2025,\n\ttitle = {Synthesis and characterisation of {\\textless}span style="font-variant:small-caps;"{\\textgreater}{DOTA}{\\textless}/span{\\textgreater} ‐kisspeptin‐10 as a potential gallium‐68/lutetium‐177 pan‐tumour radiopharmaceutical},\n\tvolume = {37},\n\tissn = {0953-8194, 1365-2826},\n\tshorttitle = {Synthesis and characterisation of {\\textless}span style="font-variant},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/jne.13487},\n\tdoi = {10.1111/jne.13487},\n\tabstract = {Abstract \n            Kisspeptin (KISS1) and its cognate receptor (KISS1R) are implicated in the progression of various cancers. A gallium‐68 labelled kisspeptin‐10 (KP10), the minimal biologically active structure, has potential as a pan‐tumour radiopharmaceutical for the detection of cancers. Furthermore, a lutetium‐177 labelled KP10 could find therapeutic application in treating oncological diseases. DOTA (1,4,7,10‐tetraazacyclododecane‐1,4,7,10‐tetraacetic acid) was attached to the NH2‐terminus of KP10 as we posited from our previous publications that this modification would not impair biological activity. Here, we showed that the biological activity, as monitored by stimulation of inositol phosphate accumulation in HEK293 transfected with the KISS1R gene, was indeed similar for KP10 and DOTA‐KP10. The optimisation of radiolabelling with gallium‐68 and lutetium‐177 is described. Stability in serum, plasma and whole blood was also investigated. Pharmacokinetics and biodistribution were established with micro‐PET/CT (positron emission tomography/computerised tomography) and ex vivo measurements. Dynamic studies with micro‐PET/CT demonstrated that background clearance for the radiopharmaceutical was rapid with a blood half‐life of 18 ± 3 min. DOTA‐KP10 demonstrated preserved functionality at KISS1R and good blood clearance. These results lay the foundation for the further development of DOTA‐KP10 analogues that have high binding affinity along with proteolytic resistance.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-27},\n\tjournal = {Journal of Neuroendocrinology},\n\tauthor = {Kleynhans, Janke and Reeve, Robert and Driver, Cathryn H. S. and Marjanovic‐Painter, Biljana and Sathekge, Mike and Zeevaart, Jan Rijn and Ebenhan, Thomas and Millar, Robert P.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {e13487},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Clinical trials of broadly neutralizing monoclonal antibodies in people living with HIV – a review.\n \n \n \n \n\n\n \n Mahomed, S.; Pillay, K.; Hassan-Moosa, R.; Galvão, B. P. G. V.; Burgers, W. A.; Moore, P. L.; Rose-Abrahams, M.; Williamson, C.; and Garrett, N.\n\n\n \n\n\n\n AIDS Research and Therapy, 22(1): 44. April 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{mahomed_clinical_2025,\n\ttitle = {Clinical trials of broadly neutralizing monoclonal antibodies in people living with {HIV} – a review},\n\tvolume = {22},\n\tissn = {1742-6405},\n\turl = {https://aidsrestherapy.biomedcentral.com/articles/10.1186/s12981-025-00734-8},\n\tdoi = {10.1186/s12981-025-00734-8},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-27},\n\tjournal = {AIDS Research and Therapy},\n\tauthor = {Mahomed, Sharana and Pillay, Kayla and Hassan-Moosa, Razia and Galvão, Bruna P. G. V. and Burgers, Wendy A. and Moore, Penny L. and Rose-Abrahams, Melissa and Williamson, Carolyn and Garrett, Nigel},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {44},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Diagnostic accuracy of a commercial AI digital stethoscope for diagnosis of TB.\n \n \n \n \n\n\n \n Cox, H.; Rani, Y.; Nakiyingi, L.; Francia, K.; Xie, Y.; Hoang, C.; Hapeela, N.; Romero, G.; Nasinghe, E.; Van Hung, N.; Kim, S.; Penn-Nicholson, A.; Dorman, S.; and for the FEND-TB Consortium\n\n\n \n\n\n\n IJTLD Open, 2(10): 610–615. October 2025.\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{cox_diagnostic_2025,\n\ttitle = {Diagnostic accuracy of a commercial {AI} digital stethoscope for diagnosis of {TB}},\n\tvolume = {2},\n\tissn = {3005-7590},\n\turl = {https://journals.theunion.org/lookup/doi/10.5588/ijtldopen.25.0360},\n\tdoi = {10.5588/ijtldopen.25.0360},\n\tabstract = {SUMMARY \n             \n              BACKGROUND \n              Improved TB screening requires non-invasive, low-cost, and rapid diagnostics. Digital stethoscopes utilising machine-learning approaches to analyse respiratory sounds have potential. \n             \n             \n              METHODS \n              We assessed accuracy of a commercial digital stethoscope for TB diagnosis among TB symptomatic participants. The microbiological reference standard (MRS) was sputum TB-positive on either liquid culture, solid culture, or Xpert MTB/RIF Ultra. Adults were enrolled from South Africa, Uganda, Vietnam, and Peru, with pre-defined sampling of 60 MRS-positive and 180 MRS-negative participants over two stages. Respiratory sounds from six auscultation positions on the participant’s torso were analysed. The manufacturer (blinded to MRS status) provided participant scores and a test-positivity cut-off. \n             \n             \n              RESULTS \n              Among 240 participants, 135 (56\\%) were female, 62 (26\\%) living with HIV, 35 (15\\%) current smokers, and 31 (13\\%) previously treated for TB. Estimates of sensitivity and specificity, adjusted for country-stratified sampling, were 77\\% (95\\% confidence interval [CI]: 65–85) and 50\\% (95\\% CI: 43–57), respectively. Sensitivity was lower among people living with HIV and those with sputum smear–negative TB and varied by country. Testing took 5 min per participant (median, interquartile range 4–6). \n             \n             \n              CONCLUSION \n              These early data suggest that further refinement of this test is warranted. The device is simple to use, is inexpensive, and can be used offline.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-27},\n\tjournal = {IJTLD Open},\n\tauthor = {Cox, H. and Rani, Y. and Nakiyingi, L. and Francia, K.A. and Xie, Y. and Hoang, C. and Hapeela, N. and Romero, G.P. and Nasinghe, E. and Van Hung, N. and Kim, S. and Penn-Nicholson, A. and Dorman, S.E. and {for the FEND-TB Consortium}},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {610--615},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Population pharmacokinetics of pyrazinamide and isoniazid in plasma and cerebrospinal fluid from South African adults with tuberculous meningitis.\n \n \n \n \n\n\n \n Calderin, J. M.; Wasserman, S.; Resendiz-Galvan, J. E.; Abdelgawad, N.; Davis, A.; Stek, C.; Wiesner, L.; Wilkinson, R. J.; and Denti, P.\n\n\n \n\n\n\n Antimicrobial Agents and Chemotherapy, 69(8): e00099–25. August 2025.\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{calderin_population_2025,\n\ttitle = {Population pharmacokinetics of pyrazinamide and isoniazid in plasma and cerebrospinal fluid from {South} {African} adults with tuberculous meningitis},\n\tvolume = {69},\n\tissn = {0066-4804, 1098-6596},\n\turl = {https://journals.asm.org/doi/10.1128/aac.00099-25},\n\tdoi = {10.1128/aac.00099-25},\n\tabstract = {ABSTRACT \n             \n               \n              Pyrazinamide and isoniazid are first-line drugs for tuberculous meningitis (TBM), but limited information is available on their plasma pharmacokinetics, and particularly cerebrospinal fluid (CSF) penetration, in patients with TBM. Any potential effect of co-administration with high-dose rifampicin, also being evaluated in trials for TBM, is unknown. Understanding this is important for dose optimisation. We characterized pyrazinamide and isoniazid plasma and CSF pharmacokinetics among adults enrolled in a phase 2 clinical trial of intensified antibiotic therapy for HIV-associated TBM. Participants were randomized to receive either standard TBM treatment (including rifampicin 10 mg/kg) or high-dose rifampicin (35 mg/kg) plus linezolid, with or without aspirin. Plasma and lumbar CSF samples were collected on days 3 and 28 after study enrollment, and drug concentrations were measured using liquid chromatography-tandem mass spectrometry. Data were analysed using nonlinear mixed-effects modeling. Forty-nine participants provided 414 plasma and 44 CSF concentrations. Pyrazinamide CSF concentrations equilibrated with plasma with a half-life of 0.66 h and a pseudo-partition coefficient of 1.05. Isoniazid concentrations equilibrated with a half-life of 3.87 h and a pseudo-partition coefficient of 1.04. Pyrazinamide clearance increased by 30\\% from day 3 to day 28. NAT2 phenotype determined multi-modal isoniazid clearance. High-dose rifampicin did not affect pyrazinamide or isoniazid plasma pharmacokinetics or CSF penetration. Both drugs achieved exposure in CSF similar to plasma, supporting their crucial role in TBM treatment. Plasma pharmacokinetics of pyrazinamide and isoniazid in TBM were consistent with previously reported values in pulmonary tuberculosis, even when co-administered with high-dose rifampicin.},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-27},\n\tjournal = {Antimicrobial Agents and Chemotherapy},\n\tauthor = {Calderin, Jose M. and Wasserman, Sean and Resendiz-Galvan, Juan Eduardo and Abdelgawad, Noha and Davis, Angharad and Stek, Cari and Wiesner, Lubbe and Wilkinson, Robert J. and Denti, Paolo},\n\teditor = {Doernberg, Sarah},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {e00099--25},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n World TB Day 2025 Theme “Yes! We Can End TB: Commit, Invest, Deliver” can be made a reality through concerted global efforts to advance diagnosis, treatment and research of tuberculosis infection and disease.\n \n \n \n \n\n\n \n Goletti, D.; Matteelli, A.; Cliff, J. M.; Meintjes, G.; Graham, S.; Esmail, H.; and Shan Lee, S.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 155: 107892. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"World$ Paper\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{goletti_world_2025,\n\ttitle = {World {TB} {Day} 2025 {Theme} “{Yes}! {We} {Can} {End} {TB}: {Commit}, {Invest}, {Deliver}” can be made a reality through concerted global efforts to advance diagnosis, treatment and research of tuberculosis infection and disease},\n\tvolume = {155},\n\tissn = {12019712},\n\tshorttitle = {World {TB} {Day} 2025 {Theme} “{Yes}! {We} {Can} {End} {TB}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971225001158},\n\tdoi = {10.1016/j.ijid.2025.107892},\n\tlanguage = {en},\n\turldate = {2026-05-27},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Goletti, Delia and Matteelli, Alberto and Cliff, Jacqueline M. and Meintjes, Graeme and Graham, Steve and Esmail, Hanif and Shan Lee, Shui},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {107892},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Assessment of γ-herpesvirus infection dynamics in non-hospitalised people living with HIV during the COVID-19 pandemic in South Africa.\n \n \n \n \n\n\n \n Chinna, P.; Blumenthal, M. J.; Lambarey, H.; Jennings, L.; Orrell, C.; and Schäfer, G.\n\n\n \n\n\n\n Virology, 611: 110666. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Assessment$ Paper\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{chinna_assessment_2025,\n\ttitle = {Assessment of γ-herpesvirus infection dynamics in non-hospitalised people living with {HIV} during the {COVID}-19 pandemic in {South} {Africa}},\n\tvolume = {611},\n\tissn = {00426822},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0042682225002806},\n\tdoi = {10.1016/j.virol.2025.110666},\n\tlanguage = {en},\n\turldate = {2026-05-27},\n\tjournal = {Virology},\n\tauthor = {Chinna, Prishanta and Blumenthal, Melissa J. and Lambarey, Humaira and Jennings, Lauren and Orrell, Catherine and Schäfer, Georgia},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {110666},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Insights from the 2024 WHO Global Tuberculosis Report – More Comprehensive Action, Innovation, and Investments required for achieving WHO End TB goals.\n \n \n \n \n\n\n \n Goletti, D.; Meintjes, G.; Andrade, B. B.; Zumla, A.; and Shan Lee, S.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 150: 107325. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Insights$ Paper\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{goletti_insights_2025,\n\ttitle = {Insights from the 2024 {WHO} {Global} {Tuberculosis} {Report} – {More} {Comprehensive} {Action}, {Innovation}, and {Investments} required for achieving {WHO} {End} {TB} goals},\n\tvolume = {150},\n\tissn = {12019712},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971224004004},\n\tdoi = {10.1016/j.ijid.2024.107325},\n\tlanguage = {en},\n\turldate = {2026-05-27},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Goletti, Delia and Meintjes, Graeme and Andrade, Bruno B. and Zumla, Alimuddin and Shan Lee, Shui},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {107325},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Oral antiretroviral adherence interventions in the era of U=U.\n \n \n \n \n\n\n \n Keene, C. M; Sabin, L. L; Jennings, L.; Schreuder, C.; Källström-Ståhlgren, C.; Katz, I. T; Singh, Y.; Orrell, C.; and Rivet Amico, K\n\n\n \n\n\n\n The Lancet HIV, 12(8): e587–e595. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Oral$ Paper\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{keene_oral_2025,\n\ttitle = {Oral antiretroviral adherence interventions in the era of {U}={U}},\n\tvolume = {12},\n\tissn = {23523018},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352301825000967},\n\tdoi = {10.1016/S2352-3018(25)00096-7},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-27},\n\tjournal = {The Lancet HIV},\n\tauthor = {Keene, Claire M and Sabin, Lora L and Jennings, Lauren and Schreuder, Chantel and Källström-Ståhlgren, Carl-Oscar and Katz, Ingrid T and Singh, Yashna and Orrell, Catherine and Rivet Amico, K},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {e587--e595},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Neurological Sequelae After Paediatric Cryptococcal Meningitis.\n \n \n \n \n\n\n \n Gifford, A.; Patel, S. A.; Matlakala, M.; Dangarembizi, R.; and Warris, A.\n\n\n \n\n\n\n Journal of Fungi, 11(11): 767. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Neurological$ Paper\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{gifford_neurological_2025,\n\ttitle = {Neurological {Sequelae} {After} {Paediatric} {Cryptococcal} {Meningitis}},\n\tvolume = {11},\n\tissn = {2309-608X},\n\turl = {https://www.mdpi.com/2309-608X/11/11/767},\n\tdoi = {10.3390/jof11110767},\n\tabstract = {An infectious insult to a child’s developing brain has the potential to result in life-long neurological and neurodevelopmental consequences. Adult survivors of cryptococcal meningitis (CM) can suffer from long-term neurological sequelae such as blindness and motor weakness, but little is known about outcomes in children. A PubMed and Ovid Global Health search identified all children {\\textless}19 yrs of age with proven cryptococcal disease of the central nervous system until October 2024. A total of 868 children were included from 108 publications. In total, 555 (67\\%) were HIV positive, 67 (8\\%) non-HIV immunocompromised and 204 (25\\%) immunocompetent. The mortality rate was 24\\% (104/430). No child had a documented formal neurodevelopmental assessment after CM. Of those with a documented clinical outcome, 20\\% (36/184) had neurological sequelae, but this was higher in HIV-positive children (25\\%, 11/44). Visual impairment was most commonly observed (13\\%, 23/184) and remarkably higher in those with Cryptococcus gattii meningitis (32\\%, 10/31). Other sequelae included limb weakness (n = 8), learning difficulties (n = 7), hearing loss (n = 3) and recurrent seizures (n = 2). The burden of neurological sequelae is likely even more extensive than captured, with little data available from the populations most affected by CM. It is vital that neurodevelopmental assessment of children after CM is standard in all countries to support rehabilitation and the best functional outcomes.},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-27},\n\tjournal = {Journal of Fungi},\n\tauthor = {Gifford, Alison and Patel, Simran Atulkumar and Matlakala, Masilo and Dangarembizi, Rachael and Warris, Adilia},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {767},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Overcoming endosomal/lysosomal barriers: Advanced strategies for cytosolic siRNA delivery.\n \n \n \n \n\n\n \n Li, R.; Zhu, M.; Hu, X.; Chen, J.; Yu, F.; Barth, S.; Sun, L.; and He, H.\n\n\n \n\n\n\n Chinese Chemical Letters, 36(9): 110736. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Overcoming$ Paper\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{li_overcoming_2025,\n\ttitle = {Overcoming endosomal/lysosomal barriers: {Advanced} strategies for cytosolic {siRNA} delivery},\n\tvolume = {36},\n\tissn = {10018417},\n\tshorttitle = {Overcoming endosomal/lysosomal barriers},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S100184172401252X},\n\tdoi = {10.1016/j.cclet.2024.110736},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-27},\n\tjournal = {Chinese Chemical Letters},\n\tauthor = {Li, Rui and Zhu, Mengxi and Hu, Xiwen and Chen, Jiaxuan and Yu, Fei and Barth, Stefan and Sun, Lu and He, Huining},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {110736},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Ex Vivo Host Transcriptomics During Cryptococcus neoformans , Cryptococcus gattii , and Candida albicans Infection of Peripheral Blood Mononuclear Cells From South African Volunteers.\n \n \n \n \n\n\n \n Doyle, R. M; Kannambath, S.; Pittman, A.; Goliath, R.; Kumar, V.; Meintjes, G.; Milburn, J.; Netea, M. G; Harrison, T. S; Jarvis, J. N; and Bicanic, T.\n\n\n \n\n\n\n The Journal of Infectious Diseases, 231(1): e254–e262. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Ex$ Paper\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{doyle_ex_2025,\n\ttitle = {Ex {Vivo} {Host} {Transcriptomics} {During} \\textit{{Cryptococcus} neoformans} , \\textit{{Cryptococcus} gattii} , and \\textit{{Candida} albicans} {Infection} of {Peripheral} {Blood} {Mononuclear} {Cells} {From} {South} {African} {Volunteers}},\n\tvolume = {231},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/231/1/e254/7735862},\n\tdoi = {10.1093/infdis/jiae410},\n\tabstract = {Abstract \n            Cryptococcus neoformans, Cryptococcus gattii, and Candida albicans are opportunistic fungal pathogens associated with infections in immunocompromised hosts. Cryptococcal meningitis (CM) is the leading fungal cause of human immunodeficiency virus–related deaths globally, with the majority occurring in Africa. The human immune response to C albicans infection has been studied extensively in large genomics studies whereas cryptococcal infections, despite their severity, are comparatively understudied. Here we investigated the transcriptional response of immune cells after in vitro stimulation with in vitro C neoformans, C gattii, and C albicans infection of peripheral blood mononuclear cells collected from healthy South African volunteers. We found a lower transcriptional response to cryptococcal stimuli compared to C albicans and unique expression signatures from all 3 fungal stimuli. This work provides a starting point for further studies comparing the transcriptional signature of CM in immunocompromised patients, with the goal of identifying biomarkers of disease severity and possible novel treatment targets.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-27},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Doyle, Ronan M and Kannambath, Shichina and Pittman, Alan and Goliath, Rene and Kumar, Vinod and Meintjes, Graeme and Milburn, James and Netea, Mihai G and Harrison, Thomas S and Jarvis, Joseph N and Bicanic, Tihana},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {e254--e262},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Challenges of microscopy technology dissemination to resource-constrained communities.\n \n \n \n \n\n\n \n Aaron, J. S.; Jacobs, C. A.; Malacrida, L.; Keppler, A.; French, P.; Fletcher, D. A.; Wood, C.; Brown, C. M.; Wright, G. D.; Ogawa, S.; Maina, M.; and Chew, T.\n\n\n \n\n\n\n Nature Methods. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Challenges$ Paper\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{aaron_challenges_2025,\n\ttitle = {Challenges of microscopy technology dissemination to resource-constrained communities},\n\tissn = {1548-7091, 1548-7105},\n\turl = {https://www.nature.com/articles/s41592-025-02690-7},\n\tdoi = {10.1038/s41592-025-02690-7},\n\tlanguage = {en},\n\turldate = {2026-05-27},\n\tjournal = {Nature Methods},\n\tauthor = {Aaron, Jesse S. and Jacobs, Caron A. and Malacrida, Leonel and Keppler, Antje and French, Paul and Fletcher, Daniel A. and Wood, Christopher and Brown, Claire M. and Wright, Graham D. and Ogawa, Satoshi and Maina, Mahmoud and Chew, Teng-Leong},\n\tmonth = may,\n\tyear = {2025},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Population Pharmacokinetics of Rifampicin in Plasma and Cerebrospinal Fluid in Adults With Tuberculosis Meningitis.\n \n \n \n \n\n\n \n Abdelgawad, N.; Wasserman, S.; Gausi, K.; Davis, A.; Stek, C.; Wiesner, L.; Meintjes, G.; Wilkinson, R. J; and Denti, P.\n\n\n \n\n\n\n The Journal of Infectious Diseases, 232(2): e234–e241. August 2025.\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{abdelgawad_population_2025,\n\ttitle = {Population {Pharmacokinetics} of {Rifampicin} in {Plasma} and {Cerebrospinal} {Fluid} in {Adults} {With} {Tuberculosis} {Meningitis}},\n\tvolume = {232},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/232/2/e234/8121427},\n\tdoi = {10.1093/infdis/jiaf178},\n\tabstract = {Abstract \n             \n              Background \n              Several ongoing clinical trials are evaluating high-dose rifampicin (up to 35 mg/kg) for tuberculous meningitis (TBM). However, rifampicin pharmacokinetics at higher doses is not fully characterized, particularly in cerebrospinal fluid (CSF), the site of TBM disease. \n             \n             \n              Methods \n              In a randomized controlled trial, adults with HIV-associated TBM were assigned to experimental arms of high-dose rifampicin (oral, 35 mg/kg; intravenous, 20 mg/kg) plus linezolid, with or without aspirin, or a control arm that received the standard of care with 10 mg/kg of oral rifampicin. Rifampicin concentrations, including the unbound fraction, were measured on plasma samples, and CSF was collected on days 3 and 28 of study enrollment. Data were analyzed by nonlinear mixed effects modeling. \n             \n             \n              Results \n              In total, 400 plasma and 44 CSF rifampicin concentrations from 48 participants were used for model development. The median (range) age and weight were 39 years (25–78) and 60 kg (30–107). Rifampicin pharmacokinetics was best described by a 2-compartment disposition model with first-order transit oral absorption and elimination via saturable hepatic extraction. Typical clearance values for the standard dose for days 3 and 28 were 33.1 and 41.4 L/h, respectively; high-dose values were 46.1 and 70.2 L/h. The CSF-plasma ratio was approximately 6\\% and the equilibration half-life was 3.2 hours. Simulated standard-dose rifampicin did not reach CSF concentrations above the critical concentration for Mycobacterium tuberculosis. \n             \n             \n              Conclusions \n              CSF penetration with standard-dose rifampicin is low. Our findings support continued evaluation of high-dose rifampicin for TBM treatment.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Abdelgawad, Noha and Wasserman, Sean and Gausi, Kamunkhwala and Davis, Angharad and Stek, Cari and Wiesner, Lubbe and Meintjes, Graeme and Wilkinson, Robert J and Denti, Paolo},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {e234--e241},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Exploring the female genital tract mycobiome in young South African women using metaproteomics.\n \n \n \n \n\n\n \n Gangiah, T. K.; Alisoltani, A.; Potgieter, M.; Bell, L.; Ross, E.; Iranzadeh, A.; McDonald, Z.; Allali, I.; Dabee, S.; Barnabas, S.; Blackburn, J. M.; Tabb, D. L.; Bekker, L.; Jaspan, H. B.; Passmore, J. S.; Mulder, N.; and Masson, L.\n\n\n \n\n\n\n Microbiome, 13(1): 76. March 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{gangiah_exploring_2025,\n\ttitle = {Exploring the female genital tract mycobiome in young {South} {African} women using metaproteomics},\n\tvolume = {13},\n\tissn = {2049-2618},\n\turl = {https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-025-02066-1},\n\tdoi = {10.1186/s40168-025-02066-1},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Microbiome},\n\tauthor = {Gangiah, Tamlyn K. and Alisoltani, Arghavan and Potgieter, Matthys and Bell, Liam and Ross, Elizabeth and Iranzadeh, Arash and McDonald, Zac and Allali, Imane and Dabee, Smritee and Barnabas, Shaun and Blackburn, Jonathan M. and Tabb, David L. and Bekker, Linda-Gail and Jaspan, Heather B. and Passmore, Jo-Ann S. and Mulder, Nicola and Masson, Lindi},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {76},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Immunogenicity of DNA, mRNA and Subunit Vaccines Against Beak and Feather Disease Virus.\n \n \n \n \n\n\n \n Ndlovu, B.; Van Zyl, A. R.; Verwoerd, D.; Rybicki, E. P.; and Hitzeroth, I. I.\n\n\n \n\n\n\n Vaccines, 13(7): 762. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Immunogenicity$ Paper\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{ndlovu_immunogenicity_2025,\n\ttitle = {Immunogenicity of {DNA}, {mRNA} and {Subunit} {Vaccines} {Against} {Beak} and {Feather} {Disease} {Virus}},\n\tvolume = {13},\n\tissn = {2076-393X},\n\turl = {https://www.mdpi.com/2076-393X/13/7/762},\n\tdoi = {10.3390/vaccines13070762},\n\tabstract = {Background/Objectives: Beak and feather disease virus (BFDV) is the causative agent of psittacine beak and feather disease (PBFD), affecting psittacine birds. There is currently no commercial vaccine or treatment for this disease. This study developed a novel BFDV coat protein mRNA vaccine encapsidated by TMV coat protein to form pseudovirions (PsVs) and tested its immunogenicity alongside BFDV coat protein (CP) subunit and DNA vaccine candidates. Methods: mRNA and BFDV CP subunit vaccine candidates were produced in Nicotiana benthamiana and subsequently purified using PEG precipitation and gradient ultracentrifugation, respectively. The DNA vaccine candidate was produced in E. coli cells harbouring a plasmid with a BFDV1.1mer pseudogenome. Immunogenicity of the vaccine candidates was evaluated in African grey parrot chicks. Results: Successful purification of TMV PsVs harbouring the mRNA vaccine, and of the BFDV-CP subunit vaccine, was confirmed by SDS-PAGE and western blot analysis. TEM analyses confirmed formation of TMV PsVs, while RT-PCR and RT-qPCR cDNA amplification confirmed encapsidation of the mRNA vaccine candidate within TMV particles. Restriction digests verified presence of the BFDV1.1mer genome in the plasmid. Four groups of 5 ten-week-old African grey parrot (Psittacus erithacus) chicks were vaccinated and received two boost vaccinations 2 weeks apart. Blood samples were collected from all four groups on day 14, 28 and 42, and sera were analysed using indirect ELISA, which showed that all vaccine candidates successfully elicited specific anti-BFDV-CP immune responses. The subunit vaccine candidate showed the strongest immune response, indicated by higher binding titres ({\\textgreater}6400), followed by the mRNA and DNA vaccine candidates. Conclusions: The candidate vaccines present an important milestone in the search for a protective vaccine against PBFD, and their inexpensive manufacture could considerably aid commercial vaccine development.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-19},\n\tjournal = {Vaccines},\n\tauthor = {Ndlovu, Buyani and Van Zyl, Albertha R. and Verwoerd, Dirk and Rybicki, Edward P. and Hitzeroth, Inga I.},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {762},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Emergence of the BA.2.87.1 lineage of SARS-CoV-2 in South Africa, a highly diverged BA.2-related lineage.\n \n \n \n \n\n\n \n Kekana, D.; Ntozini, B.; Hisner, R.; Yousif, M.; Ntuli, P.; Ndlovu, N.; McCarthy, K.; Mnguni, A.; Mahlangu, B.; Nzimande, A.; Stock, N.; Tegally, H.; Davis, M.; Moir, M.; Wilkinson, E.; Baxter, C.; Bhiman, J.; Cohen, C.; Walaza, S.; Von Gottberg, A.; De Oliveira, T.; Wolter, N.; and Martin, D.\n\n\n \n\n\n\n Virus Evolution, 11(1): veaf083. January 2025.\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{kekana_emergence_2025,\n\ttitle = {Emergence of the {BA}.2.87.1 lineage of {SARS}-{CoV}-2 in {South} {Africa}, a highly diverged {BA}.2-related lineage},\n\tvolume = {11},\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/veaf083/8313344},\n\tdoi = {10.1093/ve/veaf083},\n\tabstract = {Abstract \n            The emergence of various SARS-CoV-2 lineages with adaptive mutations is of significant concern worldwide, especially when these mutations enhance the virus’s ability to either evade immune responses or transmit more efficiently. Between September and December 2023, a highly diverged BA.2-related lineage, designated BA.2.87.1, was detected through diagnostic testing, syndromic surveillance, and wastewater surveillance in the Limpopo, Mpumalanga, Western Cape, Eastern Cape, and Gauteng provinces of South Africa. This lineage harbours 20 amino acid substitutions in Spike protein relative to baseline BA.2, including at antigenic sites of the receptor-binding domain (including N417T, K444N, V445G, L452M, N460K, K478T, N481K, and R493Q) and, most strikingly, large deletions of the N-terminal domain (NTD) residues 15–26 and 136–146. Such large NTD deletions have never been observed in circulating lineages but do sometimes occur in highly mutated sequences originating in chronic infections. Phylodynamic analysis supports the possibility that the BA.2.87.1 lineage originated in a chronic infection in that the nearest known ancestor of this lineage last circulated at least 18 months prior to its first detection. Although BA.2.87.1 had immune evasion and/or transmission potential, its detection was not associated with a surge of infections and it was displaced by the globally dominant BA.2.86 lineage, JN.1, in the last few weeks of 2023. Our findings further strengthen the case for genomic surveillance through clinical and wastewater surveillance systems. SARS-CoV-2 continues to circulate and evolve within the global population. Multiple divergent Omicron lineages such as BA.1, BA.2, BA.3, BA.4, and BA.5 that have emerged from the southern African region have had a major impact on the epidemiology of the virus worldwide. This is likely driven by the large population of immunocompromised individuals due to the high burden of HIV/AIDS and TB in the region that facilitates long-term chronic infections. This article provides insights into the emergence of the BA.2.87.1 lineage, which briefly circulated in South Africa. The lineage displayed a unique mutational profile, including major substitutions in the receptor-binding domain and N-terminal domain deletions. The study also highlights the critical role of syndromic and wastewater surveillance in monitoring the circulation and evolution of SARS-CoV-2.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Virus Evolution},\n\tauthor = {Kekana, Dikeledi and Ntozini, Buhle and Hisner, Ryan and Yousif, Mukhlid and Ntuli, Phindile and Ndlovu, Nkosenhle and McCarthy, Kerrigan and Mnguni, Anele and Mahlangu, Boitshoko and Nzimande, Ayanda and Stock, Nadine and Tegally, Houriiyah and Davis, Mary-Ann and Moir, Monika and Wilkinson, Eduan and Baxter, Cheryl and Bhiman, Jinal and Cohen, Cheryl and Walaza, Sibongile and Von Gottberg, Anne and De Oliveira, Tulio and Wolter, Nicole and Martin, Darren},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {veaf083},\n}\n\n\n\n

\n

\n\n\n

\n Abstract The emergence of various SARS-CoV-2 lineages with adaptive mutations is of significant concern worldwide, especially when these mutations enhance the virus’s ability to either evade immune responses or transmit more efficiently. Between September and December 2023, a highly diverged BA.2-related lineage, designated BA.2.87.1, was detected through diagnostic testing, syndromic surveillance, and wastewater surveillance in the Limpopo, Mpumalanga, Western Cape, Eastern Cape, and Gauteng provinces of South Africa. This lineage harbours 20 amino acid substitutions in Spike protein relative to baseline BA.2, including at antigenic sites of the receptor-binding domain (including N417T, K444N, V445G, L452M, N460K, K478T, N481K, and R493Q) and, most strikingly, large deletions of the N-terminal domain (NTD) residues 15–26 and 136–146. Such large NTD deletions have never been observed in circulating lineages but do sometimes occur in highly mutated sequences originating in chronic infections. Phylodynamic analysis supports the possibility that the BA.2.87.1 lineage originated in a chronic infection in that the nearest known ancestor of this lineage last circulated at least 18 months prior to its first detection. Although BA.2.87.1 had immune evasion and/or transmission potential, its detection was not associated with a surge of infections and it was displaced by the globally dominant BA.2.86 lineage, JN.1, in the last few weeks of 2023. Our findings further strengthen the case for genomic surveillance through clinical and wastewater surveillance systems. SARS-CoV-2 continues to circulate and evolve within the global population. Multiple divergent Omicron lineages such as BA.1, BA.2, BA.3, BA.4, and BA.5 that have emerged from the southern African region have had a major impact on the epidemiology of the virus worldwide. This is likely driven by the large population of immunocompromised individuals due to the high burden of HIV/AIDS and TB in the region that facilitates long-term chronic infections. This article provides insights into the emergence of the BA.2.87.1 lineage, which briefly circulated in South Africa. The lineage displayed a unique mutational profile, including major substitutions in the receptor-binding domain and N-terminal domain deletions. The study also highlights the critical role of syndromic and wastewater surveillance in monitoring the circulation and evolution of SARS-CoV-2.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Bridging data gaps: African reference genomes advancing inclusive microbiome research.\n \n \n \n \n\n\n \n Kouidhi, S.; Passmore, J. S.; Setati, M. E.; Mwapagha, L. M.; Jimoh, A.; and Oduaran, O. H.\n\n\n \n\n\n\n Trends in Microbiology, 33(5): 479–483. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Bridging$ Paper\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{kouidhi_bridging_2025,\n\ttitle = {Bridging data gaps: {African} reference genomes advancing inclusive microbiome research},\n\tvolume = {33},\n\tissn = {0966842X},\n\tshorttitle = {Bridging data gaps},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0966842X25000320},\n\tdoi = {10.1016/j.tim.2025.02.001},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-19},\n\tjournal = {Trends in Microbiology},\n\tauthor = {Kouidhi, Soumaya and Passmore, Jo-Ann S. and Setati, Mathabatha Evodia and Mwapagha, Lamech M. and Jimoh, Adijat and Oduaran, Ovokeraye H.},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {479--483},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Summary of taxonomy changes ratified by the International Committee on Taxonomy of Viruses from the Plant Viruses Subcommittee, 2025.\n \n \n \n \n\n\n \n Rubino, L.; Abrahamian, P.; An, W.; Aranda, M. A.; Ascencio-Ibañez, J. T.; Bejerman, N.; Blouin, A. G.; Candresse, T.; Canto, T.; Cao, M.; Carr, J. P.; Cho, W. K.; Constable, F.; Dasgupta, I.; Debat, H.; Dietzgen, R. G.; Digiaro, M.; Donaire, L.; Elbeaino, T.; Fargette, D.; Filardo, F.; Fischer, M. G.; Fontdevila, N.; Fox, A.; Freitas-Astua, J.; Fuchs, M.; Geering, A. D.; Ghafari, M.; Hafrén, A.; Hammond, J.; Hammond, R.; Hasiów-Jaroszewska, B.; Hebrard, E.; Hernández, C.; Hily, J.; Hosseini, A.; Hull, R.; Inoue-Nagata, A. K.; Jordan, R.; Kondo, H.; Kreuze, J. F.; Krupovic, M.; Kubota, K.; Kuhn, J. H.; Leisner, S.; Lett, J.; Li, C.; Li, F.; Li, J. M.; López-Lambertini, P. M.; Lopez-Moya, J. J.; Maclot, F.; Mäkinen, K.; Martin, D.; Massart, S.; Miller, W. A.; Mohammadi, M.; Mollov, D.; Muller, E.; Nagata, T.; Navas-Castillo, J.; Neriya, Y.; Ochoa-Corona, F. M.; Ohshima, K.; Pallás, V.; Pappu, H.; Petrzik, K.; Pooggin, M.; Prigigallo, M. I.; Ramos-González, P. L.; Ribeiro, S.; Richert-Pöggeler, K. R.; Roumagnac, P.; Roy, A.; Sabanadzovic, S.; Šafářová, D.; Saldarelli, P.; Sanfaçon, H.; Sarmiento, C.; Sasaya, T.; Scheets, K.; Schravesande, W. E.; Seal, S.; Shimomoto, Y.; Sõmera, M.; Stavolone, L.; Stewart, L. R.; Teycheney, P.; Thomas, J. E.; Thompson, J. R.; Tiberini, A.; Tomitaka, Y.; Tzanetakis, I.; Umber, M.; Urbino, C.; Van Den Burg, H. A.; Van Der Vlugt, R. A.; Varsani, A.; Verhage, A.; Villamor, D.; Von Bargen, S.; Walker, P. J.; Wetzel, T.; Whitfield, A. E.; Wylie, S. J.; Yang, C.; Zerbini, F. M.; Zhang, S.; and ICTV Taxonomy Summary Consortium\n\n\n \n\n\n\n Journal of General Virology, 106(7). July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Summary$ Paper\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{rubino_summary_2025,\n\ttitle = {Summary of taxonomy changes ratified by the {International} {Committee} on {Taxonomy} of {Viruses} from the {Plant} {Viruses} {Subcommittee}, 2025},\n\tvolume = {106},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {0022-1317, 1465-2099},\n\turl = {https://www.microbiologyresearch.org/content/journal/jgv/10.1099/jgv.0.002114},\n\tdoi = {10.1099/jgv.0.002114},\n\tabstract = {In March 2025, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote, newly proposed taxa were added to those under the mandate of the Plant Viruses Subcommittee. In brief, 1 new order, 3 new families, 6 new genera, 2 new subgenera and 206 new species were created. Some taxa were reorganized. Genus \n Cytorhabdovirus \n in the family \n Rhabdoviridae \n was abolished and its taxa were redistributed into three new genera \n Alphacytorhabdovirus \n , \n Betacytorhabdovirus \n and \n Gammacytorhabdovirus \n . Genus \n Waikavirus \n in the family \n Secoviridae \n was reorganized into two subgenera ( \n Actinidivirus \n and \n Ritunrivirus \n ). One family and four previously unaffiliated genera were moved to the newly established order \n Tombendovirales \n . Twelve species not assigned to a genus were abolished. To comply with the ICTV mandate of a binomial format for virus species, eight species were renamed. Demarcation criteria in the absence of biological information were defined in the genus \n Ilarvirus \n (family \n Bromoviridae \n ). This article presents the updated taxonomy put forth by the Plant Viruses Subcommittee and ratified by the ICTV.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-19},\n\tjournal = {Journal of General Virology},\n\tauthor = {Rubino, Luisa and Abrahamian, Peter and An, Wenxia and Aranda, Miguel A. and Ascencio-Ibañez, José T. and Bejerman, Nicolas and Blouin, Arnaud G. and Candresse, Thierry and Canto, Tomas and Cao, Mengji and Carr, John P. and Cho, Won Kyong and Constable, Fiona and Dasgupta, Indranil and Debat, Humberto and Dietzgen, Ralf G. and Digiaro, Michele and Donaire, Livia and Elbeaino, Toufic and Fargette, Denis and Filardo, Fiona and Fischer, Matthias G. and Fontdevila, Nuria and Fox, Adrian and Freitas-Astua, Juliana and Fuchs, Marc and Geering, Andrew D.W. and Ghafari, Mahan and Hafrén, Anders and Hammond, John and Hammond, Rosemarie and Hasiów-Jaroszewska, Beata and Hebrard, Eugenie and Hernández, Carmen and Hily, Jean-Michel and Hosseini, Ahmed and Hull, Roger and Inoue-Nagata, Alice K. and Jordan, Ramon and Kondo, Hideki and Kreuze, Jan F. and Krupovic, Mart and Kubota, Kenji and Kuhn, Jens H. and Leisner, Scott and Lett, Jean-Michel and Li, Chengyu and Li, Fan and Li, Jun Min and López-Lambertini, Paola M. and Lopez-Moya, Juan J. and Maclot, Francois and Mäkinen, Kristiina and Martin, Darren and Massart, Sebastien and Miller, W. Allen and Mohammadi, Musa and Mollov, Dimitre and Muller, Emmanuelle and Nagata, Tatsuya and Navas-Castillo, Jesús and Neriya, Yutaro and Ochoa-Corona, Francisco M. and Ohshima, Kazusato and Pallás, Vicente and Pappu, Hanu and Petrzik, Karel and Pooggin, Mikhail and Prigigallo, Maria Isabella and Ramos-González, Pedro L. and Ribeiro, Simone and Richert-Pöggeler, Katja R. and Roumagnac, Philippe and Roy, Avijit and Sabanadzovic, Sead and Šafářová, Dana and Saldarelli, Pasquale and Sanfaçon, Hélène and Sarmiento, Cecilia and Sasaya, Takahide and Scheets, Kay and Schravesande, Willem E.W. and Seal, Susan and Shimomoto, Yoshifumi and Sõmera, Merike and Stavolone, Livia and Stewart, Lucy R. and Teycheney, Pierre-Yves and Thomas, John E. and Thompson, Jeremy R. and Tiberini, Antonio and Tomitaka, Yasuhiro and Tzanetakis, Ioannis and Umber, Marie and Urbino, Cica and Van Den Burg, Harrold A. and Van Der Vlugt, René A.A. and Varsani, Arvind and Verhage, Adriaan and Villamor, Dan and Von Bargen, Susanne and Walker, Peter J. and Wetzel, Thierry and Whitfield, Anna E. and Wylie, Stephen J. and Yang, Caixia and Zerbini, F. Murilo and Zhang, Song and {ICTV Taxonomy Summary Consortium}},\n\tmonth = jul,\n\tyear = {2025},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Novel lineage of anelloviruses with large genomes identified in dolphins.\n \n \n \n \n\n\n \n De Koch, M. D.; Krupovic, M.; Fielding, R.; Smith, K.; Schiavone, K.; Hall, K. R.; Reid, V. S.; Boyea, D.; Smith, E. L.; Schmidlin, K.; Fontenele, R. S.; Koonin, E. V.; Martin, D. P.; Kraberger, S.; and Varsani, A.\n\n\n \n\n\n\n Journal of Virology, 99(1): e01370–24. January 2025.\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{de_koch_novel_2025,\n\ttitle = {Novel lineage of anelloviruses with large genomes identified in dolphins},\n\tvolume = {99},\n\tissn = {0022-538X, 1098-5514},\n\turl = {https://journals.asm.org/doi/10.1128/jvi.01370-24},\n\tdoi = {10.1128/jvi.01370-24},\n\tabstract = {ABSTRACT \n             \n               \n               \n                Anellovirus infections are ubiquitous in mammals but lack any clear disease association, suggesting a commensal virus-host relationship. Although anelloviruses have been identified in numerous mammalian hosts, their presence in members of the family Delphinidae has yet to be reported. Here, using a metagenomic approach, we characterize complete anellovirus genomes ( \n                n \n                = 69) from four Delphinidae host species: short-finned pilot whale ( \n                Globicephala macrorhynchus \n                , \n                n \n                = 19), killer whale ( \n                Orcinus orca \n                , \n                n \n                = 9), false killer whale ( \n                Pseudorca crassidens \n                , \n                n \n                = 6), and pantropical spotted dolphin ( \n                Steno attenuatus \n                , \n                n \n                = 1). Sequence comparison of the open reading frame 1 (ORF1) encoding the capsid protein, the only conserved gene shared by all anelloviruses, shows that the Delphinidae anelloviruses form a novel genus-level clade that encompasses 22 unique species-level groupings. We provide evidence that different Delphinidae species can be co-infected by multiple anelloviruses belonging to distinct species groupings. Notably, the ORF1 protein of the Delphinidae anelloviruses is considerably larger than those encoded by all previously described anelloviruses from other hosts (spanning 14 vertebrate orders and including 27 families). Comprehensive analysis of the ORF1 sequences and predicted protein structures showed that the increased size of these proteins results from divergent elaborations within the capsid-distal P2 subdomain and elongation of the C-terminal domain of ORF1. Comparative structural and phylogenetic analyses suggest that acquisition of the P2 subdomain and its diversification occurred convergently in the anelloviruses associated with primate and Delphinidae hosts. Collectively, our results further the appreciation of diversity and evolution of the ubiquitous and enigmatic viruses in the family \n                Anelloviridae \n                . \n               \n             \n             \n              IMPORTANCE \n               \n                Anelloviruses are ubiquitous in mammals, but their infection has not yet been linked to any disease, suggesting a commensal virus-host relationship. Here, we describe the first anelloviruses associated with diverse species of dolphins. The dolphinid anelloviruses represent a new genus (tentatively named “Qoptorquevirus”) and encode open reading frame 1 (ORF1) (capsid) proteins that are considerably larger than those encoded by previously described anelloviruses from other hosts. Comprehensive analysis of the ORF1 sequences and predicted protein structures revealed the underlying structural basis for such an extravagant ORF1 size and suggested that ORF1 size increased convergently in the anelloviruses associated with primate and Delphinidae hosts, respectively. Collectively, our results provide insights into the diversity and evolution of \n                Anelloviridae \n                . Further exploration of the anellovirus diversity, especially in the host species that have not yet been sampled, is expected to further clarify their evolutionary trajectory and explain the unusual virus-host commensal relationship. \n               \n             \n          ,  \n             \n              Anelloviruses are ubiquitous in mammals, but their infection has not yet been linked to any disease, suggesting a commensal virus-host relationship. Here, we describe the first anelloviruses associated with diverse species of dolphins. The dolphinid anelloviruses represent a new genus (tentatively named “Qoptorquevirus”) and encode open reading frame 1 (ORF1) (capsid) proteins that are considerably larger than those encoded by previously described anelloviruses from other hosts. Comprehensive analysis of the ORF1 sequences and predicted protein structures revealed the underlying structural basis for such an extravagant ORF1 size and suggested that ORF1 size increased convergently in the anelloviruses associated with primate and Delphinidae hosts, respectively. Collectively, our results provide insights into the diversity and evolution of \n              Anelloviridae \n              . Further exploration of the anellovirus diversity, especially in the host species that have not yet been sampled, is expected to further clarify their evolutionary trajectory and explain the unusual virus-host commensal relationship.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Journal of Virology},\n\tauthor = {De Koch, Matthew D. and Krupovic, Mart and Fielding, Russell and Smith, Kendal and Schiavone, Kelsie and Hall, Katharine R. and Reid, Vincent S. and Boyea, Diallo and Smith, Emma L. and Schmidlin, Kara and Fontenele, Rafaela S. and Koonin, Eugene V. and Martin, Darren P. and Kraberger, Simona and Varsani, Arvind},\n\teditor = {Van Doorslaer, Koenraad},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {e01370--24},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Anellovirus infections are ubiquitous in mammals but lack any clear disease association, suggesting a commensal virus-host relationship. Although anelloviruses have been identified in numerous mammalian hosts, their presence in members of the family Delphinidae has yet to be reported. Here, using a metagenomic approach, we characterize complete anellovirus genomes ( n = 69) from four Delphinidae host species: short-finned pilot whale ( Globicephala macrorhynchus , n = 19), killer whale ( Orcinus orca , n = 9), false killer whale ( Pseudorca crassidens , n = 6), and pantropical spotted dolphin ( Steno attenuatus , n = 1). Sequence comparison of the open reading frame 1 (ORF1) encoding the capsid protein, the only conserved gene shared by all anelloviruses, shows that the Delphinidae anelloviruses form a novel genus-level clade that encompasses 22 unique species-level groupings. We provide evidence that different Delphinidae species can be co-infected by multiple anelloviruses belonging to distinct species groupings. Notably, the ORF1 protein of the Delphinidae anelloviruses is considerably larger than those encoded by all previously described anelloviruses from other hosts (spanning 14 vertebrate orders and including 27 families). Comprehensive analysis of the ORF1 sequences and predicted protein structures showed that the increased size of these proteins results from divergent elaborations within the capsid-distal P2 subdomain and elongation of the C-terminal domain of ORF1. Comparative structural and phylogenetic analyses suggest that acquisition of the P2 subdomain and its diversification occurred convergently in the anelloviruses associated with primate and Delphinidae hosts. Collectively, our results further the appreciation of diversity and evolution of the ubiquitous and enigmatic viruses in the family Anelloviridae . IMPORTANCE Anelloviruses are ubiquitous in mammals, but their infection has not yet been linked to any disease, suggesting a commensal virus-host relationship. Here, we describe the first anelloviruses associated with diverse species of dolphins. The dolphinid anelloviruses represent a new genus (tentatively named “Qoptorquevirus”) and encode open reading frame 1 (ORF1) (capsid) proteins that are considerably larger than those encoded by previously described anelloviruses from other hosts. Comprehensive analysis of the ORF1 sequences and predicted protein structures revealed the underlying structural basis for such an extravagant ORF1 size and suggested that ORF1 size increased convergently in the anelloviruses associated with primate and Delphinidae hosts, respectively. Collectively, our results provide insights into the diversity and evolution of Anelloviridae . Further exploration of the anellovirus diversity, especially in the host species that have not yet been sampled, is expected to further clarify their evolutionary trajectory and explain the unusual virus-host commensal relationship. , Anelloviruses are ubiquitous in mammals, but their infection has not yet been linked to any disease, suggesting a commensal virus-host relationship. Here, we describe the first anelloviruses associated with diverse species of dolphins. The dolphinid anelloviruses represent a new genus (tentatively named “Qoptorquevirus”) and encode open reading frame 1 (ORF1) (capsid) proteins that are considerably larger than those encoded by previously described anelloviruses from other hosts. Comprehensive analysis of the ORF1 sequences and predicted protein structures revealed the underlying structural basis for such an extravagant ORF1 size and suggested that ORF1 size increased convergently in the anelloviruses associated with primate and Delphinidae hosts, respectively. Collectively, our results provide insights into the diversity and evolution of Anelloviridae . Further exploration of the anellovirus diversity, especially in the host species that have not yet been sampled, is expected to further clarify their evolutionary trajectory and explain the unusual virus-host commensal relationship.\n

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\n \n\n \n \n \n \n \n \n A Real-Time Urine Tenofovir Assay Improves Drug Adherence Among People With HIV With Prior Virologic Failure in a Randomized Controlled Trial.\n \n \n \n \n\n\n \n Van Zyl, G. U; Decloedt, E.; Jennings, L.; Kellermann, T.; Motha, K.; Van Schalkwyk, M.; Schreuder, C.; Coetzee, N.; Glidden, D. V; Orrell, C.; and Gandhi, M.\n\n\n \n\n\n\n Clinical Infectious Diseases, 81(5): e352–e359. December 2025.\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{van_zyl_real-time_2025,\n\ttitle = {A {Real}-{Time} {Urine} {Tenofovir} {Assay} {Improves} {Drug} {Adherence} {Among} {People} {With} {HIV} {With} {Prior} {Virologic} {Failure} in a {Randomized} {Controlled} {Trial}},\n\tvolume = {81},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1058-4838, 1537-6591},\n\turl = {https://academic.oup.com/cid/article/81/5/e352/8169862},\n\tdoi = {10.1093/cid/ciaf337},\n\tabstract = {Abstract \n             \n              Background \n              Scalable strategies to detect and address inadequate adherence to antiretroviral therapy (ART) are a high priority towards meeting UNAIDS 95-95-95 targets. A urine tenofovir rapid assay (UTRA) at the point-of-care improves adherence among pre-exposure prophylaxis recipients and virologic suppression (VS) in a pre-post study of people with HIV (PWH). Here, we conducted the first randomized trial of UTRA-enhanced adherence support vs standard of care among PWH. \n             \n             \n              Methods \n              Participants receiving dolutegravir (DTG)– or protease inhibitor (PI)–based ART were randomized to UTRA-enhanced adherence support (n = 100) vs standard of care (n = 100). The primary outcome was VS, HIV-1 RNA \\&lt;50 copies/mL, at 12-months and secondary outcome was VS at 6 months. To explore ART adherence over the preceding 6–8 weeks, tenofovir diphosphate (TFV-DP) in dried blood spots (DBS) was quantified. C-reactive protein (CRP) was measured as an inflammatory marker. \n             \n             \n              Results \n              At the 12-month visit, 59/80 (74\\%) in the intervention and 48/75 (64\\%) in the control arm achieved VS (the same proportion as at 6 months; P = .2); TFV-DP concentrations (median, IQR) in DBS were significantly higher in the intervention arm: 884 (491–1296) vs 598 (239–964) fmol/3-mm DBS punch in the control arm (P \\&lt; .01). Higher TFV-DP DBS concentrations correlated with a slight decrease in CRP (Spearman's rho = −0.19; P = .02). \n             \n             \n              Conclusions \n              UTRA-enhanced adherence support did not result in a significantly higher VS rate but was associated with increased TFV-DP in DBS—in turn, associated with lower CRP levels—suggesting that UTRA-enhanced adherence support improves long-term drug exposure and could also reduce HIV-associated inflammation. \n             \n             \n              Clinical Trials Registration \n              clinicaltrials.gov (https://clinicaltrials.gov/study/NCT05333679).},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-19},\n\tjournal = {Clinical Infectious Diseases},\n\tauthor = {Van Zyl, Gert U and Decloedt, Eric and Jennings, Lauren and Kellermann, Tracy and Motha, Khethiwe and Van Schalkwyk, Marije and Schreuder, Chantel and Coetzee, Nicola and Glidden, David V and Orrell, Catherine and Gandhi, Monica},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e352--e359},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The 96-week outcomes and pharmacokinetics of long-acting cabotegravir plus rilpivirine in South Africans.\n \n \n \n \n\n\n \n Mngqibisa, R.; Singh, Y.; Orrell, C.; Lombaard, J.; Griffith, S.; Harrington, C.; D’Amico, R.; Spreen, W.; St Clair, M.; Latham, C.; Garside, L.; Van Solingen-Ristea, R.; Van Eygen, V.; Addo Boateng, F.; Crauwels, H.; Eneh, P.; and Eshun-Wilsonova, I.\n\n\n \n\n\n\n Southern African Journal of HIV Medicine, 26(1): a1709. July 2025.\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{mngqibisa_96-week_2025,\n\ttitle = {The 96-week outcomes and pharmacokinetics of long-acting cabotegravir plus rilpivirine in {South} {Africans}},\n\tvolume = {26},\n\tissn = {1608-9693, 2078-6751},\n\turl = {https://sajhivmed.org.za/index.php/hivmed/article/view/1709},\n\tdoi = {10.4102/sajhivmed.v26i1.1709},\n\tabstract = {Background: Evaluating long-term efficacy, safety and pharmacokinetics of long-acting cabotegravir + rilpivirine (CAB+RPV LA) in sub-Saharan African populations is important because of the region’s unique demographics and antiretroviral therapy resistance patterns. \n \nObjectives: To describe the 96-week efficacy, safety and pharmacokinetics of CAB+RPV LA in South African participants from the pooled FLAIR and ATLAS-2M Phase 3/3b randomised studies. \n \nMethod: Primary endpoint: proportion of participants with plasma HIV-1 RNA levels ≥ 50 copies/mL at Week 96. Secondary endpoints: proportion of participants with plasma HIV-1 RNA levels {\\textless} 50 copies/mL, confirmed virological failure (CVF; two consecutive plasma HIV-1 RNA ≥ 200 copies/mL), adverse events and pharmacokinetics. \n \nResults: Sixty-six participants were included, (CAB+RPV LA, n = 49; current oral antiretroviral regimen [CAR], n = 17). Forty-five (92\\%) on CAB+RPV LA and 15 (88\\%) on CAR maintained HIV-1 RNA levels {\\textless} 50 copies/mL. At Week 96, two participants, one in each arm, had CVF. Ninety per cent on CAB+RPV LA and 76\\% on CAR of participants experienced an adverse event; six (12\\%) of which were drug-related (CAB+RPV LA: n = 6). Injection-site reactions were common (78\\% [Grade 1: 80\\%; Grade 2: 20\\%]). CAB and RPV trough plasma concentrations remained above respective in vitro protein-adjusted 90\\% inhibitory concentrations following all doses. \n \nConclusion: This subgroup analysis of South African participants demonstrated durable efficacy, acceptable safety profile and pharmacokinetics of injectable CAB+RPV LA up to 96 weeks, consistent with long-term data from other regions and studies.},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Southern African Journal of HIV Medicine},\n\tauthor = {Mngqibisa, Rosie and Singh, Yashna and Orrell, Catherine and Lombaard, Johan and Griffith, Sandy and Harrington, Conn and D’Amico, Ronald and Spreen, William and St Clair, Marty and Latham, Christine and Garside, Louise and Van Solingen-Ristea, Rodica and Van Eygen, Veerle and Addo Boateng, Fafa and Crauwels, Herta and Eneh, Prosperity and Eshun-Wilsonova, Ingrid},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {a1709},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Which trial do we need? A randomised controlled study to compare the protective efficacy of early post-exposure discontinuation versus standard atovaquone-proguanil malaria prophylaxis in a human Plasmodium falciparum challenge model.\n \n \n \n \n\n\n \n Schnyder, J. L.; De Jong, H. K.; Bache, E. B.; Van Hest, R. M.; Bélard, S.; Hanscheid, T.; Kremsner, P. G.; and Grobusch, M. P.\n\n\n \n\n\n\n Clinical Microbiology and Infection, 31(10): 1618–1622. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Which$ Paper\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{schnyder_which_2025,\n\ttitle = {Which trial do we need? {A} randomised controlled study to compare the protective efficacy of early post-exposure discontinuation versus standard atovaquone-proguanil malaria prophylaxis in a human {Plasmodium} falciparum challenge model},\n\tvolume = {31},\n\tissn = {1198743X},\n\tshorttitle = {Which trial do we need?},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1198743X25001867},\n\tdoi = {10.1016/j.cmi.2025.04.023},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-19},\n\tjournal = {Clinical Microbiology and Infection},\n\tauthor = {Schnyder, Jenny L. and De Jong, Hanna K. and Bache, Emmanuel B. and Van Hest, Reinier M. and Bélard, Sabine and Hanscheid, Thomas and Kremsner, Peter G. and Grobusch, Martin P.},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {1618--1622},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n NOS3 rs3918188C\\textgreaterA is associated with susceptibility to resistant hypertension while CES1 genetic variation was not associated with resistant hypertension among South Africans.\n \n \n \n \n\n\n \n Katsukunya, J. N.; Naicker, R.; Soko, N. D.; Blom, D.; Sinxadi, P.; Chimusa, E. R.; Rayner, B.; Jones, E.; and Dandara, C.\n\n\n \n\n\n\n Frontiers in Genetics, 16: 1608423. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"NOS3$ Paper\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_nos3_2025,\n\ttitle = {{NOS3} {rs3918188C}{\\textgreater}{A} is associated with susceptibility to resistant hypertension while {CES1} genetic variation was not associated with resistant hypertension among {South} {Africans}},\n\tvolume = {16},\n\tissn = {1664-8021},\n\turl = {https://www.frontiersin.org/articles/10.3389/fgene.2025.1608423/full},\n\tdoi = {10.3389/fgene.2025.1608423},\n\tabstract = {Introduction \n               \n                Genetic variation in genes coding for enzymes metabolising antihypertensive drugs, may affect the efficacy of angiotensin converting enzyme (ACE) inhibitors such as enalapril, potentially leading to resistant hypertension (RHTN). We set out to evaluate the contribution of genetic variation in \n                CES1 \n                and \n                NOS3 \n                genes on susceptibility to RHTN, as well as estimate the frequencies of \n                CES1 \n                copy number variation (CNV) in African and Mixed Ancestry (MA) populations of South Africa. \n               \n             \n             \n              Methods \n               \n                Using a retrospective age, sex and ethnicity matched case-control study design, 379 participants with hypertension belonging to the African and MA ethnic groups were recruited. Cases were participants with RHTN (i.e., blood pressure (BP) ≥140/90 mmHg on ≥3 antihypertensive drugs or BP \\&lt; 140/90 mmHg on \\&gt;3 antihypertensive drugs, including a diuretic). Cases were matched to controls with similar characteristics (age (±5 years), sex and ethnicity) in a 1:1 ratio. Controls were participants with hypertension that was under control (BP \\&lt; 140/90 mmHg on ≤3 antihypertensive drugs). Five polymorphisms in \n                CES1 \n                and \n                NOS3 \n                were characterized using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), quantitative PCR and validated using Sanger sequencing. The additive model of inheritance and multivariable logistic regression were used to determine associations between genotypes and RHTN while adjusting for potential confounding variables. \n               \n             \n             \n              Results and discussion \n               \n                NOS3 \n                rs3918188A/A (aOR: 0.13; CI: 0.04–0.41; P = 0.0009) genotype and \n                NOS3 \n                rs2070744–rs1798883–rs3918188G–T–A haplotype (OR: 0.54; CI: 0.37–0.78; P = 0.001) appeared to confer protection against RHTN among MA participants only. \n                CES1 \n                rs2244613C\\&gt;A and \n                CES1 \n                CNV were not significantly associated with RHTN. However, there appeared to be quantitative differences in \n                CES1 \n                CNV profiles across ethnic groups. We speculate that \n                NOS3 \n                rs3918188A allele may affect \n                NOS3 \n                gene expression, potentially leading to increased amounts of the vasodilator, nitric oxide (NO) and favourable outcomes in individuals taking antihypertensives drugs such as enalapril. \n               \n             \n             \n              Conclusion \n               \n                NOS3 \n                genetic variation seems important in the susceptibility to RHTN among Africans and requires further studies.},\n\turldate = {2026-05-19},\n\tjournal = {Frontiers in Genetics},\n\tauthor = {Katsukunya, Jonathan N. and Naicker, Revina and Soko, Nyarai D. and Blom, Dirk and Sinxadi, Phumla and Chimusa, Emile R. and Rayner, Brian and Jones, Erika and Dandara, Collet},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {1608423},\n}\n\n\n\n

\n

\n\n\n

\n Introduction Genetic variation in genes coding for enzymes metabolising antihypertensive drugs, may affect the efficacy of angiotensin converting enzyme (ACE) inhibitors such as enalapril, potentially leading to resistant hypertension (RHTN). We set out to evaluate the contribution of genetic variation in CES1 and NOS3 genes on susceptibility to RHTN, as well as estimate the frequencies of CES1 copy number variation (CNV) in African and Mixed Ancestry (MA) populations of South Africa. Methods Using a retrospective age, sex and ethnicity matched case-control study design, 379 participants with hypertension belonging to the African and MA ethnic groups were recruited. Cases were participants with RHTN (i.e., blood pressure (BP) ≥140/90 mmHg on ≥3 antihypertensive drugs or BP < 140/90 mmHg on >3 antihypertensive drugs, including a diuretic). Cases were matched to controls with similar characteristics (age (±5 years), sex and ethnicity) in a 1:1 ratio. Controls were participants with hypertension that was under control (BP < 140/90 mmHg on ≤3 antihypertensive drugs). Five polymorphisms in CES1 and NOS3 were characterized using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), quantitative PCR and validated using Sanger sequencing. The additive model of inheritance and multivariable logistic regression were used to determine associations between genotypes and RHTN while adjusting for potential confounding variables. Results and discussion NOS3 rs3918188A/A (aOR: 0.13; CI: 0.04–0.41; P = 0.0009) genotype and NOS3 rs2070744–rs1798883–rs3918188G–T–A haplotype (OR: 0.54; CI: 0.37–0.78; P = 0.001) appeared to confer protection against RHTN among MA participants only. CES1 rs2244613C>A and CES1 CNV were not significantly associated with RHTN. However, there appeared to be quantitative differences in CES1 CNV profiles across ethnic groups. We speculate that NOS3 rs3918188A allele may affect NOS3 gene expression, potentially leading to increased amounts of the vasodilator, nitric oxide (NO) and favourable outcomes in individuals taking antihypertensives drugs such as enalapril. Conclusion NOS3 genetic variation seems important in the susceptibility to RHTN among Africans and requires further studies.\n

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\n \n\n \n \n \n \n \n \n Graft Arteritis Due to Candida Spp. After Kidney Transplant: A Systematic Review of Individual Cases.\n \n \n \n \n\n\n \n Tirlangi, P. K.; Pothumarthy Venkata Swathi, K.; Prabhu, R. A.; Singh, G.; Barac, A.; Grobusch, M. P.; and Gupta, N.\n\n\n \n\n\n\n Open Forum Infectious Diseases, 12(10): ofaf554. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Graft$ Paper\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{tirlangi_graft_2025,\n\ttitle = {Graft {Arteritis} {Due} to \\textit{{Candida}} {Spp}. {After} {Kidney} {Transplant}: {A} {Systematic} {Review} of {Individual} {Cases}},\n\tvolume = {12},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2328-8957},\n\tshorttitle = {Graft {Arteritis} {Due} to \\textit{{Candida}} {Spp}. {After} {Kidney} {Transplant}},\n\turl = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofaf554/8246004},\n\tdoi = {10.1093/ofid/ofaf554},\n\tabstract = {Abstract \n             \n              Background \n              Graft arteritis due to Candida species (GAC) is a rare but life-threatening complication in kidney transplant recipients. This systematic review examines its clinical profile and outcomes. \n             \n             \n              Methods \n              A PRISMA-compliant systematic review was conducted. Cases of GAC in kidney transplant recipients were identified and analyzed for clinical characteristics and outcomes. \n             \n             \n              Results \n              Sixty-one patients from 31 studies were included. Median time to infection was 30 days (IQR: 12–60 days) post-transplant. Common symptoms included fever (41.5\\%) and abdominal pain (33.9\\%). Aneurysmal rupture occurred in 49.1\\%, often linked to early presentation. Surgical intervention, mainly external iliac artery ligation, was required in most cases. Mortality was 22.9\\% and was associated with candidemia and a significantly shorter interval between transplantation and clinical presentation. \n             \n             \n              Conclusions \n              GAC typically occurs early after kidney transplantation, with high rates of aneurysmal rupture and mortality.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-19},\n\tjournal = {Open Forum Infectious Diseases},\n\tauthor = {Tirlangi, Praveen Kumar and Pothumarthy Venkata Swathi, Kiran and Prabhu, Ravindra Attur and Singh, Gagandeep and Barac, Aleksandra and Grobusch, Martin Peter and Gupta, Nitin},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {ofaf554},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Incidence and prevalence of traumatic and non-traumatic wounds and burns and access to wound care in Sierra Leone; data from a nationwide household survey (PRESSCO) 2020.\n \n \n \n \n\n\n \n Vas Nunes, J. H.; Van Duinen, A. J.; Boateng, D.; Tommy, A. J.; Sankoh, O.; Grobusch, M. P.; and Bolkan, H. A.\n\n\n \n\n\n\n Heliyon, 11(1): e38693. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Incidence$ Paper\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{vas_nunes_incidence_2025,\n\ttitle = {Incidence and prevalence of traumatic and non-traumatic wounds and burns and access to wound care in {Sierra} {Leone}; data from a nationwide household survey ({PRESSCO}) 2020},\n\tvolume = {11},\n\tissn = {24058440},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S240584402414724X},\n\tdoi = {10.1016/j.heliyon.2024.e38693},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Heliyon},\n\tauthor = {Vas Nunes, Jonathan H. and Van Duinen, Alex J. and Boateng, Daniel and Tommy, Amidu J. and Sankoh, Osman and Grobusch, Martin P. and Bolkan, Håkon A.},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {e38693},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Southern African HIV Clinicians Society guideline on pre-exposure prophylaxis to prevent HIV.\n \n \n \n \n\n\n \n Macdonald, P.; Nair, G.; Wattrus, C.; Mullick, S.; Pleaner, M.; Rousseau, E.; Subedar, H.; Joseph-Davey, D.; Hugo, J.; Delany-Moretlwe, S.; and Bekker, L.\n\n\n \n\n\n\n Southern African Journal of HIV Medicine, 26(1): a1713. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Southern$ Paper\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{macdonald_southern_2025,\n\ttitle = {Southern {African} {HIV} {Clinicians} {Society} guideline on pre-exposure prophylaxis to prevent {HIV}},\n\tvolume = {26},\n\tissn = {1608-9693, 2078-6751},\n\turl = {https://sajhivmed.org.za/index.php/hivmed/article/view/1713},\n\tdoi = {10.4102/sajhivmed.v26i1.1713},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Southern African Journal of HIV Medicine},\n\tauthor = {Macdonald, Pippa and Nair, Gonasagrie and Wattrus, Camilla and Mullick, Saiqa and Pleaner, Melanie and Rousseau, Elzette and Subedar, Hasina and Joseph-Davey, Dvora and Hugo, Johan and Delany-Moretlwe, Sinead and Bekker, Linda-Gail},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {a1713},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Effect of long-term azithromycin treatment on gut microbial diversity in children and adolescents with HIV-associated chronic lung disease.\n \n \n \n \n\n\n \n Flygel, T. T.; Bargheet, A.; Abotsi, R. E.; Claassen-Weitz, S.; Simms, V.; Hjerde, E.; Mwaikono, K. S.; Mchugh, G.; Hameiri-Bowen, D.; Pettersen, V. K.; Ferrand, R. A.; Nicol, M.; Cavanagh, J. P.; Flaegstad, T.; and Sovershaeva, E.\n\n\n \n\n\n\n eBioMedicine, 118: 105832. August 2025.\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{flygel_effect_2025,\n\ttitle = {Effect of long-term azithromycin treatment on gut microbial diversity in children and adolescents with {HIV}-associated chronic lung disease},\n\tvolume = {118},\n\tissn = {23523964},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352396425002762},\n\tdoi = {10.1016/j.ebiom.2025.105832},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {eBioMedicine},\n\tauthor = {Flygel, Trym Thune and Bargheet, Ahmed and Abotsi, Regina Esinam and Claassen-Weitz, Shantelle and Simms, Victoria and Hjerde, Erik and Mwaikono, Kilaza Samson and Mchugh, Grace and Hameiri-Bowen, Dan and Pettersen, Veronika Kuchařová and Ferrand, Rashida Abbas and Nicol, Mark and Cavanagh, Jorunn Pauline and Flaegstad, Trond and Sovershaeva, Evgeniya},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {105832},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Safety and immunogenicity of investigational tuberculosis vaccine M72/AS01E–4 in people living with HIV in South Africa: an observer-blinded, randomised, controlled, phase 2 trial.\n \n \n \n \n\n\n \n Dagnew, A. F; Han, L. L; Naidoo, K.; Fairlie, L.; Innes, J. C; Middelkoop, K.; Tameris, M.; Wilkinson, R. J; Ananworanich, J.; Bower, D.; Schlehuber, L.; Frahm, N.; Cinar, A.; Dunne, M.; and Schmidt, A. C\n\n\n \n\n\n\n The Lancet HIV, 12(8): e546–e555. August 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{dagnew_safety_2025,\n\ttitle = {Safety and immunogenicity of investigational tuberculosis vaccine {M72}/{AS01E}–4 in people living with {HIV} in {South} {Africa}: an observer-blinded, randomised, controlled, phase 2 trial},\n\tvolume = {12},\n\tissn = {23523018},\n\tshorttitle = {Safety and immunogenicity of investigational tuberculosis vaccine {M72}/{AS01E}–4 in people living with {HIV} in {South} {Africa}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352301825001249},\n\tdoi = {10.1016/S2352-3018(25)00124-9},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet HIV},\n\tauthor = {Dagnew, Alemnew F and Han, Linda L and Naidoo, Kogieleum and Fairlie, Lee and Innes, James C and Middelkoop, Keren and Tameris, Michele and Wilkinson, Robert J and Ananworanich, Jintanat and Bower, Daniel and Schlehuber, Lisa and Frahm, Nicole and Cinar, Amy and Dunne, Michael and Schmidt, Alexander C},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {e546--e555},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Quantifying prevalence and risk factors of HIV multiple infection in Uganda from population-based deep-sequence data.\n \n \n \n \n\n\n \n Martin, M. A.; Brizzi, A.; Xi, X.; Galiwango, R. M.; Moyo, S.; Ssemwanga, D.; Blenkinsop, A.; Redd, A. D.; Abeler-Dörner, L.; Fraser, C.; Reynolds, S. J.; Quinn, T. C.; Kagaayi, J.; Bonsall, D.; Serwadda, D.; Nakigozi, G.; Kigozi, G.; Grabowski, M. K.; Ratmann, O.; with the PANGEA-HIV Consortium; and Program, t. R. H. S.\n\n\n \n\n\n\n PLOS Pathogens, 21(4): e1013065. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Quantifying$ Paper\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{martin_quantifying_2025,\n\ttitle = {Quantifying prevalence and risk factors of {HIV} multiple infection in {Uganda} from population-based deep-sequence data},\n\tvolume = {21},\n\tissn = {1553-7374},\n\turl = {https://dx.plos.org/10.1371/journal.ppat.1013065},\n\tdoi = {10.1371/journal.ppat.1013065},\n\tabstract = {People living with HIV can acquire secondary infections through a process called superinfection, giving rise to simultaneous infection with genetically distinct variants (multiple infection). Multiple infection provides the necessary conditions for the generation of novel recombinant forms of HIV and may worsen clinical outcomes and increase the rate of transmission to HIV seronegative sexual partners. To date, studies of HIV multiple infection have relied on insensitive bulk-sequencing, labor intensive single genome amplification protocols, or deep-sequencing of short genome regions. Here, we identified multiple infections in whole-genome or near whole-genome HIV RNA deep-sequence data generated from plasma samples of 2,029 people living with viremic HIV who participated in the population-based Rakai Community Cohort Study (RCCS). We estimated individual- and population-level probabilities of being multiply infected and assessed epidemiological risk factors using the novel Bayesian deep-phylogenetic multiple infection model ( \n              deep \n               −  \n              phyloMI \n              ) which accounts for bias due to partial sequencing success and false-negative and false-positive detection rates. We estimated that between 2010 and 2020, 4.09\\% (95\\% highest posterior density interval (HPD) 2.95\\%–5.45\\%) of RCCS participants with viremic HIV multiple infection at time of sampling. Participants living in high-HIV prevalence communities along Lake Victoria were 2.33-fold (95\\% HPD 1.3–3.7) more likely to harbor a multiple infection compared to individuals in lower prevalence neighboring communities. This work introduces a high-throughput surveillance framework for identifying people with multiple HIV infections and quantifying population-level prevalence and risk factors of multiple infection for clinical and epidemiological investigations.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-19},\n\tjournal = {PLOS Pathogens},\n\tauthor = {Martin, Michael A. and Brizzi, Andrea and Xi, Xiaoyue and Galiwango, Ronald Moses and Moyo, Sikhulile and Ssemwanga, Deogratius and Blenkinsop, Alexandra and Redd, Andrew D. and Abeler-Dörner, Lucie and Fraser, Christophe and Reynolds, Steven J. and Quinn, Thomas C. and Kagaayi, Joseph and Bonsall, David and Serwadda, David and Nakigozi, Gertrude and Kigozi, Godfrey and Grabowski, M. Kate and Ratmann, Oliver and {with the PANGEA-HIV Consortium and the Rakai Health Sciences Program}},\n\teditor = {Moore, Penny L.},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {e1013065},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Taurine transport is a critical modulator of ionic fluxes during NLRP3 inflammasome activation.\n \n \n \n \n\n\n \n Rossi-Smith, P.; Kim, J.; Skirlo, K.; Ferris, T.; Green, J. P.; Stek, C.; Huse, K. K.; Mortimer, P. M.; Olona, A.; Wieder, C.; Moseki, R.; Silva Dos Santos, M.; MacRae, J. I.; Sriskandan, S.; Ebbels, T. M.; Wilkinson, R. J.; Denton, A. E.; Matheson, N. J.; Anand, P. K.; Meintjes, G.; Thomas, D. C.; and Lai, R. P.\n\n\n \n\n\n\n Cell Reports, 44(10): 116317. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Taurine$ Paper\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{rossi-smith_taurine_2025,\n\ttitle = {Taurine transport is a critical modulator of ionic fluxes during {NLRP3} inflammasome activation},\n\tvolume = {44},\n\tissn = {22111247},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2211124725010885},\n\tdoi = {10.1016/j.celrep.2025.116317},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-19},\n\tjournal = {Cell Reports},\n\tauthor = {Rossi-Smith, Peter and Kim, Joohee and Skirlo, Kamil and Ferris, Trevor and Green, Jack P. and Stek, Cari and Huse, Kristin K. and Mortimer, Paige M. and Olona, Antoni and Wieder, Cecilia and Moseki, Raymond and Silva Dos Santos, Mariana and MacRae, James I. and Sriskandan, Shiranee and Ebbels, Timothy M.D. and Wilkinson, Robert J. and Denton, Alice E. and Matheson, Nicholas J. and Anand, Paras K. and Meintjes, Graeme and Thomas, David C. and Lai, Rachel P.J.},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {116317},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Implementation of a genotyped African population cohort, with virtual follow-up: A feasibility study in the Western Cape Province, South Africa.\n \n \n \n \n\n\n \n Tamuhla, T.; Coussens, A. K; Abrahams, M.; Blumenthal, M. J; Lakay, F.; Wilkinson, R. J; Riou, C.; Raubenheimer, P.; Dave, J. A; and Tiffin, N.\n\n\n \n\n\n\n Wellcome Open Research, 9: 620. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Implementation$ Paper\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{tamuhla_implementation_2025,\n\ttitle = {Implementation of a genotyped {African} population cohort, with virtual follow-up: {A} feasibility study in the {Western} {Cape} {Province}, {South} {Africa}},\n\tvolume = {9},\n\tissn = {2398-502X},\n\tshorttitle = {Implementation of a genotyped {African} population cohort, with virtual follow-up},\n\turl = {https://wellcomeopenresearch.org/articles/9-620/v2},\n\tdoi = {10.12688/wellcomeopenres.23009.2},\n\tabstract = {Background There is limited knowledge regarding African genetic drivers of disease due to prohibitive costs of large-scale genomic research in Africa. Methods We piloted a scalable virtual genotyped cohort in South Africa that was affordable in this resource-limited context, cost-effective, scalable virtual genotyped cohort in South Africa, with participant recruitment using a tiered informed consent model and DNA collection by buccal swab. Genotype data was generated using the H3Africa Illumina micro-array, and phenotype data was derived from routine health data of participants. We demonstrated feasibility of nested case control genome wide association studies using these data for phenotypes type 2 diabetes mellitus (T2DM) and severe COVID-19. Results 2267346 variants were analysed in 459 participant samples, of which 229 (66.8\\%) are female. 78.6\\% of SNPs and 74\\% of samples passed quality control (QC). Principal component analysis showed extensive ancestry admixture in study participants. Of the 343 samples that passed QC, 93 participants had T2DM and 63 had severe COVID-19. For 1780 previously published COVID-19-associated variants, 3 SNPs in the pre-imputation data and 23 SNPS in the imputed data were significantly associated with severe COVID-19 cases compared to controls (p{\\textless}0.05). For 2755 published T2DM associated variants, 69 SNPs in the pre-imputation data and 419 SNPs in the imputed data were significantly associated with T2DM cases when compared to controls (p{\\textless}0.05). Conclusions The results shown here are illustrative of what will be possible as the cohort expands in the future. Here we demonstrate the feasibility of this approach, recognising that the findings presented here are preliminary and require further validation once we have a sufficient sample size to improve statistical significance of findings. We implemented a genotyped population cohort with virtual follow up data in a resource-constrained African environment, demonstrating feasibility for scale up and novel health discoveries through nested case-control studies.},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {Wellcome Open Research},\n\tauthor = {Tamuhla, Tsaone and Coussens, Anna K and Abrahams, Maleeka and Blumenthal, Melissa J and Lakay, Francisco and Wilkinson, Robert J and Riou, Catherine and Raubenheimer, Peter and Dave, Joel A and Tiffin, Nicki},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {620},\n}\n\n\n\n

\n

\n\n\n

\n Background There is limited knowledge regarding African genetic drivers of disease due to prohibitive costs of large-scale genomic research in Africa. Methods We piloted a scalable virtual genotyped cohort in South Africa that was affordable in this resource-limited context, cost-effective, scalable virtual genotyped cohort in South Africa, with participant recruitment using a tiered informed consent model and DNA collection by buccal swab. Genotype data was generated using the H3Africa Illumina micro-array, and phenotype data was derived from routine health data of participants. We demonstrated feasibility of nested case control genome wide association studies using these data for phenotypes type 2 diabetes mellitus (T2DM) and severe COVID-19. Results 2267346 variants were analysed in 459 participant samples, of which 229 (66.8%) are female. 78.6% of SNPs and 74% of samples passed quality control (QC). Principal component analysis showed extensive ancestry admixture in study participants. Of the 343 samples that passed QC, 93 participants had T2DM and 63 had severe COVID-19. For 1780 previously published COVID-19-associated variants, 3 SNPs in the pre-imputation data and 23 SNPS in the imputed data were significantly associated with severe COVID-19 cases compared to controls (p\\textless0.05). For 2755 published T2DM associated variants, 69 SNPs in the pre-imputation data and 419 SNPs in the imputed data were significantly associated with T2DM cases when compared to controls (p\\textless0.05). Conclusions The results shown here are illustrative of what will be possible as the cohort expands in the future. Here we demonstrate the feasibility of this approach, recognising that the findings presented here are preliminary and require further validation once we have a sufficient sample size to improve statistical significance of findings. We implemented a genotyped population cohort with virtual follow up data in a resource-constrained African environment, demonstrating feasibility for scale up and novel health discoveries through nested case-control studies.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Pulmonary tuberculosis in a rural hospital in Sierra Leone.\n \n \n \n \n\n\n \n Rottmann, H.; Olaru, I. D.; Kanu, E. M.; Theiler, T.; Kargbo, I. M.; Kelling, E.; Kalkman, L.; Grobusch, M. P.; and Schaumburg, F.\n\n\n \n\n\n\n New Microbes and New Infections, 64: 101570. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Pulmonary$ Paper\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{rottmann_pulmonary_2025,\n\ttitle = {Pulmonary tuberculosis in a rural hospital in {Sierra} {Leone}},\n\tvolume = {64},\n\tissn = {20522975},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2052297525000083},\n\tdoi = {10.1016/j.nmni.2025.101570},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {New Microbes and New Infections},\n\tauthor = {Rottmann, Henning and Olaru, Ioana D. and Kanu, Emmanuel Marx and Theiler, Tom and Kargbo, Islam M. and Kelling, Emil and Kalkman, Laura and Grobusch, Martin P. and Schaumburg, Frieder},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {101570},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n An Integrative Genotyping and Gene Expression Profiling of the Mutated Human FAM111B Gene and Fibrosis‐Associated Pathway in the POIKTMP Syndrome.\n \n \n \n \n\n\n \n Tambwe, N.; Sinkala, M.; Oluwole, O. G.; Khumalo, N. P.; and Arowolo, A.\n\n\n \n\n\n\n Journal of Cellular and Molecular Medicine, 29(19): e70871. October 2025.\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

\n

@article{tambwe_integrative_2025,\n\ttitle = {An {Integrative} {Genotyping} and {Gene} {Expression} {Profiling} of the {Mutated} {Human} \\textit{{FAM111B}} {Gene} and {Fibrosis}‐{Associated} {Pathway} in the {POIKTMP} {Syndrome}},\n\tvolume = {29},\n\tissn = {1582-1838, 1582-4934},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/jcmm.70871},\n\tdoi = {10.1111/jcmm.70871},\n\tabstract = {ABSTRACT \n             \n              Poikiloderma with tendon contracture, myopathy and pulmonary fibrosis (POIKTMP) is a rare hereditary disorder caused by mutations in the \n              FAM111B \n              gene, characterised by multi‐organ fibrosis, particularly affecting the lungs. This study investigates the molecular mechanisms of fibrosis in POIKTMP through genotyping and gene expression profiling of \n              FAM111B \n              and associated fibrotic pathways. Post‐mortem formalin‐fixed paraffin‐embedded (FFPE) tissues from a POIKTMP patient and healthy controls were analysed. Genomic DNA was extracted, confirming the \n              FAM111B Y621D \n              mutation via Sanger sequencing. RT‐qPCR and the RT \n              2 \n              Profiler PCR Array were used to evaluate fibrosis‐related gene expression in lung and skin tissues. Disease and pathway enrichment analyses were conducted using Metascape, GeneMANIA and Enrichr tools. The \n              FAM111B Y621D \n              mutation was validated, and gene expression profiling revealed significant upregulation of fibrotic markers, such as \n              TGFβ‐3, PDGFA, ITGB1, MMP3, MMP13 \n              and \n              CCN2 \n              in the lungs, and \n              COL3A1 \n              and \n              THBS2 \n              in the skin. Pathway enrichment analysis linked FAM111B to extracellular matrix remodelling, cell adhesion, and cancer. These findings suggest that \n              FAM111B \n              mutations drive fibrosis through dysregulated gene networks, highlighting potential therapeutic targets for POIKTMP and related fibrotic diseases. Further research is required to understand \n              FAM111B \n              's role in fibrosis fully.},\n\tlanguage = {en},\n\tnumber = {19},\n\turldate = {2026-05-19},\n\tjournal = {Journal of Cellular and Molecular Medicine},\n\tauthor = {Tambwe, Nadine and Sinkala, Musalula and Oluwole, Oluwafemi G. and Khumalo, Nonhlanhla P. and Arowolo, Afolake},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {e70871},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Disruption of riboflavin biosynthesis in mycobacteria establishes riboflavin pathway intermediates as key precursors of MAIT cell agonists.\n \n \n \n \n\n\n \n Chengalroyen, M. D.; Oketade, N.; Worley, A.; Lucas, M.; Ramirez, L. M. N.; Raphela, M. L.; Swarbrick, G. M.; Soma, P. S.; Zuma, M.; Warner, D. F.; Lewinsohn, D. A.; Mehaffy, C.; Adams, E. J.; Hildebrand, W.; Dobos, K. M.; Mizrahi, V.; and Lewinsohn, D. M.\n\n\n \n\n\n\n PLOS Pathogens, 21(7): e1012632. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Disruption$ Paper\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{chengalroyen_disruption_2025,\n\ttitle = {Disruption of riboflavin biosynthesis in mycobacteria establishes riboflavin pathway intermediates as key precursors of {MAIT} cell agonists},\n\tvolume = {21},\n\tissn = {1553-7374},\n\turl = {https://dx.plos.org/10.1371/journal.ppat.1012632},\n\tdoi = {10.1371/journal.ppat.1012632},\n\tabstract = {Mucosal-associated invariant T (MAIT) cells exhibit an intrinsic ability to recognize and respond to microbial infections. The semi-invariant antigen recognition receptor of MAIT cells specifically detects the non-polymorphic antigen-presenting molecule, major histocompatibility complex class I-related protein 1 (MR1), which primarily binds riboflavin-derived metabolites of microbial origin. To further interrogate the dependence of these antigens on riboflavin biosynthesis in mycobacteria, we deleted individual genes in the riboflavin biosynthesis pathways in \n              Mycobacterium smegmatis \n              (Msm) and \n              Mycobacterium tuberculosis \n              (Mtb) and evaluated the impact thereof on MAIT cell activation. Blocking the early steps of the pathway by deletion of RibA2 or RibG profoundly reduced, but did not completely ablate, MAIT cell activation by Msm or Mtb, whereas deletion of RibC, which catalyzes the last step in the pathway, had no significant effect. Interestingly, deletion of the lumazine synthase (RibH) specifically enhanced MAIT cell recognition of Mtb whereas loss of lumazine synthase activity had no impact on MAIT cell activation by Msm. MAIT cell activation by Msm was likewise unaffected by blocking the production of the MAIT cell antagonist, F \n              o \n              (by inhibiting its conversion from the riboflavin pathway intermediate, 5-amino-6-D-ribitylaminouracil (5-A-RU), through the deletion of \n              fbiC \n              ). Together, these results confirm a central role for 5-A-RU in generating mycobacterial MR1 ligands and reveal similarities and differences between Msm and Mtb in terms of the impact of riboflavin pathway disruption on MAIT cell activation.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-19},\n\tjournal = {PLOS Pathogens},\n\tauthor = {Chengalroyen, Melissa D. and Oketade, Nurudeen and Worley, Aneta and Lucas, Megan and Ramirez, Luisa Maria Nieto and Raphela, Mabule L. and Swarbrick, Gwendolyn M. and Soma, Paul S. and Zuma, Mandisa and Warner, Digby F. and Lewinsohn, Deborah A. and Mehaffy, Carolina and Adams, Erin J. and Hildebrand, William and Dobos, Karen M. and Mizrahi, Valerie and Lewinsohn, David M.},\n\teditor = {Prince, Alice},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {e1012632},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Helminth-induced prostaglandin signaling and dietary shifts in PUFA metabolism promote colitis-associated cancer.\n \n \n \n \n\n\n \n Smith, K. A.; Reed, E. K.; Guschina, I.; Tyrrell, V. J.; Butters, C.; Darby, M. G.; Katsandegwaza, B.; Chetty, A.; Horsnell, W. G.; O’Donnell, V. B.; and Gallimore, A.\n\n\n \n\n\n\n Journal of Lipid Research, 66(7): 100837. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Helminth-induced$ Paper\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{smith_helminth-induced_2025,\n\ttitle = {Helminth-induced prostaglandin signaling and dietary shifts in {PUFA} metabolism promote colitis-associated cancer},\n\tvolume = {66},\n\tissn = {00222275},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0022227525000975},\n\tdoi = {10.1016/j.jlr.2025.100837},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-19},\n\tjournal = {Journal of Lipid Research},\n\tauthor = {Smith, Katherine A. and Reed, Ella K. and Guschina, Irina and Tyrrell, Victoria J. and Butters, Claire and Darby, Matthew G. and Katsandegwaza, Brunette and Chetty, Alisha and Horsnell, William G.C. and O’Donnell, Valerie B. and Gallimore, Awen},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {100837},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A Phosphoproteomic Analysis of Mycobacterial PknG-Mediated Host Immune Evasion.\n \n \n \n \n\n\n \n Baros-Steyl, S. S.; Nakedi, K. C.; Ganief, T. A.; Soares, N. C.; and Blackburn, J. M.\n\n\n \n\n\n\n Journal of Proteome Research, 24(11): 5585–5603. November 2025.\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{baros-steyl_phosphoproteomic_2025,\n\ttitle = {A {Phosphoproteomic} {Analysis} of {Mycobacterial} {PknG}-{Mediated} {Host} {Immune} {Evasion}},\n\tvolume = {24},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1535-3893, 1535-3907},\n\turl = {https://pubs.acs.org/doi/10.1021/acs.jproteome.5c00416},\n\tdoi = {10.1021/acs.jproteome.5c00416},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-19},\n\tjournal = {Journal of Proteome Research},\n\tauthor = {Baros-Steyl, Seanantha S. and Nakedi, Kehilwe C. and Ganief, Tariq A. and Soares, Nelson C. and Blackburn, Jonathan M.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {5585--5603},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Long COVID prevalence and risk factors in adults residing in middle- and high-income countries: secondary analysis of the multinational Anti-Coronavirus Therapies (ACT) trials.\n \n \n \n \n\n\n \n Hermans, L. E.; Wasserman, S.; Xu, L.; and Eikelboom, J.\n\n\n \n\n\n\n BMJ Global Health, 10(4): e017126. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Long$ Paper\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{hermans_long_2025,\n\ttitle = {Long {COVID} prevalence and risk factors in adults residing in middle- and high-income countries: secondary analysis of the multinational {Anti}-{Coronavirus} {Therapies} ({ACT}) trials},\n\tvolume = {10},\n\tissn = {2059-7908},\n\tshorttitle = {Long {COVID} prevalence and risk factors in adults residing in middle- and high-income countries},\n\turl = {https://gh.bmj.com/lookup/doi/10.1136/bmjgh-2024-017126},\n\tdoi = {10.1136/bmjgh-2024-017126},\n\tabstract = {Background \n              During the recent COVID-19 pandemic, reports of long-term persistence or recurrence of symptoms after SARS-CoV-2 infection emerged, which are now collectively referred to as ‘long COVID’. Most descriptions of long COVID originate from patients residing in high-income countries. We set out to characterise long COVID in a large-scale clinical trial that was conducted in low-middle, high-middle and high-income countries. \n             \n             \n              Methods \n              The Anti-Coronavirus Therapies trials enrolled 6528 adult patients with symptomatic COVID-19 in Argentina, Brazil, Canada, Colombia, Ecuador, Egypt, India, Nepal, Pakistan, Philippines, Russia, Saudi Arabia, South Africa and the United Arab Emirates. Long COVID was defined as the presence of patient-reported symptoms at 180 days after enrolment. Multivariable logistic regression was used to evaluate associations of baseline characteristics with long COVID. \n             \n             \n              Results \n              Of 4697 included participants, 1181 (25.1\\%) reported long COVID symptoms. The most frequently reported symptoms were sleeping disorders (n=601; 12.8\\%), joint pain (n=461; 9.8\\%), fatigue (n=410; 8.7\\%) and headaches (n=382; 8.1\\%). Long COVID prevalence was higher in participants from lower middle-income compared with high-income countries (29.8\\% (850/2854) vs 14.4\\% (102/706); adjusted OR (aOR) 1.53 (1.10 to 2.14); p=0.012). Prevalence also varied between participants of different ethnic backgrounds and was highest (36.1\\% (775/2145)) for patients of Arab/North African ethnicity. Patients requiring inpatient admission were at increased risk of long COVID (aOR: 2.04 (1.63 to 2.54); p{\\textless}0.001). Other independent predictors of long COVID were male sex, older age and hypertension. Vaccination, prior lung disease, smoking and diabetes mellitus conferred protective effects. \n             \n             \n              Conclusion \n              Symptoms of long COVID are reported in a quarter of cases of symptomatic COVID-19 in this study and were significantly more prevalent in participants from countries with lower income status and in patients of Arab/North African ethnicity. Research to further assess the health burden posed by long COVID in low- and middle-income countries is urgently needed.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-19},\n\tjournal = {BMJ Global Health},\n\tauthor = {Hermans, Lucas Etienne and Wasserman, Sean and Xu, Lizhen and Eikelboom, John},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {e017126},\n}\n\n\n\n

\n

\n\n\n

\n Background During the recent COVID-19 pandemic, reports of long-term persistence or recurrence of symptoms after SARS-CoV-2 infection emerged, which are now collectively referred to as ‘long COVID’. Most descriptions of long COVID originate from patients residing in high-income countries. We set out to characterise long COVID in a large-scale clinical trial that was conducted in low-middle, high-middle and high-income countries. Methods The Anti-Coronavirus Therapies trials enrolled 6528 adult patients with symptomatic COVID-19 in Argentina, Brazil, Canada, Colombia, Ecuador, Egypt, India, Nepal, Pakistan, Philippines, Russia, Saudi Arabia, South Africa and the United Arab Emirates. Long COVID was defined as the presence of patient-reported symptoms at 180 days after enrolment. Multivariable logistic regression was used to evaluate associations of baseline characteristics with long COVID. Results Of 4697 included participants, 1181 (25.1%) reported long COVID symptoms. The most frequently reported symptoms were sleeping disorders (n=601; 12.8%), joint pain (n=461; 9.8%), fatigue (n=410; 8.7%) and headaches (n=382; 8.1%). Long COVID prevalence was higher in participants from lower middle-income compared with high-income countries (29.8% (850/2854) vs 14.4% (102/706); adjusted OR (aOR) 1.53 (1.10 to 2.14); p=0.012). Prevalence also varied between participants of different ethnic backgrounds and was highest (36.1% (775/2145)) for patients of Arab/North African ethnicity. Patients requiring inpatient admission were at increased risk of long COVID (aOR: 2.04 (1.63 to 2.54); p\\textless0.001). Other independent predictors of long COVID were male sex, older age and hypertension. Vaccination, prior lung disease, smoking and diabetes mellitus conferred protective effects. Conclusion Symptoms of long COVID are reported in a quarter of cases of symptomatic COVID-19 in this study and were significantly more prevalent in participants from countries with lower income status and in patients of Arab/North African ethnicity. Research to further assess the health burden posed by long COVID in low- and middle-income countries is urgently needed.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Comparative insight: hereditary colorectal cancer registries in Iran, Singapore, and South Africa.\n \n \n \n \n\n\n \n Goshayeshi, L.; Eu, E. W.; Ramesar, R.; Goldberg, P.; Tan, Y. B.; Algar, U.; Manisekaran, R. G.; Li, S.; Caeser, R.; Boutall, A.; Goshayeshi, L.; Monahan, K. J.; and Ngeow, J.\n\n\n \n\n\n\n Familial Cancer, 24(4): 70. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Comparative$ Paper\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{goshayeshi_comparative_2025,\n\ttitle = {Comparative insight: hereditary colorectal cancer registries in {Iran}, {Singapore}, and {South} {Africa}},\n\tvolume = {24},\n\tissn = {1573-7292},\n\tshorttitle = {Comparative insight},\n\turl = {https://link.springer.com/10.1007/s10689-025-00494-4},\n\tdoi = {10.1007/s10689-025-00494-4},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-19},\n\tjournal = {Familial Cancer},\n\tauthor = {Goshayeshi, Ladan and Eu, Ernest Wencong and Ramesar, Raj and Goldberg, Paul and Tan, Yu Bin and Algar, Ursula and Manisekaran, Rutharra Ghayadthri and Li, Shao-Tzu and Caeser, Rebecca and Boutall, Adam and Goshayeshi, Lena and Monahan, Kevin J. and Ngeow, Joanne},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {70},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Ten simple rules for building and maintaining sustainable high-performance computing infrastructure for research in resource-limited settings.\n \n \n \n \n\n\n \n Galiwango, R.; Whalen, C. J.; Kebirungi, G.; Atwine, M. T.; Kimera, R.; Ssekagiri, A.; Kimbowa, T. W.; Lukyamuzi, E.; Nsubuga, M.; eLwazi ODSP; Ssentongo, L.; Mutegeki, H.; Fonner, J. M.; Wuerthwein, F.; Berman, A.; Okalebo, L. B.; McCarthy, M.; Kramer, V. S.; Quinones, M.; Cruz, P.; Hurt, D.; Giovanni, M. Y.; Mulder, N.; Tartakovsky, M.; Kayondo, J.; and Jjingo, D.\n\n\n \n\n\n\n PLOS Computational Biology, 21(9): e1013481. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Ten$ Paper\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{galiwango_ten_2025,\n\ttitle = {Ten simple rules for building and maintaining sustainable high-performance computing infrastructure for research in resource-limited settings},\n\tvolume = {21},\n\tissn = {1553-7358},\n\turl = {https://dx.plos.org/10.1371/journal.pcbi.1013481},\n\tdoi = {10.1371/journal.pcbi.1013481},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-19},\n\tjournal = {PLOS Computational Biology},\n\tauthor = {Galiwango, Ronald and Whalen, Christopher J. and Kebirungi, Grace and Atwine, Mugume T. and Kimera, Rodgers and Ssekagiri, Alfred and Kimbowa, Timothy W. and Lukyamuzi, Edward and Nsubuga, Mike and {eLwazi ODSP} and Ssentongo, Lloyd and Mutegeki, Henry and Fonner, John M. and Wuerthwein, Frank and Berman, Ari and Okalebo, Laura B. and McCarthy, Meghan and Kramer, Victor S. and Quinones, Mariam and Cruz, Phillip and Hurt, Darrell and Giovanni, Maria Y. and Mulder, Nicola and Tartakovsky, Michael and Kayondo, Jonathan and Jjingo, Daudi},\n\teditor = {Markel, Scott},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {e1013481},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Reduced plasma levels of GM-CSF is a common feature of Schistosoma mansoni-infected school-aged children.\n \n \n \n \n\n\n \n Kamdem, S. D.; Kamguia, L. M.; Oumarou, A.; Bitye, B. M. Z.; Lennard, K.; Brombacher, F.; Spangenberg, T.; Demarta-Gatsi, C.; and Nono, J. K.\n\n\n \n\n\n\n Frontiers in Immunology, 16: 1474575. February 2025.\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 abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{kamdem_reduced_2025,\n\ttitle = {Reduced plasma levels of {GM}-{CSF} is a common feature of {Schistosoma} mansoni-infected school-aged children},\n\tvolume = {16},\n\tissn = {1664-3224},\n\turl = {https://www.frontiersin.org/articles/10.3389/fimmu.2025.1474575/full},\n\tdoi = {10.3389/fimmu.2025.1474575},\n\tabstract = {Background \n              Currently available schistosomiasis diagnostic and monitoring tools are limited, and the development of novel technologies is necessary to enhance disease diagnostic and surveillance by supporting elimination efforts. Novel disease-specific biomarkers can facilitate the development of these technologies. Through the comparison of parasite burden and host factors, we assessed whether host plasma cytokines could be used as robust biomarkers for intestinal schistosomiasis and associated pathology in school-aged children (SAC) living in endemic areas. \n             \n             \n              Methods \n              Levels of host plasma cytokines were measured in SAC from a low-to-moderate burden region five months deworming with praziquantel, using Luminex assay for exploration analysis and ELISA for validation. \n             \n             \n              Results \n               \n                The concentration of GM-CSF, IL-2, and VEGF in plasma was significantly lower in schistosome-infected compared to non-infected children, as determined by Luminex assay. Further evaluation by ELISA revealed a negative correlation between GM-CSF plasma levels, but not those of IL-2 or VEGF, and \n                S. mansoni \n                egg burdens in infected individuals. Common coinfections in the study area such as geohelminths, hepatitis or malaria failed to alter plasma GM-CSF levels arguing in favor of a potential specific effect of \n                S. mansoni \n                infection on this cytokine. Receiver operating characteristic analysis confirmed GM-CSF as an acceptable predictive marker of \n                S. mansoni \n                infection, with an area under the curve (AUC) of 75\\%. Finally, the adjunct use of plasmatic GM-CSF thresholds for screening \n                S. mansoni \n                at-risk children and identify \n                S. mansoni \n                -infected ones increased the sensitivity of a single Kato-Katz test by averagely 15\\%. \n               \n             \n             \n              Conclusions \n               \n                Our findings highlight the potential of using plasma GM-CSF levels to biomark \n                S. mansoni \n                infection and improve the sensitivity of single Kato-Katz based diagnostic for low- to-moderate burden infections.},\n\turldate = {2026-05-19},\n\tjournal = {Frontiers in Immunology},\n\tauthor = {Kamdem, Severin Donald and Kamguia, Leonel Meyo and Oumarou, Alim and Bitye, Bernard Marie Zambo and Lennard, Katie and Brombacher, Frank and Spangenberg, Thomas and Demarta-Gatsi, Claudia and Nono, Justin Komguep},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {1474575},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Population pharmacokinetics of ritonavir as a booster of lopinavir, atazanavir, or darunavir in African children with HIV.\n \n \n \n \n\n\n \n Tsirizani, L.; Waalewijn, H.; Szubert, A.; Mulenga, V.; Chabala, C.; Bwakura-Dangarembizi, M.; Chitsamatanga, M.; Rutebarika, D. A.; Musiime, V.; Kasozi, M.; Lugemwa, A.; McIlleron, H. M.; Burger, D. M.; Gibb, D. M.; Colbers, A.; Denti, P.; Wasmann, R. E.; the CHAPAS-4 trial team; 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, N.; Au, C.; Sweeney, H.; Cissy, U.; Musiime, V.; Natukunda, E.; Nambi, E.; Rutebarika, 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, P.; Ankunda, J.; Naabalamba, M.; Nannungi, M.; Musiime, A.; Mbasani, F.; Enoch, B.; Namusanje, J.; Odoch, D.; Bagirigomwa, E.; Rubanga, E.; Mulima, D.; Oronon, P.; David, E.; Baliruno, D.; Kobusingye, J.; Uyungrwoth, A.; Mukanza, B.; Okello, J.; Ninsiima, E.; Ezra, L.; Nambi, C.; Mangadalen, N.; Sharif, M.; Nobert, B.; Thomas, O.; Abbas, U.; Makumbi, S.; Musumba, S.; Mawejje, E.; Yawe, I.; Jovia, L.; Kasozi, M.; Ankunda, R.; Kariisa, S.; Inyakuwa, C.; Ninsiima, E.; Atwine, L.; Tumusiime, B.; Ahuura, J.; Tukwasibwe, D.; Nagasha, V.; Kukundakwe, J.; Zahara, M.; Winnie, R.; Tukamushaba, M.; Baker, R.; Keminyeto, E.; Ainebyoona, B.; Myalo, S.; Acen, J.; Jinta, N.; Natuhurira, I.; Kananura, G.; Veronica, Z.; Chabala, C.; Chipili, J.; Kapasa, M.; Zyambo, K.; Zimba, K.; Zangata, D.; Shingalili, E.; and Mumba, N.\n\n\n \n\n\n\n Antimicrobial Agents and Chemotherapy, 69(11): e00771–25. November 2025.\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{tsirizani_population_2025,\n\ttitle = {Population pharmacokinetics of ritonavir as a booster of lopinavir, atazanavir, or darunavir in {African} children with {HIV}},\n\tvolume = {69},\n\tissn = {0066-4804, 1098-6596},\n\turl = {https://journals.asm.org/doi/10.1128/aac.00771-25},\n\tdoi = {10.1128/aac.00771-25},\n\tabstract = {ABSTRACT \n             \n               \n              Ritonavir is important in antiretroviral therapy (ART) because it is used to \n                        boost the drug exposure of its fellow protease inhibitors (PIs). While PIs \n                        are commonly used in children, ritonavir data in this population are quite \n                        scarce. We investigated the population pharmacokinetics of ritonavir given \n                        to boost exposures of lopinavir, atazanavir, or darunavir, and \n                        co-administered with nucleoside reverse transcriptase inhibitors (NRTIs) in \n                        African children, and investigated factors affecting its exposure. We \n                        conducted a pharmacokinetic sub-study within the CHAPAS-4 (ISRCTN22964075) \n                        trial, which randomized children to two NRTIs with twice-daily \n                        lopinavir/ritonavir, once-daily atazanavir/ritonavir, or once-daily \n                        darunavir/ritonavir, as second-line ART. Intensive pharmacokinetic blood \n                        samples were collected at week 6, and nonlinear mixed-effects modeling was \n                        used to identify factors affecting ritonavir pharmacokinetics. In all, 170 \n                        children were enrolled in the ritonavir-boosted PI arms of the CHAPAS-4 \n                        pharmacokinetic sub-study, with median age 10.6 (range 3.2–15.6) \n                        years and weight 26.0 (14.2–64.2) kg. Despite similar dose levels, \n                        ritonavir exposure varied widely depending on the companion PI. Compared to \n                        children on darunavir/ritonavir, those on atazanavir/ritonavir had 137\\% (95\\% \n                        CI 107\\%–190\\%) higher bioavailability and 20\\% (95\\% CI \n                        11.3\\%–31.3\\%) faster clearance, while those on lopinavir/ritonavir had \n                        23.4\\% (95\\% CI 8.20\\%–34.4\\%) lower bioavailability. No effect of NRTIs \n                        on ritonavir pharmacokinetics was observed. Ritonavir exposure is higher \n                        with atazanavir than with lopinavir or darunavir. These data provide greater \n                        insight into the use of ritonavir for boosting PIs in children and help \n                        reduce the knowledge gap regarding its exposure in children.},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-19},\n\tjournal = {Antimicrobial Agents and Chemotherapy},\n\tauthor = {Tsirizani, Lufina 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 McIlleron, Helen M. and Burger, David M. and Gibb, Diana M. and Colbers, Angela and Denti, Paolo and Wasmann, Roeland E. and {the CHAPAS-4 trial team} 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, Nadine and Au, Carly and Sweeney, Hannah and Cissy, Uganda and Musiime, Victor and Natukunda, Eva and Nambi, Esether and Rutebarika, 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, Phyllis and Ankunda, Juliet and Naabalamba, Mariam and Nannungi, Mary and Musiime, Alex and Mbasani, Faith and Enoch, Babu and Namusanje, Josephine and Odoch, Denis and Bagirigomwa, Edward and Rubanga, Eddie and Mulima, Disan and Oronon, Paul and David, 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 Nobert, B. and Thomas, Otim and Abbas, Uganda and Makumbi, Shafic and Musumba, Sharif and Mawejje, Edward and Yawe, Ibrahim and Jovia, 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, Mariam and Winnie, Ritah and Tukamushaba, Mercy and Baker, Rubinga and Keminyeto, Edridah and Ainebyoona, Barbara and Myalo, Sula and Acen, Juliet and Jinta, Nicholas and Natuhurira, Ian and Kananura, Gershom and Veronica, Zambia and Chabala, Chishala and Chipili, Joyce and Kapasa, Monica and Zyambo, Khonzya and Zimba, Kevin and Zangata, Dorothy and Shingalili, Ellen and Mumba, Naomi},\n\teditor = {Groll, Andreas H.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {e00771--25},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Rethinking BCG vaccine delivery for enhanced efficacy: Are two distinct routes of BCG administration better than one?.\n \n \n \n \n\n\n \n Moseki, R. M.; and Chengalroyen, M. D.\n\n\n \n\n\n\n hLife, 3(2): 61–63. February 2025.\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

\n

@article{moseki_rethinking_2025,\n\ttitle = {Rethinking {BCG} vaccine delivery for enhanced efficacy: {Are} two distinct routes of {BCG} administration better than one?},\n\tvolume = {3},\n\tissn = {29499283},\n\tshorttitle = {Rethinking {BCG} vaccine delivery for enhanced efficacy},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2949928324001007},\n\tdoi = {10.1016/j.hlife.2024.12.002},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {hLife},\n\tauthor = {Moseki, Raymond Moeketsi and Chengalroyen, Melissa Dalcina},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {61--63},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Effectiveness of the primary Bacillus Calmette-Guérin vaccine against the risk of Mycobacterium tuberculosis infection and tuberculosis disease: a meta-analysis of individual participant data.\n \n \n \n \n\n\n \n Pelzer, P. T; Stuck, L.; Martinez, L.; Richards, A. S; Acuña-Villaorduña, C.; Aronson, N. E; Bonnet, M.; Carvalho, A. C; Chan, P.; Huang, L.; Fang, C.; Churchyard, G.; Corral-Londoño, H. D.; Datta, M.; Espinal, M. A; Fielding, K.; Fiore-Gartland, A. J; Garcia-Basteiro, A.; Hanekom, W.; Hatherill, M.; Hill, P. C; Huerga, H.; Jones-López, E. C; Kritski, A.; Mandalakas, A. M; Mangtani, P.; Martins Netto, E.; Mayanja, H.; Mazahir, R.; Murray, M.; Rangaka, M.; Scriba, T.; Singh, J.; Singh, S.; Stein, C. M; Vekemans, J.; Verhagen, L. M; Villalba, J. A; Wajja, A.; Watson, B.; White, R. G; and Cobelens, F. G J\n\n\n \n\n\n\n The Lancet Microbe, 6(2): 100961. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Effectiveness$ Paper\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{pelzer_effectiveness_2025,\n\ttitle = {Effectiveness of the primary {Bacillus} {Calmette}-{Guérin} vaccine against the risk of {Mycobacterium} tuberculosis infection and tuberculosis disease: a meta-analysis of individual participant data},\n\tvolume = {6},\n\tissn = {26665247},\n\tshorttitle = {Effectiveness of the primary {Bacillus} {Calmette}-{Guérin} vaccine against the risk of {Mycobacterium} tuberculosis infection and tuberculosis disease},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2666524724002143},\n\tdoi = {10.1016/j.lanmic.2024.100961},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet Microbe},\n\tauthor = {Pelzer, Puck T and Stuck, Logan and Martinez, Leonardo and Richards, Alexandra S and Acuña-Villaorduña, Carlos and Aronson, Naomi E and Bonnet, Maryline and Carvalho, Anna C and Chan, Pei-Chun and Huang, Li-Min and Fang, Chi-Tai and Churchyard, Gavin and Corral-Londoño, Helena Del and Datta, Manjula and Espinal, Marcos A and Fielding, Katherine and Fiore-Gartland, Andrew J and Garcia-Basteiro, Alberto and Hanekom, Willem and Hatherill, Mark and Hill, Phillip C and Huerga, Helena and Jones-López, Edward C and Kritski, Afranio and Mandalakas, Anna M and Mangtani, Punam and Martins Netto, Eduardo and Mayanja, Harriet and Mazahir, Rufaida and Murray, Megan and Rangaka, Molebogeng and Scriba, Thomas and Singh, Jitendra and Singh, Sarman and Stein, Catherine M and Vekemans, Johan and Verhagen, Lilly M and Villalba, Julian A and Wajja, Anne and Watson, Basilea and White, Richard G and Cobelens, Frank G J},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {100961},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Unveiling a hidden phenotype of early tuberculosis.\n \n \n \n \n\n\n \n Ehrlich, J.; Suñer, C.; Churchyard, G.; Cobelens, F.; Hatherill, M.; Mendelsohn, S. C; Nelson, K. N; Scriba, T.; Theron, G.; Martinez, L.; and Garcia-Basteiro, A. L\n\n\n \n\n\n\n The Lancet Respiratory Medicine, 13(5): 385–387. May 2025.\n \n\n\n\n
\n\n\n\n \n \n Paper\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{ehrlich_unveiling_2025,\n\ttitle = {Unveiling a hidden phenotype of early tuberculosis},\n\tvolume = {13},\n\tissn = {22132600},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S221326002500092X},\n\tdoi = {10.1016/S2213-2600(25)00092-X},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet Respiratory Medicine},\n\tauthor = {Ehrlich, Joanna and Suñer, Clara and Churchyard, Gavin and Cobelens, Frank and Hatherill, Mark and Mendelsohn, Simon C and Nelson, Kristin N and Scriba, Tom and Theron, Grant and Martinez, Leonardo and Garcia-Basteiro, Alberto L},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {385--387},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Mycobacterium tuberculosis biology, pathogenicity and interaction with the host.\n \n \n \n \n\n\n \n Warner, D. F.; Barczak, A. K.; Gutierrez, M. G.; and Mizrahi, V.\n\n\n \n\n\n\n Nature Reviews Microbiology, 23(12): 788–804. December 2025.\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

\n

@article{warner_mycobacterium_2025,\n\ttitle = {Mycobacterium tuberculosis biology, pathogenicity and interaction with the host},\n\tvolume = {23},\n\tissn = {1740-1526, 1740-1534},\n\turl = {https://www.nature.com/articles/s41579-025-01201-x},\n\tdoi = {10.1038/s41579-025-01201-x},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2026-05-19},\n\tjournal = {Nature Reviews Microbiology},\n\tauthor = {Warner, Digby F. and Barczak, Amy K. and Gutierrez, Maximiliano G. and Mizrahi, Valerie},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {788--804},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Immune correlates analysis of antibody responses against SARS-CoV-2 variants in the ENSEMBLE vaccine efficacy trial.\n \n \n \n \n\n\n \n Luedtke, A.; Fong, Y.; Van Der Laan, L.; Heng, F.; Huang, Y.; Lu, Y.; Yu, C.; Carpp, L. N.; Roels, S.; Le Gars, M.; Van Roey, G. A.; Stieh, D. J.; Van Dromme, I.; Kenny, A.; Carone, M.; Hyrien, O.; Ayala, V.; 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.; Dziubla, G.; Randhawa, A. K.; Andrasik, M. P.; Hendriks, J.; Truyers, C.; Struyf, F.; Schuitemaker, H.; Douoguih, M.; Kublin, J. G.; Corey, L.; Neuzil, K. M.; Bekker, L.; Garrett, N.; Cardoso, S. W.; DelaFontaine, P.; Magaret, C. A.; Vingerhoets, J.; Casapia, M.; Losso, M. H.; Little, S. J.; Gaur, A.; Swann, E.; Petropoulos, C. J.; McDermott, A. B.; Sadoff, J.; Gray, G. E.; Grinsztejn, B.; Goepfert, P. A.; Follmann, D.; Roychoudhury, P.; Greninger, A. L.; Koup, R. A.; Donis, R. O.; and Gilbert, P. B.\n\n\n \n\n\n\n iScience, 28(11): 113660. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Immune$ Paper\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{luedtke_immune_2025,\n\ttitle = {Immune correlates analysis of antibody responses against {SARS}-{CoV}-2 variants in the {ENSEMBLE} vaccine efficacy trial},\n\tvolume = {28},\n\tissn = {25890042},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2589004225019212},\n\tdoi = {10.1016/j.isci.2025.113660},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-19},\n\tjournal = {iScience},\n\tauthor = {Luedtke, Alex and Fong, Youyi and Van Der Laan, Lars and Heng, Fei and Huang, Ying and Lu, Yiwen and Yu, Chenchen and Carpp, Lindsay N. and Roels, Sanne and Le Gars, Mathieu and Van Roey, Griet A. and Stieh, Daniel J. and Van Dromme, Ilse and Kenny, Avi and Carone, Marco and Hyrien, Ollivier and Ayala, Victor 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 Dziubla, Gabrielle and Randhawa, April K. and Andrasik, Michele P. and Hendriks, Jenny and Truyers, Carla and Struyf, Frank and Schuitemaker, Hanneke and Douoguih, Macaya and Kublin, James G. and Corey, Lawrence and Neuzil, Kathleen M. and Bekker, Linda-Gail and Garrett, Nigel and Cardoso, Sandra W. and DelaFontaine, Patrice and Magaret, Craig A. and Vingerhoets, Johan and Casapia, Martin and Losso, Marcelo H. and Little, Susan J. and Gaur, Aditya and Swann, Edith and Petropoulos, Christos J. and McDermott, Adrian B. and Sadoff, Jerald and Gray, Glenda E. and Grinsztejn, Beatriz and Goepfert, Paul A. and Follmann, Dean and Roychoudhury, Pavitra and Greninger, Alexander L. and Koup, Richard A. and Donis, Ruben O. and Gilbert, Peter B.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {113660},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Human alveolar macrophage function is impaired in tuberculosis contacts with diabetes.\n \n \n \n \n\n\n \n Kleynhans, L.; Kunsevi-Kilola, C.; Tshivhula, H.; Webber, T.; Keyser, A.; Prins, N.; Snyders, C. I.; Shabangu, A.; Rozot, V.; Kidd, M.; Zhang, H.; Cai, H.; Wang, Y.; Ewing, A. D.; Malherbe, S. T.; Azad, A. K.; Arnett, E.; Restrepo, B. I.; Schlesinger, L. S.; and Ronacher, K.\n\n\n \n\n\n\n eBioMedicine, 122: 106050. December 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{kleynhans_human_2025,\n\ttitle = {Human alveolar macrophage function is impaired in tuberculosis contacts with diabetes},\n\tvolume = {122},\n\tissn = {23523964},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352396425004943},\n\tdoi = {10.1016/j.ebiom.2025.106050},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {eBioMedicine},\n\tauthor = {Kleynhans, Léanie and Kunsevi-Kilola, Carine and Tshivhula, Happy and Webber, Tariq and Keyser, Alana and Prins, Nicole and Snyders, Candice I. and Shabangu, Ayanda and Rozot, Virginie and Kidd, Martin and Zhang, Hao and Cai, Hong and Wang, Yufeng and Ewing, Adam D. and Malherbe, Stephanus T. and Azad, Abul K. and Arnett, Eusondia and Restrepo, Blanca I. and Schlesinger, Larry S. and Ronacher, Katharina},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {106050},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n FLT1 and other candidate fetal haemoglobin modifying loci in sickle cell disease in African ancestries.\n \n \n \n \n\n\n \n Wonkam, A.; Esoh, K.; Levine, R. M.; Ngo Bitoungui, V. J.; Mnika, K.; Nimmagadda, N.; Dempsey, E. A. D.; Nkya, S.; Sangeda, R. Z.; Nembaware, V.; Morrice, J.; Osman, F.; Beer, M. A.; Makani, J.; Mulder, N.; Lettre, G.; Steinberg, M. H.; Latanich, R.; Casella, J. F.; Drehmer, D.; Arking, D. E.; Chimusa, E. R.; Yen, J. S.; Newby, G. A.; and Antonarakis, S. E.\n\n\n \n\n\n\n Nature Communications, 16(1): 2092. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"FLT1$ Paper\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{wonkam_flt1_2025,\n\ttitle = {{FLT1} and other candidate fetal haemoglobin modifying loci in sickle cell disease in {African} ancestries},\n\tvolume = {16},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-025-57413-5},\n\tdoi = {10.1038/s41467-025-57413-5},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Nature Communications},\n\tauthor = {Wonkam, Ambroise and Esoh, Kevin and Levine, Rachel M. and Ngo Bitoungui, Valentina Josiane and Mnika, Khuthala and Nimmagadda, Nikitha and Dempsey, Erin A. D. and Nkya, Siana and Sangeda, Raphael Z. and Nembaware, Victoria and Morrice, Jack and Osman, Fujr and Beer, Michael A. and Makani, Julie and Mulder, Nicola and Lettre, Guillaume and Steinberg, Martin H. and Latanich, Rachel and Casella, James F. and Drehmer, Daiana and Arking, Dan E. and Chimusa, Emile R. and Yen, Jonathan S. and Newby, Gregory A. and Antonarakis, Stylianos E.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {2092},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Comprehensive chemoanatomical mapping, and the gonadal regulation, of seven kisspeptin neuronal populations in the mouse brain.\n \n \n \n \n\n\n \n Hernández, V. S.; Zetter, M. A.; Hernández‐Pérez, O. R.; Hernández‐González, R.; Camacho‐Arroyo, I.; Millar, R. P.; Eiden, L. E.; and Zhang, L.\n\n\n \n\n\n\n Journal of Neuroendocrinology, 37(5): e70019. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Comprehensive$ Paper\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{hernandez_comprehensive_2025,\n\ttitle = {Comprehensive chemoanatomical mapping, and the gonadal regulation, of seven kisspeptin neuronal populations in the mouse brain},\n\tvolume = {37},\n\tissn = {0953-8194, 1365-2826},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/jne.70019},\n\tdoi = {10.1111/jne.70019},\n\tabstract = {Abstract \n             \n              Kisspeptinergic signaling is well‐established as crucial for the regulation of reproduction, but its potential broader role in brain function is less understood. This study investigates the distribution and chemotyping of kisspeptin‐expressing neurons within the mouse brain. RNAscope single, dual, and multiplex in situ hybridization methods were used to assess kisspeptin mRNA ( \n              Kiss1 \n              ) expression and its co‐expression with other neuropeptides, excitatory and inhibitory neurotransmitter markers, and sex steroid receptors in wild‐type intact and gonadectomized young adult mice. Seven distinct kisspeptin neuronal chemotypes were characterized, including two novel kisspeptin‐expressing groups described for the first time, that is, the \n              Kiss1 \n              population in the ventral premammillary nucleus and the nucleus of the solitary tract. \n              Kiss1 \n              mRNA was also observed to localize in both somatic and dendritic compartments of hypothalamic neurons. High androgen receptor expression and changes in medial amygdala and septo‐hypothalamic \n              Kiss1 \n              expression following GDX in males, but not in females, suggest a role for androgen receptors in regulating kisspeptin signaling. This study provides a detailed chemoanatomical map of kisspeptin‐expressing neurons, highlighting their potential functional diversity. The discovery of a new kisspeptin‐expressing group and gonadectomy‐induced changes in \n              Kiss1 \n              expression patterns suggest broader roles for kisspeptin in brain functions beyond those of reproduction.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-19},\n\tjournal = {Journal of Neuroendocrinology},\n\tauthor = {Hernández, Vito S. and Zetter, Mario A. and Hernández‐Pérez, Oscar R. and Hernández‐González, Rafael and Camacho‐Arroyo, Ignacio and Millar, Robert P. and Eiden, Lee E. and Zhang, Limei},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {e70019},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The Therapeutic Potential of Photoimmunotherapy as a Safe, Effective and Non‐Toxic Treatment Option for Superficial Triple Negative Breast Cancer.\n \n \n \n \n\n\n \n Biteghe, F. A. N.; Mungra, N.; Malindi, Z.; Chalomie, N. E. T.; Stanislas, K. A.; Yasmin‐Karim, S.; Mike Makrigiorgos, G.; Chipidza, F. E.; Akinrinmade, O. A.; Sridhar, S.; Barth, S.; and Ngwa, W.\n\n\n \n\n\n\n Cancer Medicine, 14(18): e71255. September 2025.\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{biteghe_therapeutic_2025,\n\ttitle = {The {Therapeutic} {Potential} of {Photoimmunotherapy} as a {Safe}, {Effective} and {Non}‐{Toxic} {Treatment} {Option} for {Superficial} {Triple} {Negative} {Breast} {Cancer}},\n\tvolume = {14},\n\tissn = {2045-7634, 2045-7634},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/cam4.71255},\n\tdoi = {10.1002/cam4.71255},\n\tabstract = {ABSTRACT \n            Triple‐negative breast cancer (TNBC) is the most aggressive breast cancer subtype, lacking estrogen (ER), progesterone (PR), and human epidermal growth factor receptor (HER‐2) expression. It disproportionately affects women of African descent and has a poor clinical prognosis attributed to its acute heterogeneity, thereby causing elevated mortality rates. Due to the lack of well‐defined molecular targets in TNBC, treatment relies heavily on a trimodality approach (surgery, radiotherapy, and chemotherapy), despite growing evidence of adverse effects and disease relapses. Therefore, there is an urgency to identify targetable aberrations for more effective approaches capable of selectively detecting and killing targeted cells while sparing healthy tissues. The emergence of monoclonal antibodies (mAbs) targeting tumor‐associated antigens (TAAs), which can be used as a carrier to deliver highly cytotoxic drugs, raised hopes that antibody‐drug conjugates (ADCs) might solve the toxicity‐therapy challenge by shifting the balance more toward beneficial therapeutic efficacy. Despite their therapeutic benefits, their clinical translation is limited by key developmental barriers, including immune‐related adverse events. To address these limitations, a novel approach using antibody‐photoconjugates (APCs) was developed for photoimmunotherapy (PIT) applications, whereby local exposure to near‐infrared (NIR) light induces targeted phototoxic damage, culminating in apoptotic, necrotic, and immunogenic cell death (ICD) with minimal toxicities. Therefore, this review highlights the potential of PIT as an inherently safer and efficient light‐dependent therapeutic option for treating TNBC. \n             \n              Trial Registration: \n              NCT06449222},\n\tlanguage = {en},\n\tnumber = {18},\n\turldate = {2026-05-19},\n\tjournal = {Cancer Medicine},\n\tauthor = {Biteghe, Fleury Augustin Nsole and Mungra, Neelakshi and Malindi, Zaria and Chalomie, Nyangone Ekome Toung and Stanislas, Ketum Ateh and Yasmin‐Karim, Sayeda and Mike Makrigiorgos, G. and Chipidza, Fallon Ester and Akinrinmade, Olusiji Alex and Sridhar, Srinivas and Barth, Stefan and Ngwa, Wilfred},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {e71255},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Performance of 2 Finger-Stick Blood Tests to Triage Adults With Symptoms of Pulmonary Tuberculosis: A Prospective Multisite Diagnostic Accuracy Study.\n \n \n \n \n\n\n \n Sutherland, J. S; Van Der Spuy, G. D; Shaw, J. A; Richardson, T.; Tjon Kon Fat, E. M; Gindeh, A.; Owolabi, O.; Thuong, N. T. T.; Van, L. H.; Van, N. H.; Thao, D. T. T.; Mayanja-Kizza, H.; Nsereko, M.; Namuganga, A.; Nalukwago, S.; Belisle, J.; Moreau, E.; Penn-Nicholson, A.; Thwaites, G.; Winter, J.; Dockrell, H. M; Scriba, T. J; Stanley, K.; Smith, B.; Chegou, N. N; Malherbe, S. T; Geluk, A.; Corstjens, P.; Walzl, G.; the TrENDx-TB consortium; Sutherland, J. S; Owolabi, O.; Secka, A.; Njai, B.; Sillah, A. K; Daffeh, G. K; Gindeh, A; Barry, A.; Rashid, M.; Mendy, J.; Sarr, B.; Riley, A.; Jobe, A.; Davies, M.; Kanyi, K.; Jallow, M.; Barry, S.; Cham, O.; Walzl, G.; Malherbe, S. T; Smith, B.; Van Der Spuy, G. D; Stanley, K.; Shaw, J. A; Chetram, A.; Richardson, T.; Fransman, B.; Johnson, I.; Finn, M.; Hiemstra, A.; Chegou, N. N; Kuivaniemi, H.; Tromp, G.; Tonsing, S.; Smit, E.; Carstens, B.; Mayanja-Kizza, H.; Nsereko, M.; Namuganga, A.; Nalukwago, S.; Akol, J.; Menya, S.; Kizza, V.; Kironde, Y.; Banturaki, D.; Nahereza, I.; Okiror, S.; Kemigisha, I.; Mutumba, P.; Ojiambo, H.; Murungi, L.; Nassuna, J.; Mpalanyi, G.; Odie, M.; Thwaites, G.; Thuong, N. T. T.; Van Le; Thanh, S. V.; Thi, H. N.; Thi Ngoc, H. V.; Le Hong, N.; Belisle, J.; Dobos, K.; Dockrell, H. M; Scriba, T. J; Hatherill, M.; Hadley, K.; Shenje, J.; Kimbung, S.; Mulenga, H.; Oelofse, R.; Bilek, N.; Van Rooyen, E.; Mabwe, S.; Corstjens, P.; Geluk, A; Tjon Kon Fat, E. M; Pierneef, L.; Van Hooij, A.; Winter, J.; Ruhwald, M.; Moreau, E.; Penn-Nicholson, A.; Schacht, C.; and Büech, J.\n\n\n \n\n\n\n Clinical Infectious Diseases, 81(4): 857–866. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Performance$ Paper\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{sutherland_performance_2025,\n\ttitle = {Performance of 2 {Finger}-{Stick} {Blood} {Tests} to {Triage} {Adults} {With} {Symptoms} of {Pulmonary} {Tuberculosis}: {A} {Prospective} {Multisite} {Diagnostic} {Accuracy} {Study}},\n\tvolume = {81},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1058-4838, 1537-6591},\n\tshorttitle = {Performance of 2 {Finger}-{Stick} {Blood} {Tests} to {Triage} {Adults} {With} {Symptoms} of {Pulmonary} {Tuberculosis}},\n\turl = {https://academic.oup.com/cid/article/81/4/857/8113579},\n\tdoi = {10.1093/cid/ciaf105},\n\tabstract = {Abstract \n             \n              Background \n              Non–sputum-based, point-of-care triage tests for pulmonary tuberculosis could enhance tuberculosis diagnostic programs. We assessed the diagnostic accuracy of 2 finger-stick blood tests: the Cepheid 3 gene host-response cartridge (Xpert-HR), which measures 3 host messenger RNA transcripts, and the 3-host protein multibiomarker test (MBT). \n             \n             \n              Methods \n              We performed a prospective diagnostic accuracy study of consecutive participants with symptoms compatible with pulmonary tuberculosis in The Gambia, South Africa, Uganda, and Vietnam. A composite reference standard for active pulmonary tuberculosis incorporated chest radiography, symptom resolution, and sputum microbiological test results. A training-test set approach was used to evaluate test cutoff specificities at 90\\% sensitivity. \n             \n             \n              Results \n              Between 1 November 2020 and 1 May 2023, we screened 1262 participants aged 12–70 years with cough lasting \\&gt;2 weeks and another symptom suggestive of tuberculosis. Of those who were classifiable by reference tests, 1154 participants had evaluable Xpert-HR results and 961 had evaluable MBT results. Xpert-HR had an area under the receiver operating characteristic (AUROC) curve of 0.92 at a cutoff of −1.275 or below, with a sensitivity of 92.8\\%, specificity of 62.5\\%, positive predictive value of 47.9\\%, and negative predictive value of 95.9\\%. The MBT had an AUROC of 0.91 at a cutoff of ≥0.42, with a sensitivity of 91.4\\%, specificity of 73.2\\%, positive predictive value of 52.0\\%, and negative predictive value of 96.4\\%. \n             \n             \n              Conclusions \n              Our results show that both Xpert-HR and the MBT are promising non–sputum-based point-of-care tests. The MBT met the World Health Organization target product profile for a triage test, which suggests it should be further developed.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-19},\n\tjournal = {Clinical Infectious Diseases},\n\tauthor = {Sutherland, Jayne S and Van Der Spuy, Gian D and Shaw, Jane A and Richardson, Tracy and Tjon Kon Fat, Elisa M and Gindeh, Awa and Owolabi, Olumuyiwa and Thuong, Nguyen Thuy Thuong and Van, Le Hong and Van, Nguyen Hoang and Thao, Dang Thi Thanh and Mayanja-Kizza, Harriet and Nsereko, Mary and Namuganga, AnnRitah and Nalukwago, Sophie and Belisle, John and Moreau, Emmanuel and Penn-Nicholson, Adam and Thwaites, Guy and Winter, Jill and Dockrell, Hazel M and Scriba, Thomas J and Stanley, Kim and Smith, Bronwyn and Chegou, Novel N and Malherbe, Stephanus T and Geluk, Annemieke and Corstjens, Paul and Walzl, Gerhard and {the TrENDx-TB consortium} and Sutherland, Jayne S and Owolabi, Olumuyiwa and Secka, Amie and Njai, Bintou and Sillah, Abdou K and Daffeh, Georgetta K and Gindeh, A and Barry, Amadou and Rashid, Momodou and Mendy, Joseph and Sarr, Binta and Riley, Abi-Janet and Jobe, Alhaji and Davies, Monica and Kanyi, Kairaba and Jallow, Momodou and Barry, Salieu and Cham, Ousainou and Walzl, Gerhard and Malherbe, Stephanus T and Smith, Bronwyn and Van Der Spuy, Gian D and Stanley, Kim and Shaw, Jane A and Chetram, Alicia and Richardson, Tracy and Fransman, Bernadine and Johnson, Isaac and Finn, Marika and Hiemstra, Andriette and Chegou, Novel N and Kuivaniemi, Helena and Tromp, Gerard and Tonsing, Susanne and Smit, Elizma and Carstens, Balie and Mayanja-Kizza, Harriet and Nsereko, Mary and Namuganga, AnnRitah and Nalukwago, Sophie and Akol, Joseph and Menya, Saidah and Kizza, Veronica and Kironde, Yusuf and Banturaki, Deborah and Nahereza, Immaculate and Okiror, Simon and Kemigisha, Immaculate and Mutumba, Paul and Ojiambo, Henry and Murungi, Lilian and Nassuna, Joan and Mpalanyi, Gladys and Odie, Michael and Thwaites, Guy and Thuong, Nguyen Thuy Thuong and {Van Le} and Thanh, Son Vo and Thi, Hau Nguyen and Thi Ngoc, Ha Vu and Le Hong, Ngoc and Belisle, John and Dobos, Karen and Dockrell, Hazel M and Scriba, Thomas J and Hatherill, Mark and Hadley, Kate and Shenje, Justin and Kimbung, Stanley and Mulenga, Humphrey and Oelofse, Rachel and Bilek, Nicole and Van Rooyen, Elma and Mabwe, Simba and Corstjens, Paul and Geluk, A and Tjon Kon Fat, Elisa M and Pierneef, Louise and Van Hooij, Anouk and Winter, Jill and Ruhwald, Morten and Moreau, Emmanuel and Penn-Nicholson, Adam and Schacht, Claudia and Büech, Julia},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {857--866},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Urgent request for pretomanid label expansion to align with WHO guidelines and improve treatment accessibility and efficacy.\n \n \n \n \n\n\n \n Kuksa, L.; Andrejak, C.; Haecker, B.; Bothamley, G.; Calcagno, A.; Cirillo, D.; Duarte, R.; Fatima, R.; Ferlazzo, G.; Guglielmetti, L.; Günther, G.; Hewison, C.; Horsburgh, C.; Jäger, T.; Kalancha, Y.; Otto-Knapp, R.; Kranzer, K.; Lillebaek, T.; Marks, G.; Middelkoop, K.; Motta, I.; Rabinova, V.; Sommerfeld, P.; Tattevin, P.; and Lange, C.\n\n\n \n\n\n\n IJTLD Open, 2(3): 117–119. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Urgent$ Paper\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{kuksa_urgent_2025,\n\ttitle = {Urgent request for pretomanid label expansion to align with {WHO} guidelines and improve treatment accessibility and efficacy},\n\tvolume = {2},\n\tissn = {3005-7590},\n\turl = {https://journals.theunion.org/lookup/doi/10.5588/ijtldopen.25.0152},\n\tdoi = {10.5588/ijtldopen.25.0152},\n\tabstract = {SUMMARY \n            Pretomanid is a key anti-TB drug included in the WHO list of essential medications. The current EMA-approved label for pretomanid restricts its use to the regimen comprising bedaquiline, pretomanid and linezolid (BPaL) and only for extensively drug-resistant-TB or multidrug-resistant TB, “when antibiotics used for the latter form of TB do not work or cause unacceptable side effects.” This restricted use implies that the older, prolonged and poorly tolerated regimens remain the recommended treatment for most cases of drug-resistant TB. The authors, representing many respiratory groups and societies, call for the label expansion of pretomanid to align with global guidelines, allowing for broader use.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-19},\n\tjournal = {IJTLD Open},\n\tauthor = {Kuksa, L. and Andrejak, C. and Haecker, B. and Bothamley, G. and Calcagno, A. and Cirillo, D.M. and Duarte, R. and Fatima, R. and Ferlazzo, G. and Guglielmetti, L. and Günther, G. and Hewison, C. and Horsburgh, C.R. and Jäger, T. and Kalancha, Y. and Otto-Knapp, R. and Kranzer, K. and Lillebaek, T. and Marks, G. and Middelkoop, K. and Motta, I. and Rabinova, V. and Sommerfeld, P. and Tattevin, P. and Lange, C.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {117--119},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Standard of care in advanced HIV disease: review of HIV treatment guidelines in sub-Saharan African countries—an extension study of eight countries.\n \n \n \n \n\n\n \n Scheier, T. C.; Tufa, T. B.; Feldt, T.; Hardy, Y.; Minga, A.; Moh, R.; Damasceno, A.; Chambal, L.; Ntoumi, F.; Kades, C.; Bitunguhari, L.; Sebatunzi, O. R.; Missanga, M.; Njekwa, K.; Muyoyeta, M.; Rangarajan, S.; Meintjes, G.; Mertz, D.; Eikelboom, J. W.; and Wasserman, S.\n\n\n \n\n\n\n AIDS Research and Therapy, 22(1): 39. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Standard$ Paper\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{scheier_standard_2025,\n\ttitle = {Standard of care in advanced {HIV} disease: review of {HIV} treatment guidelines in sub-{Saharan} {African} countries—an extension study of eight countries},\n\tvolume = {22},\n\tissn = {1742-6405},\n\tshorttitle = {Standard of care in advanced {HIV} disease},\n\turl = {https://aidsrestherapy.biomedcentral.com/articles/10.1186/s12981-025-00733-9},\n\tdoi = {10.1186/s12981-025-00733-9},\n\tabstract = {Abstract \n             \n              Introduction \n              The World Health Organization (WHO) has published guidelines for the management of patients with advanced HIV disease (AHD) but mortality remains high. Adoption of WHO recommendations by national guidelines is poorly documented. We aimed to extend our prior review of six national management guidelines by including additional countries from sub-Saharan Africa. \n             \n             \n              Methods \n              We identified guidelines of eight additional countries participating in a multicountry trial of azithromycin prophylaxis for AHD. Data was extracted in five domains including definition of AHD (1 item), screening (6 items), prophylaxis (6 items), supportive care (1 items), and HIV treatment (4 items) and scored agreement of each national guideline with the WHO guidelines. \n             \n             \n              Results \n              Six of the eight national guidelines had a designated section for AHD. Compared with the WHO guideline, the agreement score for national guidelines was between 7 and 17 out of 18, whereby disagreement is mainly driven by missing information. None of the national guidelines had more than three items not in agreement with the WHO guidelines, and the maximum number of items not addressed by any one guideline was eight. Main areas of disagreement were the targeted population for start of ART in presence of tuberculosis meningitis (1/8 in agreement) and urine lipoarabinomannan screening (2/8 in agreement). The targeted population group for cotrimoxazole prophylaxis and its discontinuation was in line with the WHO recommendations in 3/8 national guidelines. Except one guideline, all documents showed similar overall agreement, irrespectively of publication date. \n             \n             \n              Conclusion \n              National guidelines for the management of people with AHD are broadly in agreement with WHO guidelines. Main areas of disagreement are recommendations regarding urine lipoarabinomannan screening, cotrimoxazole prophylaxis and start of antiretroviral therapy in presence of tuberculosis.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {AIDS Research and Therapy},\n\tauthor = {Scheier, Thomas C. and Tufa, Tafese Beyene and Feldt, Torsten and Hardy, Yasmine and Minga, Albert and Moh, Raoul and Damasceno, Albertino and Chambal, Lucia and Ntoumi, Francine and Kades, Carine and Bitunguhari, Leopold and Sebatunzi, Osee R. and Missanga, Marco and Njekwa, Katanekwa and Muyoyeta, Monde and Rangarajan, Sumathy and Meintjes, Graeme and Mertz, Dominik and Eikelboom, John W. and Wasserman, Sean},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {39},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A new serological autoantibody signature associated with multiple sclerosis.\n \n \n \n \n\n\n \n Abdesselem, H.; De La Fuente, A.; Bensmail, I.; Elbashir, I. E.; Anuar, D.; Ti-Myen, T.; Abylova, B.; Blackburn, J. M.; Malik, R. A.; and Petropoulos, I. N.\n\n\n \n\n\n\n Neurobiology of Disease, 216: 107116. November 2025.\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{abdesselem_new_2025,\n\ttitle = {A new serological autoantibody signature associated with multiple sclerosis},\n\tvolume = {216},\n\tissn = {09699961},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S096999612500333X},\n\tdoi = {10.1016/j.nbd.2025.107116},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {Neurobiology of Disease},\n\tauthor = {Abdesselem, Houari and De La Fuente, Alberto and Bensmail, Ilham and Elbashir, Israa E. and Anuar, Diana and Ti-Myen, Tan and Abylova, Bermet and Blackburn, Jonathan M. and Malik, Rayaz A. and Petropoulos, Ioannis N.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {107116},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Advancements in single-cell techniques for examining the HIV reservoir: pathways to a cure.\n \n \n \n \n\n\n \n Mbhele, N.; Chimukangara, B.; Tyers, L.; Maldarelli, F.; and Redd, A. D.\n\n\n \n\n\n\n mBio, 16(7): e00655–25. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Advancements$ Paper\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{mbhele_advancements_2025,\n\ttitle = {Advancements in single-cell techniques for examining the {HIV} reservoir: pathways to a cure},\n\tvolume = {16},\n\tissn = {2150-7511},\n\tshorttitle = {Advancements in single-cell techniques for examining the {HIV} reservoir},\n\turl = {https://journals.asm.org/doi/10.1128/mbio.00655-25},\n\tdoi = {10.1128/mbio.00655-25},\n\tabstract = {ABSTRACT \n             \n               \n               \n                Human immunodeficiency virus (HIV) is largely incurable, due to the presence of a viral reservoir, which primarily consists of resting CD4 \n                + \n                T cells and other long-lived cells like macrophages. These reservoir cells, which persist despite suppressive antiretroviral therapy (ART), are thought to be influenced by several key factors such as position and orientation of chromosomal proviral integration, proviral intactness, and antigen specificity. The host’s immune status and immune selection pressures also likely play a significant role. Recent data suggest that the HIV provirus integrates into specific chromosomal regions, such as centromeric areas with low RNA expression, allowing the virus to evade detection. To effectively disrupt HIV latency, enhance immune recognition, and eliminate reservoir cells, a precise understanding of these viral reservoirs at single-cell level will be crucial. Gaining insights into the unique characteristics of these reservoir cells, including data on integration sites and gene expression profiles, is essential for designing targeted interventions. This review highlights current single-cell approaches, including single-cell sequencing, chromatin accessibility assays, and multiomic techniques, as tools for uncovering the heterogeneity and resilience of HIV reservoirs. Taken together, these methods aim to reveal the complexities of the HIV reservoir and promote the development of novel therapeutic strategies.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-19},\n\tjournal = {mBio},\n\tauthor = {Mbhele, Nokuzola and Chimukangara, Benjamin and Tyers, Lynn and Maldarelli, Frank and Redd, Andrew D.},\n\teditor = {Prasad, Vinayaka R.},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {e00655--25},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Testing tongue swab samples by Cepheid Xpert MTB/RIF Ultra: comparison of two protocols applied to samples from persons with low-bacillary load TB.\n \n \n \n \n\n\n \n Wood, R. C.; Goodgion, S.; Olson, A. M.; Luabeya, A. K.; Hatherill, M.; and Cangelosi, G. A.\n\n\n \n\n\n\n Microbiology Spectrum, 13(12): e01493–25. December 2025.\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{wood_testing_2025,\n\ttitle = {Testing tongue swab samples by {Cepheid} {Xpert} {MTB}/{RIF} {Ultra}: comparison of two protocols applied to samples from persons with low-bacillary load {TB}},\n\tvolume = {13},\n\tissn = {2165-0497},\n\tshorttitle = {Testing tongue swab samples by {Cepheid} {Xpert} {MTB}/{RIF} {Ultra}},\n\turl = {https://journals.asm.org/doi/10.1128/spectrum.01493-25},\n\tdoi = {10.1128/spectrum.01493-25},\n\tabstract = {ABSTRACT \n             \n               \n               \n                Tongue swabs (TS) are non-sputum specimens for molecular diagnosis of tuberculosis (TB). Analysis of swabs by Cepheid Xpert MTB/RIF Ultra (Xpert Ultra) is less sensitive than the use of certain manual quantitative polymerase chain reaction methods, but is desirable given the widespread use and familiarity of Xpert Ultra. This study evaluated an easy-to-use protocol for analyzing TS by Xpert Ultra. TS samples from symptomatic South African patients were previously collected and tested by Xpert Ultra using a protocol that requires a heating block (termed Heat + TE). Replicate, paired samples from the same patients were tested by a newly reported method that does not require heating (termed 2:1 SR). The diagnostic accuracy of the two methods was compared. This paired comparison prioritized samples from participants with low sputum bacillary loads, a population in whom TS sensitivity is lowest. Eighty-eight were TB-positive by sputum microbiological reference standard (MRS) and 20 were TB-negative (total \n                N \n                = 180). Within this sample set, the Heat + TE method was 42.5\\% (38/88; 95\\% confidence interval [CI]: 33–54\\%) sensitive, and the 2:1 SR method was not significantly different at 52.3\\% (46/88; 95\\% CI: 41–63\\%) sensitive relative to sputum MRS. Both methods were 100\\% (20/20; 95\\% CI: 83–100\\%) specific. A secondary analysis compared the sensitivities of single-sample versus dual-sample testing within a cohort ( \n                N \n                = 241) that included both high- and low-bacillary load participants. Testing of a single sample was 75.5\\% (182/241; 95\\% CI: 70-81\\%) sensitive relative to sputum MRS, whereas dual sampling was 81.3\\% (196/241; 95\\% CI: 76–86\\%) sensitive; the difference was not significant. \n               \n               \n                IMPORTANCE \n                 \n                  Tongue swab (TS) samples are novel, non-invasive, easy-to-collect diagnostic specimens for tuberculosis testing. This study compared two methods for processing TS samples in preparation for analysis using Xpert Ultra, a popular commercial platform for molecular detection of \n                  Mycobacterium tuberculosis \n                  DNA in human specimens. A newly described method has logistical advantages over a previously described method, in that it does not require additional equipment and is less prone to errors. The newly described method was found to be at least as sensitive and specific as the previous method. Therefore, the logistical advantages of the new method come at no cost in terms of diagnostic accuracy, and its adoption is recommended. A secondary analysis indicated that dual-sample testing can modestly boost diagnostic yield relative to testing a single sample. \n                 \n               \n             \n          ,  \n             \n              Tongue swab (TS) samples are novel, non-invasive, easy-to-collect diagnostic specimens for tuberculosis testing. This study compared two methods for processing TS samples in preparation for analysis using Xpert Ultra, a popular commercial platform for molecular detection of \n              Mycobacterium tuberculosis \n              DNA in human specimens. A newly described method has logistical advantages over a previously described method, in that it does not require additional equipment and is less prone to errors. The newly described method was found to be at least as sensitive and specific as the previous method. Therefore, the logistical advantages of the new method come at no cost in terms of diagnostic accuracy, and its adoption is recommended. A secondary analysis indicated that dual-sample testing can modestly boost diagnostic yield relative to testing a single sample.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2026-05-19},\n\tjournal = {Microbiology Spectrum},\n\tauthor = {Wood, Rachel C. and Goodgion, Sophie and Olson, Alaina M. and Luabeya, Angelique K. and Hatherill, Mark and Cangelosi, Gerard A.},\n\teditor = {Georghiou, Sophia B.},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e01493--25},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Tongue swabs (TS) are non-sputum specimens for molecular diagnosis of tuberculosis (TB). Analysis of swabs by Cepheid Xpert MTB/RIF Ultra (Xpert Ultra) is less sensitive than the use of certain manual quantitative polymerase chain reaction methods, but is desirable given the widespread use and familiarity of Xpert Ultra. This study evaluated an easy-to-use protocol for analyzing TS by Xpert Ultra. TS samples from symptomatic South African patients were previously collected and tested by Xpert Ultra using a protocol that requires a heating block (termed Heat + TE). Replicate, paired samples from the same patients were tested by a newly reported method that does not require heating (termed 2:1 SR). The diagnostic accuracy of the two methods was compared. This paired comparison prioritized samples from participants with low sputum bacillary loads, a population in whom TS sensitivity is lowest. Eighty-eight were TB-positive by sputum microbiological reference standard (MRS) and 20 were TB-negative (total N = 180). Within this sample set, the Heat + TE method was 42.5% (38/88; 95% confidence interval [CI]: 33–54%) sensitive, and the 2:1 SR method was not significantly different at 52.3% (46/88; 95% CI: 41–63%) sensitive relative to sputum MRS. Both methods were 100% (20/20; 95% CI: 83–100%) specific. A secondary analysis compared the sensitivities of single-sample versus dual-sample testing within a cohort ( N = 241) that included both high- and low-bacillary load participants. Testing of a single sample was 75.5% (182/241; 95% CI: 70-81%) sensitive relative to sputum MRS, whereas dual sampling was 81.3% (196/241; 95% CI: 76–86%) sensitive; the difference was not significant. IMPORTANCE Tongue swab (TS) samples are novel, non-invasive, easy-to-collect diagnostic specimens for tuberculosis testing. This study compared two methods for processing TS samples in preparation for analysis using Xpert Ultra, a popular commercial platform for molecular detection of Mycobacterium tuberculosis DNA in human specimens. A newly described method has logistical advantages over a previously described method, in that it does not require additional equipment and is less prone to errors. The newly described method was found to be at least as sensitive and specific as the previous method. Therefore, the logistical advantages of the new method come at no cost in terms of diagnostic accuracy, and its adoption is recommended. A secondary analysis indicated that dual-sample testing can modestly boost diagnostic yield relative to testing a single sample. , Tongue swab (TS) samples are novel, non-invasive, easy-to-collect diagnostic specimens for tuberculosis testing. This study compared two methods for processing TS samples in preparation for analysis using Xpert Ultra, a popular commercial platform for molecular detection of Mycobacterium tuberculosis DNA in human specimens. A newly described method has logistical advantages over a previously described method, in that it does not require additional equipment and is less prone to errors. The newly described method was found to be at least as sensitive and specific as the previous method. Therefore, the logistical advantages of the new method come at no cost in terms of diagnostic accuracy, and its adoption is recommended. A secondary analysis indicated that dual-sample testing can modestly boost diagnostic yield relative to testing a single sample.\n

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\n \n\n \n \n \n \n \n \n Signatures of omicron-like adaptation in early SARS-CoV-2 variants and chronic infection.\n \n \n \n \n\n\n \n Cheng, M. T. K.; Altaf, M.; Castin, J.; Reuschl, A.; Sievers, B. L.; Kamelian, K.; Mesner, D.; Morse, R. B.; Abdullahi, A.; Meng, B.; Csiba, K.; Kemp, S. A.; P. Martin, D.; Jolly, C.; Ruis, C.; Thukral, L.; and Gupta, R. K.\n\n\n \n\n\n\n Cell Reports, 44(8): 116135. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Signatures$ Paper\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{cheng_signatures_2025,\n\ttitle = {Signatures of omicron-like adaptation in early {SARS}-{CoV}-2 variants and chronic infection},\n\tvolume = {44},\n\tissn = {22111247},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2211124725009064},\n\tdoi = {10.1016/j.celrep.2025.116135},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-19},\n\tjournal = {Cell Reports},\n\tauthor = {Cheng, Mark Tsz Kin and Altaf, Mazharul and Castin, Jesu and Reuschl, Ann-Kathrin and Sievers, Benjamin L. and Kamelian, Kimia and Mesner, Dejan and Morse, Rebecca B. and Abdullahi, Adam and Meng, Bo and Csiba, Kata and Kemp, Steven A. and P. Martin, Darren and Jolly, Clare and Ruis, Christopher and Thukral, Lipi and Gupta, Ravindra K.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {116135},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Treatment Outcomes With an Oral Short Course Regimen for Rifampicin-resistant Tuberculosis in a High HIV Prevalence, Programmatic Setting in South Africa.\n \n \n \n \n\n\n \n Stadler, J. A M; Kuhlin, J.; Molloy, S. F; Mtwa, N.; Hayes, C.; Stead, D.; Maartens, G.; Warren, R.; Meintjes, G.; and Wasserman, S.\n\n\n \n\n\n\n Clinical Infectious Diseases, 81(4): e153–e162. November 2025.\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 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{stadler_treatment_2025,\n\ttitle = {Treatment {Outcomes} {With} an {Oral} {Short} {Course} {Regimen} for {Rifampicin}-resistant {Tuberculosis} in a {High} {HIV} {Prevalence}, {Programmatic} {Setting} in {South} {Africa}},\n\tvolume = {81},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {1058-4838, 1537-6591},\n\turl = {https://academic.oup.com/cid/article/81/4/e153/8127637},\n\tdoi = {10.1093/cid/ciaf112},\n\tabstract = {Abstract \n             \n              Background \n              Bedaquiline-based oral short-course regimens (SCR) for rifampicin-resistant tuberculosis (RR-TB) are highly effective in clinical trials but outcomes in programmatic settings may be more modest. We evaluated clinical and bacteriological outcomes with a seven-drug, linezolid-containing SCR in a high-burden programmatic setting. \n             \n             \n              Methods \n              This prospective cohort study enrolled adults with newly diagnosed RR-TB who were started on the oral SCR in the Eastern Cape Province, South Africa. The primary outcome was World Health Organization-defined end-of-treatment success. Secondary outcomes were TB-free survival (composite of alive, absence of a positive Mycobacterium tuberculosis culture, and treatment completed or in care) at 18 months and time to sputum culture conversion (SCC). \n             \n             \n              Results \n              In total, 248 participants were included, 173 (69.8\\%) of whom were human immunodeficiency virus (HIV) positive. Culture conversion by 90 days was 96.8\\% (median time to SCC: 29 days, 95\\% confidence interval [CI]: 27–31). Treatment success was 37.5\\% (93/248). Reasons for unsuccessful treatment included switching to individualised regimens (35.1\\%, 87/248), loss to follow-up (19.4\\%, 48/348), and death (8.1\\%, 20/248). At 18 months, 157 (63.3\\%) participants achieved TB-free survival, with a cumulative mortality of 21.6\\% (95\\% CI: 16.1–29.0). Baseline 3+ smear (adjusted odds ratio [aOR]: 3.38, 95\\% CI: 1.28–8.95), higher age (aOR: 1.05, 1.01–1.08), and lower albumin (aOR: 0.94, 0.88–0.99), but not HIV status, were associated with unfavourable outcome at 18 months. \n             \n             \n              Conclusions \n              The oral SCR performed poorly in a high-burden TB programme. Strategies to support the implementation of effective new regimens for RR-TB are needed to translate outcomes from clinical trials into practice.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-19},\n\tjournal = {Clinical Infectious Diseases},\n\tauthor = {Stadler, Jacob A M and Kuhlin, Johanna and Molloy, Síle F and Mtwa, Nomfuneko and Hayes, Cindy and Stead, David and Maartens, Gary and Warren, Robin and Meintjes, Graeme and Wasserman, Sean},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {e153--e162},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Autologous Human Dendritic Cells from XDR-TB Patients Polarize a Th1 Response Which Is Bactericidal to Mycobacterium tuberculosis.\n \n \n \n \n\n\n \n Londt, R.; Semple, L.; Esmail, A.; Pooran, A.; Meldau, R.; Davids, M.; Dheda, K.; and Tomasicchio, M.\n\n\n \n\n\n\n Microorganisms, 13(2): 345. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Autologous$ Paper\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{londt_autologous_2025,\n\ttitle = {Autologous {Human} {Dendritic} {Cells} from {XDR}-{TB} {Patients} {Polarize} a {Th1} {Response} {Which} {Is} {Bactericidal} to {Mycobacterium} tuberculosis},\n\tvolume = {13},\n\tissn = {2076-2607},\n\turl = {https://www.mdpi.com/2076-2607/13/2/345},\n\tdoi = {10.3390/microorganisms13020345},\n\tabstract = {Extensively drug-resistant tuberculosis (XDR-TB) is a public health concern as drug resistance is outpacing the drug development pipeline. Alternative immunotherapeutic approaches are needed. Peripheral blood mononuclear cells (PBMCs) were isolated from pre-XDR/XDR-TB (n = 25) patients and LTBI (n = 18) participants. Thereafter, monocytic-derived dendritic cells (mo-DCs) were co-cultured with M. tb antigens, with/without a maturation cocktail (interferon-γ, interferon-α, CD40L, IL-1β, and TLR3 and TLR7/8 agonists). Two peptide pools were evaluated: (i) an ECAT peptide pool (ESAT6, CFP10, Ag85B, and TB10.4 peptides) and (ii) a PE/PPE peptide pool. Sonicated lysate of the M. tb HN878 strain served as a control. Mo-DCs were assessed for DC maturation markers, Th1 cytokines, and the ability of the DC-primed PBMCs to restrict the growth of M. tb-infected monocyte-derived macrophages. In pre-XDR/XDR-TB, mo-DCs matured with M. tb antigens (ECAT or PE/PPE peptide pool, or HN878 lysate) + cocktail, compared to mo-DCs matured with M. tb antigens only, showed higher upregulation of co-stimulatory molecules and IL-12p70 (p {\\textless} 0.001 for both comparisons). The matured mo-DCs had enhanced antigen-specific CD8+ T-cell responses to ESAT-6 (p = 0.05) and Ag85B (p = 0.03). Containment was higher with mo-DCs matured with the PE/PPE peptide pool cocktail versus mo-DCs matured with the PE/PPE peptide pool (p = 0.0002). Mo-DCs matured with the PE/PPE peptide pool + cocktail achieved better containment than the ECAT peptide pool + cocktail [50\\%, (IQR:39–75) versus 46\\%, (IQR:15–62); p = 0.02]. In patients with pre-XDR/XDR-TB, an effector response primed by mo-DCs matured with an ECAT or PE/PPE peptide pool + cocktail was capable of restricting the growth of M. tb in vitro.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {Microorganisms},\n\tauthor = {Londt, Rolanda and Semple, Lynn and Esmail, Aliasgar and Pooran, Anil and Meldau, Richard and Davids, Malika and Dheda, Keertan and Tomasicchio, Michele},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {345},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Endothelial Cells Stably Infected with Recombinant Kaposi’s Sarcoma-Associated Herpesvirus Display Distinct Viscoelastic and Morphological Properties.\n \n \n \n \n\n\n \n Shabangu, M. M.; Blumenthal, M. J.; Sass, D. T.; Lang, D. M.; Schafer, G.; and Franz, T.\n\n\n \n\n\n\n Cellular and Molecular Bioengineering, 18(2): 123–135. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Endothelial$ Paper\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{shabangu_endothelial_2025,\n\ttitle = {Endothelial {Cells} {Stably} {Infected} with {Recombinant} {Kaposi}’s {Sarcoma}-{Associated} {Herpesvirus} {Display} {Distinct} {Viscoelastic} and {Morphological} {Properties}},\n\tvolume = {18},\n\tissn = {1865-5025, 1865-5033},\n\turl = {https://link.springer.com/10.1007/s12195-025-00848-z},\n\tdoi = {10.1007/s12195-025-00848-z},\n\tabstract = {Abstract \n             \n              Purpose \n              Kaposi’s sarcoma-associated herpesvirus (KSHV) is a γ-herpesvirus that has a tropism for endothelial cells and leads to the development of Kaposi’s sarcoma, especially in people living with HIV. The present study aimed to quantify morphological and mechanical changes in endothelial cells after infection with KSHV to assess their potential as diagnostic and therapeutic markers. \n             \n             \n              Methods \n              Vascular (HuARLT2) and lymphatic endothelial cells (LEC) were infected with recombinant KSHV (rKSHV) by spinoculation, establishing stable infections (HuARLT2-rKSHV and LEC-rKSHV). Cellular changes were assessed using mitochondria-tracking microrheology and morphometric analysis. \n             \n             \n              Results \n              rKSHV infection increased cellular deformability, indicated by higher mitochondrial mean squared displacement (MSD) for short lag times. Specifically, MSD at τ = 0.19 s was 49.4\\% and 42.2\\% higher in HuARLT2-rKSHV and LEC-rKSHV, respectively, compared to uninfected controls. There were 23.9\\% and 36.7\\% decreases in the MSD power law exponents for HuARLT2-rKSHV and LEC-rKSHV, respectively, indicating increased cytosolic viscosity associated with rKSHV infection. Infected cells displayed a marked spindloid phenotype with an increase in aspect ratio (29.7\\%) and decreases in roundness (26.1\\%) and circularity (25.7\\%) in HuARLT2-rKSHV, with similar changes observed in LEC-rKSHV. \n             \n             \n              Conclusions \n              The quantification of distinct KSHV-induced morpho-mechanical changes in endothelial cells demonstrates the potential of these changes as diagnostic markers and therapeutic targets.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {Cellular and Molecular Bioengineering},\n\tauthor = {Shabangu, Majahonkhe M. and Blumenthal, Melissa J. and Sass, Danielle T. and Lang, Dirk M. and Schafer, Georgia and Franz, Thomas},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {123--135},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Association between human papillomavirus and behaviour, clinicopathology, and cervical cancer outcome in Zimbabwean women: a cross-sectional study.\n \n \n \n \n\n\n \n Kuguyo, O.; Matimba, A.; Tsikai, N.; Madziyire, M.; Magwali, T.; and Dandara, C.\n\n\n \n\n\n\n Reproductive Health, 22(1): 190. October 2025.\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{kuguyo_association_2025,\n\ttitle = {Association between human papillomavirus and behaviour, clinicopathology, and cervical cancer outcome in {Zimbabwean} women: a cross-sectional study},\n\tvolume = {22},\n\tissn = {1742-4755},\n\tshorttitle = {Association between human papillomavirus and behaviour, clinicopathology, and cervical cancer outcome in {Zimbabwean} women},\n\turl = {https://reproductive-health-journal.biomedcentral.com/articles/10.1186/s12978-025-02100-3},\n\tdoi = {10.1186/s12978-025-02100-3},\n\tabstract = {Abstract \n             \n              Background \n              Less than 10\\% of women infected with distinct human papillomavirus (HPV) develop cervical cancer, suggesting the need for secondary driving factors for carcinogenesis. This study describes factors associated with distinct HPV infections using cervical cancer cohort as a model. Moreover, we also determined the role of distinct HPV in the outcome of cervical cancer therapy. \n             \n             \n              Methods \n              This cross-sectional study comprised of 240 Zimbabwean women aged {\\textgreater} 18 years with histologically confirmed cervical cancer. Tumour tissue was obtained for genomic DNA analysis of 14 HPV genotypes. Demographic, behavioural and clinical information of study participants were collected for analysis. Logistic regression was used to determine factors associated with HR-HPV positivity, and outcomes of therapy. \n             \n             \n              Results \n               \n                The mean age(SD) of the group was 52(12) years. High HIV-positivity (48\\%) and sexually transmitted infection history (30\\%) were observed. HPV16 (35\\%), HPV35 (33\\%) and HPV18 (32\\%) were most prevalent. In unadjusted analyses, STI history (OR = 2.5, 95\\% CI 1.8–4.4, \n                p \n                 {\\textless} 0.01) was associated with HPV51 infections. Alcohol consumption was associated with HPV35 (OR = 1.93, 95\\% CI 1.1–4.9, \n                p \n                 = 0.049) and HPV58 (OR = 2.5, 95\\% CI 1.6–3.8, \n                p \n                 = 0.030). Smoking history was associated with HPV39 (OR = 5.8, 95\\% CI 2.0–7.8, \n                p \n                 = 0.001) and HPV56 (OR = 2.0, 95\\% CI 1.2–4.3 \n                p \n                 = 0.001). In adjusted analyses, HPV35 positivity was associated with high BMI (aOR = 1.4; 95\\% CI 1.1–1.7, \n                p \n                 = 0.010). No HPV was associated with outcome. \n               \n             \n             \n              Conclusions \n              We describe the association between high BMI and smoking with distinct HPV genotypes. There is need for further research in a larger cohort to build predictive algorithms towards strengthening existing preventive, screening and predictive outcome interventions for HPV.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Reproductive Health},\n\tauthor = {Kuguyo, Oppah and Matimba, Alice and Tsikai, Nomsa and Madziyire, Mugove and Magwali, Thulani and Dandara, Collet},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {190},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Retiring the language of first-line and second-line ART.\n \n \n \n \n\n\n \n Vitoria, M.; Meintjes, G.; Ford, N.; Frigati, L.; Sugandhi, N.; and Calmy, A.\n\n\n \n\n\n\n The Lancet HIV, 12(9): e608–e610. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Retiring$ Paper\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{vitoria_retiring_2025,\n\ttitle = {Retiring the language of first-line and second-line {ART}},\n\tvolume = {12},\n\tissn = {23523018},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2352301825001377},\n\tdoi = {10.1016/S2352-3018(25)00137-7},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet HIV},\n\tauthor = {Vitoria, Marco and Meintjes, Graeme and Ford, Nathan and Frigati, Lisa and Sugandhi, Nandita and Calmy, Alexandra},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {e608--e610},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Sequence Demarcation Tool (SDT), a Free User-Friendly Computer Program Using Pairwise Genetic Identity Calculations to Classify Nucleotide or Amino Acid Sequences.\n \n \n \n \n\n\n \n Muhire, B. M.; Roumagnac, P.; Varsani, A.; and Martin, D. P.\n\n\n \n\n\n\n In Zerbini, F. M.; Fiallo-Olivé, E.; and Navas-Castillo, J., editor(s), Geminiviruses, volume 2912, pages 71–79. Springer US, New York, NY, 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Sequence$ Paper\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{zerbini_sequence_2025,\n\taddress = {New York, NY},\n\ttitle = {Sequence {Demarcation} {Tool} ({SDT}), a {Free} {User}-{Friendly} {Computer} {Program} {Using} {Pairwise} {Genetic} {Identity} {Calculations} to {Classify} {Nucleotide} or {Amino} {Acid} {Sequences}},\n\tvolume = {2912},\n\tisbn = {9781071644539 9781071644546},\n\turl = {https://link.springer.com/10.1007/978-1-0716-4454-6_9},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tbooktitle = {Geminiviruses},\n\tpublisher = {Springer US},\n\tauthor = {Muhire, Brejnev Muhizi and Roumagnac, Philippe and Varsani, Arvind and Martin, Darren Patrick},\n\teditor = {Zerbini, Francisco Murilo and Fiallo-Olivé, Elvira and Navas-Castillo, Jesús},\n\tyear = {2025},\n\tdoi = {10.1007/978-1-0716-4454-6_9},\n\tpages = {71--79},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Vaginal Microbiome Research Consortium for Africa: study protocol of a multicentre prospective clinical study to evaluate temporal vaginal microbial composition associated with maintenance of reproductive health in women in South Africa and Kenya.\n \n \n \n \n\n\n \n Kullin, B. R.; Gitome, S.; Happel, A.; Pidwell, T.; Lefevre, M.; Madikida, A.; Wekesa, P.; Mahlangu, K.; Ochieng, J.; Awili, L.; Agolla, W.; Otieno, R.; Mutharimi, A.; Ganief, Y.; Daniels, R.; Chicken, A.; Welp, K.; Livingstone, H.; Swanepoel, C.; Claassen-Weitz, S.; Kanyoka, P.; Ravel, J.; Humphrys, M.; Bilski, L.; Mulder, N.; Bekker, L.; Gill, K.; Jaspan, H.; Bukusi, E. A.; and Passmore, J. S.\n\n\n \n\n\n\n BMJ Open, 15(2): e090938. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Vaginal$ Paper\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{kullin_vaginal_2025,\n\ttitle = {Vaginal {Microbiome} {Research} {Consortium} for {Africa}: study protocol of a multicentre prospective clinical study to evaluate temporal vaginal microbial composition associated with maintenance of reproductive health in women in {South} {Africa} and {Kenya}},\n\tvolume = {15},\n\tissn = {2044-6055, 2044-6055},\n\tshorttitle = {Vaginal {Microbiome} {Research} {Consortium} for {Africa}},\n\turl = {https://bmjopen.bmj.com/lookup/doi/10.1136/bmjopen-2024-090938},\n\tdoi = {10.1136/bmjopen-2024-090938},\n\tabstract = {Introduction \n              The Vaginal Microbiome Research Consortium for Africa (VMRC4Africa) study is a multicentre observational cohort study. We aim to enrol parallel cohorts of 100 women from two sites in two African countries (N=200) (Desmond Tutu HIV Centre [DTHC], South Africa; Kenya Medical Research Institute [KEMRI], Kenya) to evaluate detailed temporal fluctuations in vaginal microbiota in young, generally healthy women from Southern and Eastern Africa. \n             \n             \n              Methods and analysis \n               \n                Cohorts in Kenya and South Africa will be followed up twice a week for 10 weeks to create detailed profiles of vaginal microbial community state types (CSTs; by 16S rRNA gene sequencing) and fungal communities (by internal transcribed spacer (ITS) sequencing) and to identify women with stable \n                Lactobacillus crispatus \n                -dominated microbiota, with no evidence of genital inflammation, as assessed by the measurement of inflammatory cytokines. \n               \n             \n             \n              Discussion \n               \n                Through the establishment of this African vaginal sample biorepository, the intention will be to cultivate \n                Lactobacillus \n                isolates to create a biobank from which to ultimately select geographically diverse \n                Lactobacillus \n                strains with health-promoting characteristics that can be co-formulated into live biotherapeutic products (LBPs) to treat bacterial vaginosis (BV) for women in sub-Saharan Africa. \n               \n             \n             \n              Ethics and dissemination \n              The VMRC4Africa study has been granted ethical approval by the Human Research Ethics Committees in South Africa (UCT HREC: 611/2022) and Kenya (KEMRI Scientific and Ethics Review Unit: SERU No. 4569). Deidentified microbial community compositional data will be made available on public databases. Results of the study will be published in peer-reviewed journals.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {BMJ Open},\n\tauthor = {Kullin, Brian Ronald and Gitome, Serah and Happel, Anna-Ursula and Pidwell, Tanya and Lefevre, Mellissa and Madikida, Anda and Wekesa, Pauline and Mahlangu, Karabo and Ochieng, James and Awili, Lydia and Agolla, Winnie and Otieno, Rhoda and Mutharimi, Amos and Ganief, Yacoeb and Daniels, Rezeen and Chicken, Anika and Welp, Kirsten and Livingstone, Hannah and Swanepoel, Caleb and Claassen-Weitz, Shantelle and Kanyoka, Pride and Ravel, Jacques and Humphrys, Michael and Bilski, Lisa and Mulder, Nicola and Bekker, Linda-Gail and Gill, Katherine and Jaspan, Heather and Bukusi, Elizabeth Anne and Passmore, Jo-Ann Shelley},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {e090938},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Neuroinflammation in fungal infections: from pathogen recognition to pathological manifestations.\n \n \n \n \n\n\n \n Dangarembizi, R.; Awala, A.; and De Lange, A.\n\n\n \n\n\n\n Disease Models & Mechanisms, 18(9): dmm052344. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Neuroinflammation$ Paper\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{dangarembizi_neuroinflammation_2025,\n\ttitle = {Neuroinflammation in fungal infections: from pathogen recognition to pathological manifestations},\n\tvolume = {18},\n\tcopyright = {http://creativecommons.org/licenses/by/4.0},\n\tissn = {1754-8403, 1754-8411},\n\tshorttitle = {Neuroinflammation in fungal infections},\n\turl = {https://journals.biologists.com/dmm/article/18/9/dmm052344/369429/Neuroinflammation-in-fungal-infections-from},\n\tdoi = {10.1242/dmm.052344},\n\tabstract = {ABSTRACT \n            Fungal diseases of the central nervous system (CNS) are associated with severe neurological damage and death in immunocompromised hosts, yet they remain neglected in research and policy. Neuroinflammation, a common clinical feature of fungal infection, has been implicated as a key driver of brain injury, but the mechanisms underlying its contribution to pathology are not well understood. The aim of this Review is to discuss the double-edged role of neuroinflammation in the pathogenesis of fungal infections. We provide an overview of the immune barriers that protect the CNS from fungal infection, the fungal strategies that enable immune evasion and neuroinvasion, and the complex mechanisms underlying the development of neuroinflammation during fungal infection. Finally, we explore how both insufficient and excessive neuroinflammatory responses drive neuropathology, and we conclude by outlining current challenges as well as potential directions for advancing future research in this overlooked field.},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-19},\n\tjournal = {Disease Models \\& Mechanisms},\n\tauthor = {Dangarembizi, Rachael and Awala, Amalia and De Lange, Anja},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {dmm052344},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Within-country heterogeneity in patterns of social contact relevant for tuberculosis infection transmission, prevention, and care.\n \n \n \n \n\n\n \n LeGrand, K. E.; Edwards, A.; Mohlamonyane, M.; Dayi, N.; Olivier, S.; Gareta, D.; Wood, R.; Grant, A. D.; White, R. G.; Middelkoop, K.; Khan, P.; and McCreesh, N.\n\n\n \n\n\n\n PLOS Global Public Health, 5(7): e0004257. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Within-country$ Paper\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{legrand_within-country_2025,\n\ttitle = {Within-country heterogeneity in patterns of social contact relevant for tuberculosis infection transmission, prevention, and care},\n\tvolume = {5},\n\tissn = {2767-3375},\n\turl = {https://dx.plos.org/10.1371/journal.pgph.0004257},\n\tdoi = {10.1371/journal.pgph.0004257},\n\tabstract = {Mycobacterium tuberculosis \n              ( \n              Mtb \n              ) transmission is driven by variable social, environmental, and biological factors, including the number and duration of indoor contacts. Social contact data can provide information on potential transmission patterns, but is underutilised outside the field of mathematical modelling. We explore three contexts where contact data can provide valuable insights: 1) household contact tracing; 2) infection prevention and control measures (IPC); and 3) contamination in cluster randomised trials (CRTs). A social contact survey was conducted in adults aged 18 and older from three communities with comparable population sizes in South Africa: an urban township and peri-urban and rural clinic catchment areas. Participants reported congregate settings visited over 24-hours, visit durations, and estimated number of people present. To correspond with the three contexts, we estimated the proportion of contact hours occurring 1) within the home; 2) in congregate settings outside the home; and 3) outside the participants’ communities. Participants reported a mean of 27.0 (rural), 55.2 (peri-urban), and 73.0 (urban) contact hours. The proportions of household contact were similar among rural and peri-urban participants (76.8\\% and 71.7\\%), compared to urban (48.6\\%). Congregate settings visited varied; urban participants spent the most contact hours in retail/office settings (19.9\\%), peri-urban participants in community-service buildings (20.4\\%), and rural participants in other peoples’ homes (25.5\\%). Urban participants reported the highest proportion of contact outside the community (67.0\\%) compared to rural (38.8\\%) and peri-urban (21.5\\%) participants. The observed heterogeneity in contact patterns has implications for TB interventions. Household contact tracing may be most effective in the rural community where household contact was highest. The diverse range of congregate settings visited suggests that prioritising IPC measures in these locations may enhance their overall efficacy. Considering contact patterns when designing clusters may reduce contamination in CRTs. Tailored interventions, informed by local contexts, are essential to reduce TB burden.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-19},\n\tjournal = {PLOS Global Public Health},\n\tauthor = {LeGrand, Kate E. and Edwards, Anita and Mohlamonyane, Mbali and Dayi, Njabulo and Olivier, Stephen and Gareta, Dickman and Wood, Robin and Grant, Alison D. and White, Richard G. and Middelkoop, Keren and Khan, Palwasha and McCreesh, Nicky},\n\teditor = {Martinez, Leonardo},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {e0004257},\n}\n\n\n\n

\n

\n\n\n

\n Mycobacterium tuberculosis ( Mtb ) transmission is driven by variable social, environmental, and biological factors, including the number and duration of indoor contacts. Social contact data can provide information on potential transmission patterns, but is underutilised outside the field of mathematical modelling. We explore three contexts where contact data can provide valuable insights: 1) household contact tracing; 2) infection prevention and control measures (IPC); and 3) contamination in cluster randomised trials (CRTs). A social contact survey was conducted in adults aged 18 and older from three communities with comparable population sizes in South Africa: an urban township and peri-urban and rural clinic catchment areas. Participants reported congregate settings visited over 24-hours, visit durations, and estimated number of people present. To correspond with the three contexts, we estimated the proportion of contact hours occurring 1) within the home; 2) in congregate settings outside the home; and 3) outside the participants’ communities. Participants reported a mean of 27.0 (rural), 55.2 (peri-urban), and 73.0 (urban) contact hours. The proportions of household contact were similar among rural and peri-urban participants (76.8% and 71.7%), compared to urban (48.6%). Congregate settings visited varied; urban participants spent the most contact hours in retail/office settings (19.9%), peri-urban participants in community-service buildings (20.4%), and rural participants in other peoples’ homes (25.5%). Urban participants reported the highest proportion of contact outside the community (67.0%) compared to rural (38.8%) and peri-urban (21.5%) participants. The observed heterogeneity in contact patterns has implications for TB interventions. Household contact tracing may be most effective in the rural community where household contact was highest. The diverse range of congregate settings visited suggests that prioritising IPC measures in these locations may enhance their overall efficacy. Considering contact patterns when designing clusters may reduce contamination in CRTs. Tailored interventions, informed by local contexts, are essential to reduce TB burden.\n

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\n \n\n \n \n \n \n \n \n The ATM Kinase Inhibitor AZD0156 Is a Potent Inhibitor of Plasmodium Phosphatidylinositol 4‐Kinase (PI4Kβ) and Is an Attractive Candidate for Medicinal Chemistry Optimization Against Malaria.\n \n \n \n \n\n\n \n Woodland, J. G.; Coertzen, D.; Wicht, K. J.; Hidalgo, V. F.; Pasaje, C. F. A.; Godoy, L. C.; Qahash, T.; Mmonwa, M. M.; Dziwornu, G. A.; Wambua, L.; Harries, S.; Korkor, C. M.; Njoroge, M.; Krugmann, L.; Taylor, D.; Leshabane, M.; Langeveld, H.; Rabie, T.; Reader, J.; Van Der Watt, M.; Venter, N.; Erlank, E.; Aswat, A. S.; Koekemoer, L. L.; Yeo, T.; Jeon, J. H.; Fidock, D. A.; Gamo, F. J.; Wittlin, S.; Niles, J. C.; Llinas, M.; Coulson, L. B.; Birkholtz, L.; and Chibale, K.\n\n\n \n\n\n\n Angewandte Chemie International Edition, 64(28): e202425206. July 2025.\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{woodland_atm_2025,\n\ttitle = {The {ATM} {Kinase} {Inhibitor} {AZD0156} {Is} a {Potent} {Inhibitor} of \\textit{{Plasmodium}} {Phosphatidylinositol} 4‐{Kinase} ({PI4Kβ}) and {Is} an {Attractive} {Candidate} for {Medicinal} {Chemistry} {Optimization} {Against} {Malaria}},\n\tvolume = {64},\n\tissn = {1433-7851, 1521-3773},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1002/anie.202425206},\n\tdoi = {10.1002/anie.202425206},\n\tabstract = {Abstract \n             \n              New compounds targeting human malaria parasites are critical for effective malaria control and elimination. Here, we pursued the imidazoquinolinone AZD0156 (MMV1580483), a human ataxia‐telangiectasia mutated (ATM) kinase inhibitor that completed Phase I clinical trials as an anticancer agent. We validated its in vitro activity against the two main forms of the \n              Plasmodium falciparum \n              parasite in the human host, viz. the asexual blood (symptomatic) stage and sexual gametocyte (transmission) stage. Resistance selection, cross‐resistance, biochemical, and conditional knockdown studies revealed that AZD0156 inhibits \n              P. falciparum \n              phosphatidylinositol 4‐kinase type III beta ( \n              Pf \n              PI4Kβ), a clinically‐validated target for the treatment of malaria. Metabolic perturbations, fixed‐ratio isobolograms, killing kinetics and morphological evaluation correlated AZD0156 inhibition with other known PI4Kβ inhibitors. The compound showed favorable in vivo pharmacokinetic properties and 81\\% antimalarial efficacy (4 × 50 mg kg \n              −1 \n              ) in a \n              P. berghei \n              mouse malaria infection model. Importantly, a cleaner biochemical profile was measured against human kinases (MAP4K4, MINK1) implicated in embryofoetal developmental toxicity associated with the \n              Pf \n              PI4Kβ inhibitor MMV390048. This improved kinase selectivity profile and structural differentiation from other PI4Kβ inhibitors, together with its multistage antiplasmodial activity and favorable pharmacokinetic properties, makes AZD0156 an attractive candidate for target‐based drug repositioning against malaria via a medicinal chemistry optimization approach.},\n\tlanguage = {en},\n\tnumber = {28},\n\turldate = {2026-05-19},\n\tjournal = {Angewandte Chemie International Edition},\n\tauthor = {Woodland, John G. and Coertzen, Dina and Wicht, Kathryn J. and Hidalgo, Virginia Franco and Pasaje, Charisse Flerida A. and Godoy, Luiz C. and Qahash, Tarrick and Mmonwa, Mmakwena M. and Dziwornu, Godwin A. and Wambua, Lynn and Harries, Sarah and Korkor, Constance M. and Njoroge, Mathew and Krugmann, Liezl and Taylor, Dale and Leshabane, Meta and Langeveld, Henrico and Rabie, Tayla and Reader, Janette and Van Der Watt, Mariëtte and Venter, Nelius and Erlank, Erica and Aswat, Ayesha S. and Koekemoer, Lizette L. and Yeo, Tomas and Jeon, Jin H. and Fidock, David A. and Gamo, Francisco Javier and Wittlin, Sergio and Niles, Jacquin C. and Llinas, Manuel and Coulson, Lauren B. and Birkholtz, Lyn‐Marié and Chibale, Kelly},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {e202425206},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Cross-species blood transcriptional correlates of BCG-mediated protection against tuberculosis include innate and adaptive immune processes.\n \n \n \n \n\n\n \n Bridges, K.; Awany, D.; Gela, A.; Mwambene, T.; Kurtz, S. L.; Baker, R. E.; Elkins, K. L.; Sassetti, C. M.; Scriba, T. J.; and Lauffenburger, D. A.\n\n\n \n\n\n\n JCI Insight, 10(24): e194450. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Cross-species$ Paper\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{bridges_cross-species_2025,\n\ttitle = {Cross-species blood transcriptional correlates of {BCG}-mediated protection against tuberculosis include innate and adaptive immune processes},\n\tvolume = {10},\n\tcopyright = {http://creativecommons.org/licenses/by/4.0/},\n\tissn = {2379-3708},\n\turl = {https://insight.jci.org/articles/view/194450},\n\tdoi = {10.1172/jci.insight.194450},\n\tabstract = {The immune mechanisms induced by the Bacillus Calmette-Guérin (BCG) vaccine, and the subset of which that mediate protection against tuberculosis (TB), remain poorly understood. This is further complicated by difficulties in verifying vaccine-induced protection in humans. Although research in animal models, namely mice and nonhuman primates (NHPs), has begun to close this knowledge gap, discrepancies in the relative importance of biological pathways across species limit the utility of animal model–derived biological insights in humans. To address these challenges, we applied a systems modeling framework, Translatable Components Regression (TransCompR), to identify human blood transcriptional variability that could predict \n              Mycobacterium tuberculosis \n              challenge outcomes in BCG-vaccinated NHPs. These protection-associated pathways included both innate and adaptive immune activation mechanisms, along with signaling via type I IFNs and antimycobacterial Th cytokines. We further partially validated the associations between these mechanisms and protection in humans using publicly available microarray data collected from BCG-vaccinated infants who either developed TB or remained healthy during 2 years of follow-up. Overall, our work demonstrates how species translation modeling can leverage animal studies to generate hypotheses about the mechanisms that underlie human infectious disease and vaccination outcomes, which may be difficult or impossible to ascertain using human data alone.},\n\tlanguage = {en},\n\tnumber = {24},\n\turldate = {2026-05-19},\n\tjournal = {JCI Insight},\n\tauthor = {Bridges, Kate and Awany, Denis and Gela, Anele and Mwambene, Temwa-Dango and Kurtz, Sherry L. and Baker, Richard E. and Elkins, Karen L. and Sassetti, Christopher M. and Scriba, Thomas J. and Lauffenburger, Douglas A.},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e194450},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Evidence required to evaluate the use of bacteriologically confirmed asymptomatic tuberculosis disease as a primary endpoint in prevention of tuberculosis disease vaccine licensure trials.\n \n \n \n \n\n\n \n White, R. G; Churchyard, G. J; Horton, K. C; Fiore-Gartland, A.; Behr, M. A; Clark, R. A; Cobelens, F.; Ernst, J. D; Esmail, H.; Garcia-Basteiro, A. L; Hadinegoro, S. R.; Hanekom, W. A; Hatherill, M.; Hill, P. C; Muloiwa, R.; Pelzer, P. T; Rangaka, L.; Rees, H.; Schrager, L.; Stanley, M.; Tufet, M.; Wong, E. B; and Houben, R. M G J\n\n\n \n\n\n\n The Lancet Respiratory Medicine, 13(10): 933–942. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Evidence$ Paper\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{white_evidence_2025,\n\ttitle = {Evidence required to evaluate the use of bacteriologically confirmed asymptomatic tuberculosis disease as a primary endpoint in prevention of tuberculosis disease vaccine licensure trials},\n\tvolume = {13},\n\tissn = {22132600},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S221326002500164X},\n\tdoi = {10.1016/S2213-2600(25)00164-X},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet Respiratory Medicine},\n\tauthor = {White, Richard G and Churchyard, Gavin J and Horton, Katherine C and Fiore-Gartland, Andrew and Behr, Marcel A and Clark, Rebecca A and Cobelens, Frank and Ernst, Joel D and Esmail, Hanif and Garcia-Basteiro, Alberto L and Hadinegoro, Sri Rezeki and Hanekom, Willem A and Hatherill, Mark and Hill, Philip C and Muloiwa, Rudzani and Pelzer, Puck T and Rangaka, Lele and Rees, Helen and Schrager, Lewis and Stanley, Margaret and Tufet, Marta and Wong, Emily B and Houben, Rein M G J},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {933--942},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n CaCO3-based nanomedicine with multi-functions of ferroptosis-apoptosis and microenvironment regulation in cancer.\n \n \n \n \n\n\n \n Zhang, X.; Feng, Y.; Cao, W.; Yu, F.; Sun, L.; Barth, S.; and He, H.\n\n\n \n\n\n\n Nano Today, 61: 102594. April 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"CaCO3-based$ 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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{zhang_caco3-based_2025,\n\ttitle = {{CaCO3}-based nanomedicine with multi-functions of ferroptosis-apoptosis and microenvironment regulation in cancer},\n\tvolume = {61},\n\tissn = {17480132},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S174801322400450X},\n\tdoi = {10.1016/j.nantod.2024.102594},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {Nano Today},\n\tauthor = {Zhang, Xue and Feng, Yaxuan and Cao, Weiran and Yu, Fei and Sun, Lu and Barth, Stefan and He, Huining},\n\tmonth = apr,\n\tyear = {2025},\n\tpages = {102594},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Brief Report: Resistance to Dolutegravir in Treatment-Experienced Patients in South Africa: A Retrospective Cohort Study.\n \n \n \n \n\n\n \n Zhao, Y.; Holtman, M.; Mudaly, V.; Van Zyl, G.; Maartens, G.; and Meintjes, G.\n\n\n \n\n\n\n JAIDS Journal of Acquired Immune Deficiency Syndromes, 99(3): 283–287. July 2025.\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{zhao_brief_2025,\n\ttitle = {Brief {Report}: {Resistance} to {Dolutegravir} in {Treatment}-{Experienced} {Patients} in {South} {Africa}: {A} {Retrospective} {Cohort} {Study}},\n\tvolume = {99},\n\tissn = {1525-4135, 1944-7884},\n\tshorttitle = {Brief {Report}},\n\turl = {https://journals.lww.com/10.1097/QAI.0000000000003657},\n\tdoi = {10.1097/QAI.0000000000003657},\n\tabstract = {Background: \n              Dolutegravir (DTG) resistance has been reported more frequently in patients with prior treatment experience compared with those on DTG in first-line antiretroviral therapy (ART). The widespread use of DTG in resource-limited programmatic settings might facilitate the emergence of resistance. Data on the prevalence of DTG resistance from programmatic settings in Africa are scarce. \n             \n             \n              Methods: \n              This retrospective observational cohort study assessed DTG resistance in routine care settings of the Western Cape provincial public healthcare sector program between February 2021 and June 2024. Treatment-experienced adults who developed virologic failure (2 HIV-1 RNA ≥1000 copies/mL), who had received DTG-based ART for {\\textgreater}24 months, were eligible for genotypic antiretroviral resistance testing (GART). Drug resistance mutations (DRMs) and resistance levels were classified using the Stanford database. \n             \n             \n              Results: \n              Among 99 eligible patients, 76 had GART performed, and 68 had successful sequences. Among these 68, 43 (63\\%) had DTG DRMs with: 1 potential low, 1 low, 15 intermediate, and 26 high resistance levels. The median time on DTG-based ART was 24 months (interquartile range, 23–31). Of the 43 patients with DTG DRMs, 21 (49\\%) were receiving zidovudine–lamivudine–dolutegravir and 19 (44\\%) were receiving tenofovir–lamivudine–dolutegravir; 42/43 had prior ART experience. \n             \n             \n              Conclusions: \n              Over 60\\% of patients with prior treatment experience who had been on DTG-based ART for over 2 years and experienced virologic failure had intermediate or high level DTG resistance. This suggests that criteria for GART used are too stringent, which has resource implications in programmatic settings where access to resistance testing for individual management is limited.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-19},\n\tjournal = {JAIDS Journal of Acquired Immune Deficiency Syndromes},\n\tauthor = {Zhao, Ying and Holtman, Melanie and Mudaly, Vanessa and Van Zyl, Gert and Maartens, Gary and Meintjes, Graeme},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {283--287},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Discordance between measures of Mycobacterium tuberculosis sensitization and type 2 diabetes mellitus in the United States (NHANES): A population-based cohort study.\n \n \n \n \n\n\n \n Magodoro, I. M.; Wilkinson, K. A.; Claggett, B. L.; Ntusi, N. A.; Siedner M, M. J.; and Wilkinson, R. J.\n\n\n \n\n\n\n Journal of Infection, 90(6): 106496. June 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Discordance$ Paper\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{magodoro_discordance_2025,\n\ttitle = {Discordance between measures of {Mycobacterium} tuberculosis sensitization and type 2 diabetes mellitus in the {United} {States} ({NHANES}): {A} population-based cohort study},\n\tvolume = {90},\n\tissn = {01634453},\n\tshorttitle = {Discordance between measures of {Mycobacterium} tuberculosis sensitization and type 2 diabetes mellitus in the {United} {States} ({NHANES})},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0163445325000908},\n\tdoi = {10.1016/j.jinf.2025.106496},\n\tlanguage = {en},\n\tnumber = {6},\n\turldate = {2026-05-19},\n\tjournal = {Journal of Infection},\n\tauthor = {Magodoro, Itai M. and Wilkinson, Katalin A. and Claggett, Brian L. and Ntusi, Ntobeko A.B. and Siedner M, Mark J. and Wilkinson, Robert J.},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {106496},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Infectious Morbidity and All-cause Mortality of Infants HIV-exposed Uninfected Compared to Infants HIV-unexposed Uninfected in Botswana.\n \n \n \n \n\n\n \n Dubois, M. M.; Jao, J.; Sun, S.; Legbedze, J.; Schenkel, S.; Mmasa, N.; Kgole, S. W.; Masasa, G.; Happel, A.; Iwase, S. C.; Haghighat, R.; Moyo, S.; Sharma, T. S.; Edlefsen, P. T.; Shao, D.; Jaspan, H.; and Powis, K. M.\n\n\n \n\n\n\n Pediatric Infectious Disease Journal, 44(3): 214–216. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Infectious$ Paper\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{dubois_infectious_2025,\n\ttitle = {Infectious {Morbidity} and {All}-cause {Mortality} of {Infants} {HIV}-exposed {Uninfected} {Compared} to {Infants} {HIV}-unexposed {Uninfected} in {Botswana}},\n\tvolume = {44},\n\tissn = {0891-3668, 1532-0987},\n\turl = {https://journals.lww.com/10.1097/INF.0000000000004603},\n\tdoi = {10.1097/INF.0000000000004603},\n\tabstract = {Some studies have reported increased infectious morbidity and all-cause mortality risk among infants HIV-exposed uninfected compared with infants HIV-unexposed uninfected. In a retrospective analysis of infants enrolled in the Botswana-based Tshilo Dikotla study, we found no difference in the prevalence of infectious hospitalizations or deaths from any cause in the first year of life by perinatal HIV exposure.},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-19},\n\tjournal = {Pediatric Infectious Disease Journal},\n\tauthor = {Dubois, Melanie M. and Jao, Jennifer and Sun, Shan and Legbedze, Justine and Schenkel, Sara and Mmasa, Nicholas and Kgole, Samuel W. and Masasa, Gosego and Happel, Anna-Ursula and Iwase, Saori C. and Haghighat, Roxanna and Moyo, Sikhulile and Sharma, Tanvi S. and Edlefsen, Paul T. and Shao, Danica and Jaspan, Heather and Powis, Kathleen M.},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {214--216},\n}\n\n\n\n

\n

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

\n \n\n \n \n \n \n \n \n Tuberculosis treatment outcomes and their related factors in patients with tuberculosis treated at the Antituberculosis Center of Brazzaville, Republic of Congo.\n \n \n \n \n\n\n \n Ngouama, B. B.; Mouzinga, F. H.; Dello, M. N. M.; Djontu, J. C.; Elion Assiana, D. O.; Okemba Okombi, F. H.; Tchuandom, S. B.; Ayet, M. I.; Siele, L. K.; Vouvoungui, J. C.; Grobusch, M. P.; Mouanga, A. M.; Mbozo, A. B. V.; and Ntoumi, F.\n\n\n \n\n\n\n IJID Regions, 15: 100647. June 2025.\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{ngouama_tuberculosis_2025,\n\ttitle = {Tuberculosis treatment outcomes and their related factors in patients with tuberculosis treated at the {Antituberculosis} {Center} of {Brazzaville}, {Republic} of {Congo}},\n\tvolume = {15},\n\tissn = {27727076},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2772707625000827},\n\tdoi = {10.1016/j.ijregi.2025.100647},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {IJID Regions},\n\tauthor = {Ngouama, Breli Bonheur and Mouzinga, Freisnel Hermeland and Dello, Mita Naomie Merveille and Djontu, Jean Claude and Elion Assiana, Darrel Ornelle and Okemba Okombi, Franck Hardain and Tchuandom, Salomon Bonsi and Ayet, Michel Illoye and Siele, Lemercier Khunell and Vouvoungui, Jeannhey Christevy and Grobusch, Martin Peter and Mouanga, Alain Maxime and Mbozo, Alain Brice Vouidibio and Ntoumi, Francine},\n\tmonth = jun,\n\tyear = {2025},\n\tpages = {100647},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Cobamide metabolism, regulation, and adaptation in Mycobacterium tuberculosis.\n \n \n \n \n\n\n \n Kipkorir, T.; Mbau, R. D.; Warner, D. F.; Krishnamoorthy, G.; and Moosa, A.\n\n\n \n\n\n\n Journal of Bacteriology, 207(12): e00204–25. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Cobamide$ Paper\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{kipkorir_cobamide_2025,\n\ttitle = {Cobamide metabolism, regulation, and adaptation in \\textit{{Mycobacterium} tuberculosis}},\n\tvolume = {207},\n\tissn = {0021-9193, 1098-5530},\n\turl = {https://journals.asm.org/doi/10.1128/jb.00204-25},\n\tdoi = {10.1128/jb.00204-25},\n\tabstract = {ABSTRACT \n             \n               \n               \n                Cobamides play a paradoxical but critical role in the biology of \n                Mycobacterium tuberculosis \n                ( \n                Mtb \n                ), the causative agent of tuberculosis. Although \n                Mtb \n                retains nearly all cobalamin (Cbl) biosynthetic genes and encodes multiple cobamide-requiring enzymes, experimental evidence indicates that \n                Mtb \n                is incapable of \n                de novo \n                Cbl synthesis under any tested conditions to date. Instead, an evolutionary shift appears to have occurred toward host dependency for biologically relevant cobamides or their precursors. This review highlights recent advances in our understanding of cobamide-related metabolism in \n                Mtb \n                , including: (i) the progressive erosion of \n                de novo \n                cobamide biosynthetic capacity across \n                Mtb \n                lineages; (ii) the role of host-derived cobamides in sustaining key mycobacterial metabolic pathways, including methionine synthesis and propionate catabolism; (iii) the impact of host immune pressures, including itaconate-mediated inhibition of methylmalonyl-CoA mutase; (iv) strategies employed by \n                Mtb \n                for cobamide and precursor acquisition; and (v) unique adaptations of Cbl-sensing riboswitches that regulate methionine synthesis, virulence-associated gene expression, and dormancy resuscitation. We also highlight unresolved questions, including possible niche-specific synthesis, utilization of alternate cobamide species, and the therapeutic potential of targeting cobamide-related metabolism. We review recent evidence of the centrality of cobamides in the metabolic flexibility of \n                Mtb \n                , virulence, and survival in the host environment, despite apparent loss of \n                de novo \n                biosynthetic capacity. Further mechanistic studies are required which may reveal vulnerabilities for the exploitation of cobamide acquisition, cobamide-related regulation, and the role of cobamides at the \n                Mtb \n                -host interface for innovative therapeutic interventions.},\n\tlanguage = {en},\n\tnumber = {12},\n\turldate = {2026-05-19},\n\tjournal = {Journal of Bacteriology},\n\tauthor = {Kipkorir, Terry and Mbau, Rendani D. and Warner, Digby F. and Krishnamoorthy, Gopinath and Moosa, Atica},\n\teditor = {O'Toole, George},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {e00204--25},\n}\n\n\n\n

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

\n \n\n \n \n \n \n \n \n Global, Regional, and National Burden of Cardiovascular Diseases and Risk Factors in 204 Countries and Territories, 1990-2023.\n \n \n \n \n\n\n \n Stark, B. A.; DeCleene, N. K.; Desai, E. C.; Hsu, J. M.; Johnson, C. O.; Lara-Castor, L.; LeGrand, K. E.; A, P. B.; Aalipour, M. A.; Aalruz, H.; Abafita, B. J.; Abaraogu, U. O.; Abavisani, M.; Abbas, N.; Abbasi, M.; Abbasian, M.; Abbastabar, H.; Abd Al Magied, A. H.; ElHafeez, S. A.; Abdelalim, P. A.; Abdelfattah, O. M.; Abdel-Hameed, P. R.; Abdelnabi, M.; Wael M Abdel-Rahman, P.; Abdi, P.; Abdisa, W. M.; Abdissa, D.; Abdous, A.; Abdullah, M.; Abdullahi, A.; Abdykerimova, K.; Abebe, M.; Abedi, A.; Abedi, A.; Abejew, A. A.; Abhilash, E.; Abiodun, O. O.; Abiodun, P. O.; Kasem, R. A.; Aboagye, R. G.; Abohashem, S.; Abolhassani, H.; Abonie, U. S.; Aborode, A. T.; Abourashed, N. M.; Abramov, D.; Abreu, L. G.; Abtahi, D.; Abu Farha, R. K.; Kende Abubakar, A. K.; Abubakar, I. J.; Abu-Elala, N.; Abu-Gharbieh, E.; Abukhadijah, H. J.; Aburuz, S.; Abushanab, D.; Acharya, A. B.; Acharya, A.; Acharya, S.; Achore, M.; Adal, O.; Adams, L. C.; Adamu, L. H.; Adão, R.; Addo, I. Y.; Adebayo, O. M.; Adebisi, T. A.; Adedia, D.; Adedokun, K. A.; Adegbile, O. E.; Adegboye, O. A.; Adegoke, N. A.; Adekanmbi, V.; Adeleke, O. T.; Oluwaseun Adetunji, C.; Adeyomoye, O. I.; Adha, R.; Adhikari, K.; Adhikary, R. K.; Adikusuma, W.; Parvar, T. A.; Adnan, M.; Sakilah Adnani, Q. E.; Adoma, P. O.; Adzigbli, L. A.; Adzrago, D.; Afifi, A. M.; Afolabi, H. A.; Afrashteh, F.; Afrooghe, A.; Afzal, M. S.; Afzal, S.; Agampodi, S. B.; Agarwal, D. M.; Agarwal, G.; Agarwal, P.; Ageru, T. A.; Aggarwal, N.; Aghajanian, S.; Sobrinho, C. A.; Agyemang-Duah, W.; Ahadi, M.; Ahammed, B.; Ahinkorah, B. O.; Ahmad, A.; Ahmad, F.; Ahmad, K.; Ahmad, M. M.; Ahmad, S.; Ahmad, S.; Ahmad, T.; Ahmadzadeh, K.; Ahmed, A.; Ahmed, A.; Ahmed, A.; Ahmed, G. S.; Ahmed, H.; Ahmed, J.; Ahmed, L. A.; Ahmed, M. S.; Ahmed, M. S.; Ahmed, M. B.; Ahmed, M.; Ahmed, N.; Ahmed, N.; Ahmed, S.; Ahmed, S. A.; Ajakwe, S. O.; Ajami, M.; Aji, B.; Akalu, Y.; Akeju, O.; Akhigbe, R. E.; Akhmedullin, R.; Oyeniran Akindele, M.; Akinosoglou, K.; Akiska, Y. M.; Akkaif, M. A.; Akram, H.; Akrami, A. E.; Awaidy, S. A.; Hamad, H. A.; Al Hasan, S. M.; Omari, O. A.; Qadire, M. A.; Thaher, Y. A.; Mahmoud Al Zoubi, M. A.; Al-Ajlouni, Y.; Alalwan, T. A.; Al-Aly, Z.; Alam, K.; Alam, M. K.; Alam, M.; Alam, Z.; Al-amer, R. M.; Alansari, A.; Alanzi, T. M.; Alarifi, A.; Al-Ashwal, F. Y.; Alavi, R.; Albashtawy, M.; Al-Daken, L. I.; Aldawsari, K. A.; Aldhahir, A. M.; Aldossary, M. S.; Aleidi, S. M.; Alemayehu, B. A.; Alemayehu, T. T.; Alemi, H.; Abdelazeem M Algammal, P.; Saeed Al-Gheethi, A. A.; Alhajri, N.; Alhalaiqa, F. N.; Al-Hanawi, M. K.; Alharrasi, M.; Alhumaidi, A.; Ali, A.; Ali, E. A.; Ali, K.; Ali, M. D.; Ali, M. U.; Ali, R.; Ali, S. A.; Ali, S. S.; Ali, S. Y.; Al-Ibraheem, A.; Al-Iede, M.; Alif, S. M.; Rokny, H. A.; Al-Jabi, S. W.; Aljawadi, M. H.; Aljofan, M.; Aljunid, S. M.; Alkhatib, A.; Alkousheh, H.; Alla, F.; Al-Mamun, M.; Al-Marwani, S.; Almasri, N. A.; Almazan, J. U.; Almidani, O.; Almobayed, A.; Alnaeem, M. M.; Al-Naqeb, G. N.; Alniss, H. Y.; Alomari, M. A.; Alosta, M. R.; Alqahtani, J. S.; Alqudimat, M. R.; Alrawashdeh, A.; Alrimawi, I.; Alrousan, S. M.; Alsabri, M. A.; Alsakarneh, S.; Alshehri, M. A.; Altaany, Z.; Altaf, A.; Al-Tammemi, A. B.; Al-Tawfiq, J. A.; Alvis-Guzman, N.; Alvis-Zakzuk, N. J.; Alwafi, H.; Al-Wardat, M.; Al-Worafi, Y. M.; Aly, H.; AlZahmi, A.; Alzahrani, H.; Alzoubi, A.; Alzoubi, K. H.; Al-Zubayer, M. A.; Amafah, E. J.; Amafah, J.; Amani-Beni, R.; Amanollahi, M.; Amaravadi, S. K.; Amegah, A. K.; Amegbor, P. M.; Amenah, M. A.; Amidi, B.; Amin, T. T.; Amindarolzarbi, A.; Amini-Rarani, M.; Amini-Salehi, E.; Aminorroaya, A.; Aminzare, M.; Amiri, S.; Ammirati, E.; Amobonye, A.; Ampon-Wireko, S.; Amu, H.; Amugsi, D. A.; Amusa, G. A.; Anagnostakis, F.; Ananda, R. A.; Anaraki, N.; Ancuceanu, R.; Anderlini, D.; Anderson, D. B.; Anderson, J. A.; Andrei, C. L.; Ang, S. P.; Angappan, S.; Anh, N. H.; Anil, A.; Ansari, S.; Ansariadi, A.; Anteneh, R. M.; Anuoluwa, B. S.; Anuoluwa, I. A.; Anvari, S.; Anwar, S.; Anwar, S. L.; Anwer, R.; Anyasodor, A. E.; Appiah, F.; Arab, J. P.; Arabloo, J.; Arafa, E. A.; Arafat, M.; Aravkin, A. Y.; Areda, D.; Aremu, O.; Arias De La Torre, J.; Armocida, B.; Arockiaraj, J.; Arooj, M.; Arshadi, M.; Artamonov, A. A.; Arumugam, A.; Asaduzzaman, M.; Basheeruddin Asdaq, S. M.; Melaku Asefa, S. M.; Asgary, A.; Asghari-Jafarabadi, M.; Ashagre, A. F.; Ashames, A.; Ashfaq, M.; Ashraf, H.; Basit Ashraf, M. A.; Ashraf, T.; Ashrafi, M.; Aslam, M. S.; Asrat, A. A.; Asri, Y.; Assefa, D. Z.; Assembekov, B.; Astell-Burt, P. T.; Athari, S. S.; Wahbi Atout, M. M.; Atreya, A.; Atta, J. A.; Aurangzeb, K.; Ausloos, M.; Avula, S.; Awedew, A. F.; Awoke, M. A.; Awotidebe, A. W.; Awoyomi, O. O.; Axame, W. K.; Ayele, B. A.; Ayyad, M.; Azadnajafabad, S.; Azadnia, A.; Azami, H.; Azarboo, A.; Azhar, M.; Aziz, M. Y.; Aziz, S. A.; Azizan, A.; Azizi, H.; Azzam, A. Y.; Azzolino, D.; Babatope, A. E.; Babu, A. S.; Babu, G. R.; Badar, M.; Badran, A. A.; Bagga, A.; Baghcheghi, N.; Bagheri, N.; Bagheri, S.; Baghizadeh, E.; Baghizadeh, F.; Baghizadeh, S.; Taghanaki, P. B.; Bahreini, R.; Bai, R.; Bains, L.; Bakkannavar, S. M.; Bako, A. T.; Balakrishnan, S.; Balasubramanian, M.; Balcha, W. F.; Baldereschi, M.; Balkis, M.; Baloch, F.; Balogun, S. A.; Hasankhani, M. B.; Baltatu, O. C.; Bam, K.; Banda, K. J.; Reddy Bandaru, P. K.; Chandra Banik, P.; Banik, R.; Bansal, H.; Bansal, K.; Barati, S.; Barbic, F.; Bardhan, M.; Barengo, N. C.; Barker-Collo, S. L.; Barqawi, H. J.; Barteit, S.; Barua, L.; Abu Bashar, M.; Bashir, S.; Bashiri, A.; Aliabadi, S. B.; Basri, R.; Bastan, M.; Basu, S.; Batra, K.; Bauckneht, M.; Bayat, M.; Bayat, R.; Bayih, M. T.; Bayisa, F. S.; Beeraka, N. M.; Behnoush, A. H.; Bekele, A.; Belayneh, A. 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P.; Buendia Rodriguez, J. A.; Roever, L.; Rojas-Rueda, D.; Romadlon, D. S.; Ronfani, L.; Rong, J.; Roshandel, G.; Roshanshad, A.; Rotimi, K.; Sekhar Rout, P. H.; Rouzbahani, S.; Roy, A.; Roy, B.; Roy, N.; Roy, P.; Roy, S.; Roy, S.; Roy, S.; Russo, M.; Rwegerera, G. M.; N, C. S.; Eddin, A. S.; Saadatian, Z.; Saber, K.; Saber-Ayad, M. M.; Sabet, C. J.; Sabour, S.; Sachdev, P. S.; Sachdeva, R.; Sadarangani, K. P.; Saddik, B. A.; Sadee, B. A.; Sadegh, T.; Sadeghi-Ghyassi, F.; Saeed, U.; Safari, M.; Sagar, R.; Saghafi, A.; Saghazadeh, A.; Sagoe, D.; Saha, N.; Sharif-Askari, F. S.; Sharif-Askari, N. S.; Sahebkar, A.; Sahiledengle, B.; Sahoo, P. M.; Sahu, K. S.; Sahu, M.; Sajadi, S M.; Uz Zaman Sajib, M. R.; Sajid, M. R.; Salabat, D.; Salami, A. A.; Salarabedi, M.; Salau, I. L.; Saleh, M. A.; Salehi, M.; Salehi, S.; Salehi, S.; Omran, H. S.; Salem, M. R.; Y Salem, M. Z.; Salimi, S.; Samadzadeh, S.; Samargandy, S.; Samimisedeh, P.; Samodra, Y. L.; Samuel, N. S.; Samuel, V. P.; Samy, A. 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S.; Sun, J.; Sun, X.; Sun, Z.; Sundaram, S. P.; Sundström, J.; Sunny, S.; Sunuwar, D. R.; Susianti, H.; Swain, C. K.; Swami Vetha, B. S.; Szarpak, P. L.; Damavandi, P. T.; Tabarés-Seisdedos, R.; Tabatabaei, S. M.; Tabche, C.; Tabibi, R.; Tabish, M.; Tabuchi, T.; Tadesse, G. F.; Tafida, B. A.; Arashlow, F. T.; Taiba, J.; Tajabadi, S.; Takele, W. W.; Talaat, I. M.; Talic, S.; Tampa, M.; Tamuzi, J. L.; Tanashat, M.; Tang, H.; Tantisattamo, E.; Tarekegn, G. E.; Tariq, S.; Tavakoli, K.; Tavangar, S. M.; Tavasol, A.; Tekola, A.; Temesgen, W. A.; Temsah, M.; Teramoto, M.; Tewari, J.; Teye-Kwadjo, E.; Teymourzadeh, A.; Raman Thankappan, P. K.; Thapa, R.; Thapar, R.; Thavamani, A.; Sundaram, M. T.; Thiruvengadam, M.; Thomas, J.; Tian, W.; Vera Ticoalu, J. H.; Tilakaratne, P. G.; Tiwari, K.; Tleshev, M.; Tomo, S.; Tonelli, P. M.; Topor-Madry, R.; Touvier, M.; Tovani-Palone, M. R.; Trabelsi, K.; Tran, N. M.; Tran, N. H.; Huong Tran, Q. T.; Minh Tran, T. Q.; Tran, T. H.; Minh Duc, N. T.; Trico, D.; Trihandini, I.; Tripathi, M.; Tripathi, T.; Tripathy, J. P.; Tromans, S. J.; Nguyen Truong, Q. X.; Tri Tai Truyen, T. T.; Hsiang-Te Tsai, D.; Tse, G.; Tsermpini, E. E.; Tuglo, L. S.; Tumkur Narayanappa, S. K.; Tumurkhuu, M.; Tusa, B. S.; Tye, S. C.; Tyrovolas, S.; Udoakang, A. J.; Ulhaq, I.; Ullah, A.; Ullah, S.; Ullah, S.; Umair, M.; Onozasi Umar, H. O.; Umar, L.; Umar, M.; Unim, B.; Unnikrishnan, B.; Upadhya, D.; Upadhyay, E.; Uppal, D.; Urmey, J. M.; Urso, D.; Usman, J. S.; Ussai, S.; Ustunsoz, D.; Ozsahin, D. U.; Uzunçıbuk, H.; Uzzaman, N.; Vadagam, P.; Vahdati, S.; Vaithinathan, A. G.; Vakilian, A.; Vakilpour, A.; Valizadeh, G.; Van Daalen, K. R.; Den Eynde, J. V.; Varghese, J.; Varma, R. P.; Varthya, S. B.; Varughese, S.; Vasankari, T. J.; Vasudevan, S. S.; Vellingiri, B.; Venketasubramanian, N.; Venkidasamy, B.; Verras, G.; Vervoort, D.; Vijayageetha, M.; Villafañe, J. H.; Villani, L.; Vipparthy, S. C.; Vishwakarma, M.; Vlassov, V.; Volovat, S. 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B.; Ye, P.; Yeganeh, M.; Yekdeş, A. C.; Yesodharan, R.; Yesuf, S. A.; Yezengaw, T. Y.; Yezli, S.; Yi, S.; Yin, D.; Keon Yon, D.; Yonemoto, N.; Youm, Y.; Yousefi, Z.; Yousefzadeh-Chabok, S.; Yu, C.; Yu, H.; Yu, Y.; Yuce, D.; Yunusa, I.; Yunusa, U.; Zaghampour, M.; Abidin, E. Z.; Zairov, D.; Zakham, F.; Zamagni, G.; Zanghì, A.; Zare, I.; Zaresharifi, S.; Zarinfar, Y.; Zastrozhin, M.; Zawiah, M.; Ali Zazouli, M.; Zeariya, M. G.; Birara Zemariam, A. B.; Zensen, S.; Zhan, T.; Zhang, C. J.; Zhang, H.; Zhang, J.; Zhang, L.; Zhang, L.; Zhang, X.; Zhang, Y.; Zhang, Z.; Zhao, H.; Zhao, Z.; Zheng, D. X.; Zheng, J.; Zheng, M.; Zhong, A.; Zhou, J.; Zhou, J.; Zhou, S.; Zhou, X.; Zhou, X.; Zhu, B.; Zhu, W.; Zhumagaliuly, A.; Ziegelmayer, S.; Zielińska, M.; Zoghi, G.; Ali Zoromba, M. A.; Zou, P. Z.; Zuber, M.; Zyoud, A. H.; Zyoud, S. H.; Zyoud, S. H.; L Murray, C. J.; Mensah, G. A.; and Roth, G. A.\n\n\n \n\n\n\n JACC, 86(22): 2167–2243. December 2025.\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

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@article{stark_global_2025,\n\ttitle = {Global, {Regional}, and {National} {Burden} of {Cardiovascular} {Diseases} and {Risk} {Factors} in 204 {Countries} and {Territories}, 1990-2023},\n\tvolume = {86},\n\tissn = {07351097},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0735109725074285},\n\tdoi = {10.1016/j.jacc.2025.08.015},\n\tlanguage = {en},\n\tnumber = {22},\n\turldate = {2026-05-19},\n\tjournal = {JACC},\n\tauthor = {Stark, Benjamin A. and DeCleene, Nicole K. and Desai, Emily C. and Hsu, Johnathan M. and Johnson, Catherine O. and Lara-Castor, Laura and LeGrand, Kate E. and A, Prof Bhoomadevi and Aalipour, Mohammad Amin and Aalruz, Hasan and Abafita, Bedru J. and Abaraogu, Ukachukwu O. and Abavisani, Mohammad and Abbas, Nasir and Abbasi, Madineh and Abbasian, Mohammadreza and Abbastabar, Hedayat and Abd Al Magied, Abdallah H.A. and ElHafeez, Samar Abd and Abdelalim, Prof Ahmed and Abdelfattah, Omar M. and Abdel-Hameed, Prof Reda and Abdelnabi, Mahmoud and Wael M Abdel-Rahman, Prof and Abdi, Parsa and Abdisa, Wakgari Mosisa and Abdissa, Daba and Abdous, Arman and Abdullah, Mujahid and Abdullahi, Auwal and Abdykerimova, Kulmira and Abebe, Mesfin and Abedi, Aidin and Abedi, Armita and Abejew, Asrat Agalu and Abhilash, E.S. and Abiodun, Olugbenga Olusola and Abiodun, Prof Olumide and Kasem, Rahim Abo and Aboagye, Richard Gyan and Abohashem, Shady and Abolhassani, Hassan and Abonie, Ulric Sena and Aborode, Abdullahi Tunde and Abourashed, Nagah Mohamed and Abramov, Dmitry and Abreu, Lucas Guimarães and Abtahi, Dariush and Abu Farha, Rana Kamal and Kende Abubakar, Aminu Kende and Abubakar, Ibrahim Jatau and Abu-Elala, Nermeen and Abu-Gharbieh, Eman and Abukhadijah, Hana J. and Aburuz, Salahdein and Abushanab, Dina and Acharya, Anirudh Balakrishna and Acharya, Apurba and Acharya, Swetha and Achore, Meshack and Adal, Ousman and Adams, Lisa C. and Adamu, Lawan Hassan and Adão, Rui and Addo, Isaac Yeboah and Adebayo, Oladimeji Muritala and Adebisi, Tajudeen Adesanmi and Adedia, David and Adedokun, Kamoru Ademola and Adegbile, Oluwatobi E. and Adegboye, Oyelola A. and Adegoke, Nurudeen A. and Adekanmbi, Victor and Adeleke, Olumide Thomas and Oluwaseun Adetunji, Charles and Adeyomoye, Olorunsola Israel and Adha, Rishan and Adhikari, Kishor and Adhikary, Ripon Kumar and Adikusuma, Wirawan and Parvar, Tanin Adl and Adnan, Mohd and Sakilah Adnani, Qorinah Estiningtyas and Adoma, Prince Owusu and Adzigbli, Leticia Akua and Adzrago, David and Afifi, Ahmed M. and Afolabi, Habeeb Abiodun and Afrashteh, Fatemeh and Afrooghe, Arya and Afzal, Muhammad Sohail and Afzal, Saira and Agampodi, Suneth Buddhika and Agarwal, Dhiraj Motilal and Agarwal, Gina and Agarwal, Prerna and Ageru, Temesgen Anjulo and Aggarwal, Navidha and Aghajanian, Sepehr and Sobrinho, César Agostinis and Agyemang-Duah, Williams and Ahadi, Mahsa and Ahammed, Benojir and Ahinkorah, Bright Opoku and Ahmad, Aqeel and Ahmad, Fuzail and Ahmad, Khurshid and Ahmad, Muayyad M. and Ahmad, Sajjad and Ahmad, Shoaib and Ahmad, Tauseef and Ahmadzadeh, Koohyar and Ahmed, Ali and Ahmed, Anisuddin and Ahmed, Ayman and Ahmed, Gasha Salih and Ahmed, Haroon and Ahmed, Junaid and Ahmed, Luai A. and Ahmed, Mehrunnisha Sharif and Ahmed, Meqdad Saleh and Ahmed, Muktar Beshir and Ahmed, Mushood and Ahmed, Naveed and Ahmed, Nesredin and Ahmed, Shabbir and Ahmed, Syed Anees and Ajakwe, Simeon Okechukwu and Ajami, Marjan and Aji, Budi and Akalu, Yonas and Akeju, Oluwasefunmi and Akhigbe, Roland Eghoghosoa and Akhmedullin, Ruslan and Oyeniran Akindele, Mukadas and Akinosoglou, Karolina and Akiska, Yagiz Matthew and Akkaif, Mohammed Ahmed and Akram, Hammad and Akrami, Ashley E. and Awaidy, Salah Al and Hamad, Hanadi Al and Al Hasan, Syed Mahfuz and Omari, Omar Al and Qadire, Mohammad Al and Thaher, Yazan Al and Mahmoud Al Zoubi, Mohammad Ahmmad and Al-Ajlouni, Yazan and Alalwan, Tariq A. and Al-Aly, Ziyad and Alam, Khurshid and Alam, Mohammad Khursheed and Alam, Mostafa and Alam, Zufishan and Al-amer, Rasmieh Mustafa and Alansari, Amani and Alanzi, Turki M. and Alarifi, Abdullah and Al-Ashwal, Fahmi Y. and Alavi, Rashid and Albashtawy, Mohammed and Al-Daken, Laila Ismael and Aldawsari, Khalifah A. and Aldhahir, Abdulelah Mastour and Aldossary, Mohammed S. and Aleidi, Shereen M. and Alemayehu, Bezawit Abeje and Alemayehu, Tekletsadik Tekleslassie and Alemi, Hediyeh and Abdelazeem M Algammal, Prof and Saeed Al-Gheethi, Adel Ali and Alhajri, Noora and Alhalaiqa, Fadwa Naji and Al-Hanawi, Mohammed Khaled and Alharrasi, Maryam and Alhumaidi, Ashraf and Ali, Akhtar and Ali, Endale Alemayehu and Ali, Kamran and Ali, Mohammad Daud and Ali, Mohammed Usman and Ali, Rafat and Ali, Sameer A. and Ali, Syed Shujait and Ali, Syed Yusuf and Al-Ibraheem, Akram and Al-Iede, Montaha and Alif, Sheikh Mohammad and Rokny, Hamid Alinejad and Al-Jabi, Samah W. and Aljawadi, Mohammad Hasan and Aljofan, Mohamad and Aljunid, Syed Mohamed and Alkhatib, Ahmad and Alkousheh, Hazim and Alla, François and Al-Mamun, Md and Al-Marwani, Sabah and Almasri, Nihad A. and Almazan, Joseph Uy and Almidani, Omar and Almobayed, Amr and Alnaeem, Mohmmad Minwer and Al-Naqeb, Ghanya Naji and Alniss, Hasan Yaser and Alomari, Mahmoud A. and Alosta, Mohammad R. and Alqahtani, Jaber S. and Alqudimat, Mohammad R. and Alrawashdeh, Ahmad and Alrimawi, Intima and Alrousan, Sahel Majed and Alsabri, Mohammed A. and Alsakarneh, Saqr and Alshehri, Mansour Abdullah and Altaany, Zaid and Altaf, Awais and Al-Tammemi, Alaa B. and Al-Tawfiq, Jaffar A. and Alvis-Guzman, Nelson and Alvis-Zakzuk, Nelson J. and Alwafi, Hassan and Al-Wardat, Mohammad and Al-Worafi, Yaser Mohammed and Aly, Hany and AlZahmi, Amal and Alzahrani, Hosam and Alzoubi, Abdallah and Alzoubi, Karem H. and Al-Zubayer, Md Akib and Amafah, Ekiyor Joseph and Amafah, Joy and Amani-Beni, Reza and Amanollahi, Mobina and Amaravadi, Sampath Kumar and Amegah, Adeladza Kofi and Amegbor, Prince M. and Amenah, Michel Adurayi and Amidi, Bardia and Amin, Tarek Tawfik and Amindarolzarbi, Alireza and Amini-Rarani, Mostafa and Amini-Salehi, Ehsan and Aminorroaya, Arya and Aminzare, Majid and Amiri, Sohrab and Ammirati, Enrico and Amobonye, Ayodeji and Ampon-Wireko, Sabina and Amu, Hubert and Amugsi, Dickson A. and Amusa, Ganiyu Adeniyi and Anagnostakis, Filippos and Ananda, Roshan A. and Anaraki, Nazanin and Ancuceanu, Robert and Anderlini, Deanna and Anderson, David B. and Anderson, Jason A. and Andrei, Catalina Liliana and Ang, Song Peng and Angappan, Santhalakshmi and Anh, Nguyen Hoang and Anil, Abhishek and Ansari, Sumbul and Ansariadi, Ansariadi and Anteneh, Rahel Mulatie and Anuoluwa, Boluwatife Stephen and Anuoluwa, Iyadunni Adesola and Anvari, Saeid and Anwar, Saleha and Anwar, Sumadi Lukman and Anwer, Razique and Anyasodor, Anayochukwu Edward and Appiah, Francis and Arab, Juan Pablo and Arabloo, Jalal and Arafa, Elshaimaa A. and Arafat, Mosab and Aravkin, Aleksandr Y. and Areda, Demelash and Aremu, Olatunde and Arias De La 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Shirin and Barbic, Franca and Bardhan, Mainak and Barengo, Noel C. and Barker-Collo, Suzanne Lyn and Barqawi, Hiba Jawdat and Barteit, Sandra and Barua, Lingkan and Abu Bashar, Md and Bashir, Shahid and Bashiri, Azadeh and Aliabadi, Somaye Bashiri and Basri, Rehana and Bastan, Mohammad-Mahdi and Basu, Saurav and Batra, Kavita and Bauckneht, Matteo and Bayat, Mahdis and Bayat, Reza and Bayih, Mulat Tirfie and Bayisa, Feyisa Shasho and Beeraka, Narasimha M. and Behnoush, Amir Hossein and Bekele, Alehegn and Belayneh, Asnake Gashaw and Belete, Abebe Gedefaw and Belete, Abel Cherkos and Bilgin, Gokce Belge and Bello, Bashir and Bello, Olorunjuwon Omolaja and Bello, Umar Muhammad and Belo, Luis and Belsti, Yitayeh and Benfor, Bright and Bennett, Derrick A. and Bensenor, Isabela M. and Bente Kamal Tune, Samiun Nazrin and Benziger, Catherine P. and Bera, Om Prakash and Berezvai, Zombor and Bergami, Maria and Berhe, Kenfe Tesfay and Berhie, Alemshet Yirga and Berihun, Abiye Assefa and Nazer C Bermudez, Amiel and Bernstein, Robert S. and Bhadoria, Ajeet Singh and Bhagavathula, Akshaya Srikanth and Bhandari, Buna and Bhardwaj, Nikha and Bhardwaj, Pankaj and Bhaskar, Sonu and Bhattacharjee, Priyadarshini and Bhattacharjee, Shuvarthi and Bhatti, Gurjit Kaur and Bhatti, Jasvinder Singh and Bhatti, Rajbir and Bhuyan, Soumitra S. and Biadgilign, Sibhatu Kassa and Bilgin, Can and Bilgin, Cem and Birck, Marina G. and Birhan, Mekuriaw Mesfin and Birru, Eshetie Melese and Biswas, Bijit and Biswas, Mohammad Shahangir and Biswas, Monirujjaman and Biswas, Raaj Kishore and Bizzozero-Peroni, Bruno and Bjørge, Tone and Bodhare, Trupti and Bodunrin, Aadam Olalekan and Bogale, Sitotaw Kerie and Bohn, Lucimere and Bolarinwa, Obasanjo Afolabi and Boloor, Archith and Hashemi, Milad Bonakdar and Bonakdarhashemi, Moein and Basara, Berrak Bora and Borhany, Hamed and Borran, Mina and Bosoka, Samuel Adolf and Carvajal, Alejandro Botero and Boyko, Edward J. and Bozic, Marija M. and Braithwaite, Dejana 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Anis and Cerrai, Sonia and Chadwick, Joshua and Shivamadhu, Madhu Chakkere and Chakraborty, Aditya and Chakraborty, Chiranjib and Chakraborty, Sandip and Kai Chan, Jeffrey Shi and Chandika, Rama Mohan and Chandradasa, Miyuru and Chandramouli Bellur, Vinay and Chandrasekar, Eeshwar K. and Chang, Qinghua and Charan, Jaykaran and Chattu, Vijay Kumar and Chaudhary, Anis Ahmad and Chaudhuri, Sirshendu and Chavoshi, Mohammadreza and Chen, An-Tian and Chen, Guangjin and Chen, Haiyan and Chen, Hana and Chen, Haowei and Chen, Meng Xuan and Chen, Simiao and Chen, Xiang and Cheung, Ka Ching and Chew, Derek S. and Chew, Nicholas Ws. and Chhabra, Ravindresh and Chi, Gerald and Chichagi, Fatemeh and Chimoriya, Ritesh and Ching, Patrick R. and Chiriacò, Martina and Chirinos-Caceres, Jesus Lorenzo and Chitheer, Abdulaal and Jemma Cho, So Mi and Cho, William C.S. and Chong, Bryan and Chong, Yuen Yu and Chopra, Hitesh and Chopra, Shivani and Chou, Hou In and Choudhari, Sonali Gajanan and Chowdhury, Enayet Karim and Chowdhury, Rajiv and Chowdhury, Sreshtha and Christensen, Hanne and Christopher, Devasahayam J. and Chu, Dinh-Toi and Chukwu, Isaac Sunday and Chung, Sheng-Chia and Chung, Sunghyun and Cioffi, Iolanda and Cohen, Aaron J. and Columbus, Alyssa and Conde, Joao and Congly, Stephen E. and Conrad, Nathalie and Conti, Sara and Cortesi, Paolo Angelo and Cosma, Claudia and Costa, Vera Marisa and Criqui, Michael H. and Cruz-Martins, Natalia and Da Silva, Alanna Gomes and Dababo, Nour and Dabbagh, Ali and Dabo, Bashir and Dadras, Omid and Dai, Xiaochen and Dai, Zhaoli and Dalakoti, Mayank and Moura Damasceno, Albertino Antonio and D'Amico, Emanuele and Danaei, Bardia and Dandona, Lalit and Dandona, Rakhi and Dang, Anh Kim and D'Anna, Lucio and Danpanichkul, Pojsakorn and Danso, Samuel E. and Darcho, Samuel Demissie and Darouei, Bahar and Cheshmeh Soltani, Reza Darvishi and Das, Saswati and Dashtkoohi, Mohadese and Davletov, Dimash and Davletov, Kairat and Dayasiri, Kavinda and De La Hoz, Fernando Pio and Deb, Novonil and Dehadrai, Aniket and Del Bo', Cristian and Del Riccio, Marco and Delsoz, Mohammad and Demeke, Dessalegn and Deng, Ke and Denova-Gutiérrez, Edgar and Molla, Meseret Derbew and Dergaa, Ismail and Derseh, Hunegnaw Almaw and Dervišević, Emina and Desai, Hardik Dineshbhai and Desai, Rupak and Desta, Abraham Aregay and Deuba, Keshab and Devarakonda, Pradeep Kumar and Devegowda, Devananda and Rahman Dewan, Syed Masudur and Dhali, Arkadeep and Dhama, Kuldeep and Rajinder K K Dhamija, Prof and Dhimal, Meghnath and Dhungel, Bibha and Bella, Stefano Di and Pumpo, Marcello Di and Da Silva, Diana Dias and Diaz, Luis Antonio and Dima, Adriana and Ding, Xueting and Do, Huyen and Phuong Do, Thao Huynh and Luiz Do Amaral Do Amaral Júnior, Orlando Luiz and Doegah, Phidelia Theresa and Dohare, Sushil and Dokova, Klara Georgieva and Dondi, Francesco and D'Oria, Mario and Dorostkar, Fariba and Dos Santos, Wendel Mombaque and Doshi, Ojas Prakashbhai and Dowou, Robert Kokou and Dresse, Menayit Tamrat and Dsouza, Viola Savy and Du, Mi and Dube, John and Dumbili, Emeka W. and Duncan, Bruce B. and Dunne, Jennifer and Duraes, Andre Rodrigues and Durojaiye, Oyewole Christopher and Dutta, Siddhartha and Dutta, Sulagna and E’mar, Abdel Rahman and Ebohon, Osamudiamen and Mahmoud Ebraheim, Lamiaa Labieb and Ebrahimi, Alireza and Ebrahimi, Mohammad Hossein and Ebrahimi, Rasoul and Ebrahimi, Sara and Edinur, Hisham Atan and Efendi, Ferry and Eftekhari, Behrad and Eghbali, Foolad and Eghdami, Shayan and Sedeh, Ashkan Eighaei and Eini, Ebrahim and Ekholuenetale, Michael and Ekundayo, Temitope Cyrus and El Arab, Rabie Adel and Wahab El Morsi, Doaa Abdel and Sayed Zaki, Maysaa El and Eladl, Mohamed Ahmed and Mustafa Elagali, Ahmed Elabbas and Elalfy, Aya and El-Ashker, Said and El-Dahiyat, Faris and Elgendy, Islam Y. and Elhadi, Muhammed and El-Huneidi, Waseem and Elkannishy, Sherif and Elmonem, Mohamed A. and Elmoselhi, Adel B. and Elnaem, Mohamed Hassan and Elsohaby, Ibrahim and Eltahir, Mohd Elmagzoub and Zeydi, Amir Emami and Emeto, Theophilus I. and Emran, Talha Bin and Eshraghi, Reza and Eskandari, Khalil and Eskandarieh, Sharareh and Eyawo, Oghenowede and Fabin, Natalia and Fadavian, Heidar and Fagbamigbe, Adeniyi Francis and Fahim, Ayesha and Fahimi, Saman and Fahira, Aamir and Faiz, Razana and Fakhradiyev, Ildar Ravisovich and Falzone, Luca and Fan, Qiping and Farahani, Alireza and Farahmand, Mohammad and Faraji, Seyed Nooreddin and Faramarzpour, Mahsa and Aquino Faraon, Emerito Jose and Fareed, Mohammad and Farina, Jacopo and Mahmoud Faris, MoezAlIslam Ezzat and Faro, Andre and Yousaf Farooq, Syed Muhammad and Farooqui, Maryam and Farrokhpour, Hossein and Farshad, Fatemeh and Farsi, Farima and Fatima, Zareen and Fazeli, Pooria and Feili, Afrooz and Feizkhah, Alireza and Fekadu, Ginenus and Feng, Xiaoqi and Fereshtehnejad, Seyed-Mohammad and Fernandez-Jimenez, Rodrigo and Feroze, Abdullah H. and Ferrara, Pietro and Ferreira, 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Mansueto and Goodarzian, MReza and Goshu, Abel Tibebu and Goulart, Alessandra C. and Gregorio, Ernesto Ramos and Grivna, Michal and Grover, Ashna and Guadie, Habtamu Alganeh and Guan, Shi-Yang and Guan, Zhongyang and Guarducci, Giovanni and Mohialdeen Gubari, Mohammed Ibrahim and Guha, Avirup and Guicciardi, Stefano and Gulati, Sheffali and Gulati, Snigdha and Gunawardane, Damitha Asanga and Gunturu, Sasidhar and Guo, Qianyu and Guo, Xingzhi and Guo, Zheng and Guo, Zhifeng and Gupta, Anish Kumar and Gupta, Bhawna and Gupta, Himanshu and Gupta, Lalit and Gupta, Rahul and Gupta, Rajeev and Gupta, Sapna and Gupta, Vivek Kumar and Gutiérrez-Murillo, Roberth Steven and Guzman-Esquivel, Jose and Habibzadeh, Adrina and Habibzadeh, Farrokh and Tesfaye Habteyes, Abrham Tesfaye and Habteyohannes, Awoke Derbie and Hadei, Mostafa and Hadi, Najah R. and Hadian, Zahra and Haghdoost, Faraidoon and Haghmorad, Dariush and Haghtalab, Arian and Haile, Demewoz and Hailu, Haimanot Ewnetu and Haj-Mirzaian, Arvin and Halder, Pritam and Halim, Sobia Ahsan and Halwani, Rabih and Hamad, Islam M. and Hamdy, Nadia M. and Hamidi, Samer and Hamilton, Erin B. and Hammoud, Ahmad and Hamza, Mohammad and Hamza, Umar Sabiu and Hanif, Asif and Hanifi, Nasrin and Hankey, Graeme J. and Hanna, Fahad and Haque, Moon Moon and Haque, Obaid I. and Hareru, Habtamu Endashaw and Haro, Josep Maria and Marah Has, Eka Mishbahatul and Hasaballah, Ahmed I. and Hasan, Faizul and Hasan, Md Kamrul and Hasani, Hamidreza and Hasanpour- Dehkordi, Ali and Hashemian, Maryam and Hashempour, Zahra and Hashempur, Mohammad Hashem and Hashim, Nada Tawfig and Saquib Hasnain, Md and Hassan, Amr and Hassan, Ikrama Ibrahim and Hassan, Md Imtaiyaz and Hassan, Muhammad and Hassan, Shoaib and Hassan Wada, Yusuf Wada and Hassan Zadeh Tabatabaei, Mahgol Sadat and Hassankhani, Hadi and Haubold, Johannes and Havmoeller, Rasmus J. and Hawat, Angie and Hay, Simon I. and He, Guohua and He, Jiawei and He, Qiang and Hebert, Jeffrey J. and 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Ikiroma, Adalia and Ilesanmi, Olayinka Stephen and Ilic, Irena M. and Ilic, Milena D. and Ilyas, Muhana Fawwazy and Imam, Mohammad Tarique and Immurana, Mustapha and Imoh, Lucius Chidiebere and Inok, Arit and Iqhrammullah, Muhammad and Isa, Mustafa Alhaji and Iskandar, Benni and Iskander, Teresa R. and Islam, Md Fakrul and Islam, Md Rabiul and Islam, Md Sahidul and Islam, Md Saiful and Islam, Md Shariful and Islam, Rakibul M. and Ismail, Faisal and Ismail, Nahlah Elkudssiah and Ismoldayev, Yerlan and Iso, Hiroyasu and Isola, Gaetano and Issa, Ramzy and Ituka, Mosimah Charles and Iwagami, Masao and Iyasu, Assefa N. and Jaafari, Jalil and Jacob, Louis and Jafari-Khounigh, Ali and Jaffar, Shabbar and Jaganathan, Vennila and Jaganathasamy, Nagaraj and Jahan, Shafkat and Jahangiri, Soodeh and Jahani, Shima and Jahrami, Haitham and Jain, Akhil and Jain, Ayushi and Jain, Pragati and Jairoun, Ammar Abdulrahman and Jaiswal, Swati and Jakovljevic, Mihajlo and Jaliliyan, Ali and Jalloh, Mohamed and Jamal, Armaan and Sajid Jamal, Qazi Mohammad and Jamali, Navid and Jameie, Melika and Jamshidi, Masoud and Janardhanan, Rajiv and Javadi, Nilofer and Javaid, Syed Sarmad and Javankiani, Sepide and Javanmardi, Anita and Jayanna, Krishnamurthy and Jayapal, Sathish Kumar and Jayaram, Shubha and Duminda Jayasinghe, Ruwan and Jayatilleke, Achala Upendra and Jeong, Seogsong and Jeswani, Bijay Mukesh and Jha, Anil K. and Ji, Zixiang and Jiang, Min and Jin, Wenyi and Jokar, Mohammad and Jonas, Jost B. and Joo, Tamas and Jor, Abu and Jose, Jobin and Jose, Jobinse and Joseph, Nitin and Joshua, Charity Ehimwenma and Josten, Kripa and Joukar, Farahnaz and Jozwiak, Jacek Jerzy and Jürisson, Mikk and Juweid, Malik E. and Kaambwa, Billingsley and Kabir, Ali and Kabir, Zubair and Kadashetti, Vidya and Kader, Avan and Kader, Md Lutful and Kadir, Dler Hussein and Kaibullayeva, Jamilya and Kakkar, Ashish Kumar and Kalankesh, Leila R. and Kalra, Sanjay and Kamal, Manoj and Kamarajah, Sivesh Kathir and Kamath, Ashwin and Kamel, Ibrahim and Kamireddy, Arun and Kamyari, Naser and Kamyshnyi, Oleksandr and Kan, Haidong and Kanaan, Mona and Kanaan, Saddam Fuad and Kankam, Samuel Berchi and Kazeem Kanmodi, Kehinde and Kansal, Sushil Kumar and Kantar, Rami S. and Kar, Sujita Kumar and Karagiannidis, Efstratios and Karakasis, Paschalis and Karami, Jafar and Karch, André and Kariman, Arian and Karimi, Aliasghar and Karimtabar, Hajar and Karki, Prabin and Karobari, Mohmed Isaqali and Karpiński, Tomasz M. and Kasa, Ayele Semachew and Kasozi, Derrick and Kasraei, Hengameh and Kassa, Tigabu Hailu and Kassar, Ahmad M. and Kassebaum, Nicholas J. and Kattea, Mohammad Obadah and Kazemian, Sina and Kedir, Shemsu and Keivanlou, Mohammad-Hossein and Kelly, Jaimon Terence and Kempegowda, Swetha N. and Keshwani, Ariz and Kesse-Guyot, Emmanuelle and Keykhaei, Mohammad and Khadembashiri, Mohamad Mehdi and Khadembashiri, Mohammad Amin and Khademi, Reza and Khader, Yousef Saleh and Khaing, Inn Kynn and Khajuria, Himanshu and Khaksar, Mohammad Ali and Khalid, Nauman and Khalil, Anees Ahmed and Khalili, Pantea and Khalis, Mohamed and Khan, Ajmal and Khan, Asaduzzaman and Khan, Faiz Ullah and Khan, Fayaz and Khan, Iman Waheed and Khan, Maseer and Saeed Khan, Md Abdullah and Khan, Moien Ab. and Khan, Muhammad Hamza and Khan, Muhammad Mueed and Khan, Muhammad Umer and Khan, Salman Ali and Khan, Serab and Khan, Sumaiya Khan and Khan, Ubaid and Khan, Yusuf Saleem and Khanal, Vishnu and Khashim, Zenith and Khatab, Prof Khaled and Khatatbeh, Moawiah Mohammad and Khatib, Mahalaqua Nazli and Khayat Kashani, Hamid Reza and Khazaei, Afshin and Kheirallah, Khalid A. and Zarandi, Peyman Kheirandish and Kheradmand, Daniel and Khidri, Feriha Fatima and Khokhar, Manoj and Khokhar, Sunil Kumar and Khoshrou, Alireza and Khoshvaght, Parisa and Khosla, Atulya Aman and Khosravi, Ahmad and Khosravi, Majid and Khosravi, Sepehr and Khosrowjerdi, Mahmood and Khuman, P Ratan and Kifle, Zemene Demelash and Kim, Jinho and Kim, Kwanghyun and Kim, Sungroul and Kim, Yun Jin and Kimokoti, Ruth W. and Kinfu, Yohannes and Kisa, Adnan and Kisa, Sezer and Kivimäki, Mika and Km, Shivakumar and Kobyliak, Nazarii and Kogi, Robert and Kohansal, Erfan and Kokkorakis, Michail and Kolahi, Ali-Asghar and Kolte, Dhaval and Kompani, Farzad and Koohestani, Hamid Reza and Koren, Gerbrand and Kormoker, Tapos and Korshunov, Vladimir Andreevich and Korzh, Oleksii and Koscik, Michal and Kostev, Karel and Kothari, Nikhil and Kothari, Yash Lalit and Kotnis, Ashwin Laxmikant and Koul, Parvaiz A. and Koulmane Laxminarayana, Sindhura Lakshmi and Kretchy, James-Paul and Krishan, Kewal and Krishna, Varun and Król, Zbigniew J. and Kua, Chong-Han and Hassan Kuchay, Raja Amir and Bicer, Burcu Kucuk and Kuddus, Mohammed and Kukreti, Shikha and Kulimbet, Mukhtar and Kulkarni, Vishnutheertha and Kumar, Ashish and Kumar, Dewesh and Kumar, G Anil and Kumar, Kamal and Kumar, Manasi and Kumar, Mukesh and Kumar, Narendar and Kumar, Nithin and Kumar, Rakesh and Kumar, Tushar and Kumar, Vijay and Kundu, Amartya and Kunutsor, Setor K. and Kurmi, Om P. and Kurniasari, Maria Dyah and Kusnali, Asep and Yeni Kustanti, Christina Yeni and Kusuma, Dian and Kuttybayev, Assylkhan and Patrick Kwong, Wai Hang and Kytö, Ville and C, Pallavi L. and Vecchia, Carlo La and Lahariya, Chandrakant and Ching Lai, Daphne Teck and Lakanova, Balzhan and Lallukka, Tea and Lám, Judit and Lanfranchi, Francesco and Lasrado, Savita and Latif, Areeba and Lee Lau, Kenney Ki and Lawal, Basira Kankia and Lawan, Aliyu and Thanh Le, Huyen Thi and Thu Le, Thao Thi and Le, Thoa and Thanh Le, Trang Diep and Bich Le, Trang Thi and Leasher, Janet L. and Lee, Ivan and Lee, Paul H. and Lee, Seung Won and Lee, Wei-Chen and Leivaditis, Vasileios and Leonardi, Matilde and Leong, Elvynna and Letafatkar, Negin and Li, An and Li, Daisong and Li, Jiaying and Li, Jie and Li, Ming-Chieh and Li, Wei and Li, Weilong and Li, Wenjie and Li, Yichong and Li, Zhaolong Adrian and Li, Zhihui and Lim, Lee-Ling and Lim, Stephen S. and Lin, Jialing and Lin, Queran and Lin, Ro-Ting and Lindholm, Daniel and Liu, Gang and Liu, Haipeng and Liu, Xiaofeng and Liu, Xuefeng and Liu, Zhe and Llanaj, Erand and Lohner, Valerie and Lonimath, Ashwini and López-Gil, José Francisco and Lopukhov, Platon D. and Lorenzovici, László and Lorkowski, Stefan and Lotufo, Paulo A. and Lourembam, Surbala Devi and Lucchetti, Giancarlo and Lugo, Alessandra and Luo, Peng and Lutambi, Angelina M. and Lv, Hengliang and Lv, Lei and Lwin, Kaung Suu and Lytras, Dimitrios and Lytras, Miltiadis D. and Lytvyak, Ellina and Ma, Kevin Sheng-Kai and Ma, Zheng Feei and Mabrok, Mahmoud and Machoy, Monika and Madadi, Firoozeh and Madinezad, Seyed Ataollah and Madureira-Carvalho, Aurea Marilia and Maffia, Pasquale and Magaña Gómez, Javier A. and Maghazachi, Azzam A. and Mahalingam, Sasikumar and Mahalleh, Mehrdad and Mahalwar, Gauranga and Mahamed, Abdulahi Abdiwali and Mahamed, Samatar Abshir and Mahasha, Phetole Walter and Mahjoob, Monireh and Mahmood, Nozad Hussein and Mahmoudi, Elham and Mahmoudi, Farhad and Maiti, Rituparna and Majmundar, Vidit D. and Malagón-Rojas, Jeadran N. and Rad, Elaheh Malakan and Malekzadeh, Reza and Singh Malhotra, Hardeep and Malik, Ahmad Azam and Ahmed Malik, Muhammad Sajeel and Malik, Shahid and Malik, Tabarak and Malta, Deborah Carvalho and Mangdow, Mustapha and Manirambona, Emery and Manjani, Lokesh and Manla, Yosef and Mannan, Fahmida and Mannethodi, Kamaruddeen and Mansoor, Farheen and Mansouri, Vahid and Mansourian, Marjan and Mansournia, Mohammad Ali and Manu, Emmanuel and Maqsood, Sajid and Marasini, Bishnu P. and Marateb, Hamid Reza and Marino, Mirko and Marks-Hultström, Michael and Marques, Adilson and Martinez-Piedra, Ramon and Martins-Melo, Francisco Rogerlândio and Martorell, Miquel and März, Winfried and Rillera Marzo, Roy and Marzouk, Sammer and Masi, Stefano and Masoudi, Alireza and Masrouri, Soroush and Matei, Clara N. and Mathangasinghe, Yasith and Mathew, Don and Mathur, Medha and Mathur, Neeta and Penido Matozinhos, Fernanda and Mattiello, Rita and Mattoo, Khurshid A. and Maude, Richard James and Maugeri, Andrea and Mazidi, Mohsen and Mazzaglia, Giampiero and McPhail, Steven M. and Medel Salas, María Paz and Mehboob, Riffat and Mehmood, Asim and Mehravar, Fatemeh and Mehrotra, Ravi and Mehta, Vini and Meto, Tesfahun Mekene and Mekonnen, Berhanu Abebaw and Mekonnen, Eskedar Getie and Meles, Hadush Negash and Melisa, Septi and Memish, Ziad Ahmed and Mendoza, Walter and Menezes, Godfred Antony and Menezes, Ritesh G. and Mengesha, Endalkachew Worku and Mengistie, Emiru Ayalew and Mentis, Alexios-Fotios A and Mercogliano, Michelangelo and Meretoja, Atte and Mestrovic, Tomislav and Kukulege Mettananda, Chamila Dinushi and Mettananda, Sachith and Metwally, Mohamed and Miezah, Dennis and Miller, Ted R. and Minervini, Giuseppe and Ming, Wai-kit and Mini, G.K. and Mirdamadi, Arian and Mirdamadi, Niloofar and Mirghafourvand, Mojgan and Mirrakhimov, Erkin M. and Mirzaei, Roya and Mishra, Amaresh and Mishra, Archana and Mishra, Shivangi and Mishra, Vinaytosh and Mithra, Prasanna and Mittal, Chaitanya and Mobayen, Mohammadreza and Modi, Natansh Deepak and Mogessie, Yidnek and Mohamed, Abdalla Z. and Mohamed, Ahmed Ismail and Mohamed, Heba M. and Mohamed, Hebatalla and Mohamed, Jama and Mohamed, Mona Gamal and Mohamed, Nouh Saad and Mohammad, Ameen Mosa and Mohammad, Taj and Mohammad-Alizadeh-Charandabi, Sakineh and Mohammadi, Abdolreza and Mohammadi, Ida and Mohammadi, Saeed and Mohammadi, Sammy and Mohammadi, Seyed Omid and Mohammadian-Hafshejani, Abdollah and Mohammadpour, Saeed and Mohammadzadeh, Ibrahim and Mohammed, Hussen and Mohammed, Shafiu and Mohammed, Yahaya and Mohan, Syam and Mohsen, Yazan and Mohsenzadeh, Amin and Mohsin, Aleenah and Mokdad, Ali H. and Mokhirev, Alexandr and Vardanjani, Hossein Molavi and Molinaro, Sabrina and Momani, Shaher and Momeni, Hamidreza and Monasta, Lorenzo and Monazzami, Amirabbas and Moni, Mohammad Ali and Mons, Ute and Namin, Sara Montazeri and Moradi, Tayebeh and Moraga, Paula and Morales-Juárez, Linda and Morawska, Lidia and Moreira, Rafael Silveira and Morgan, Anthony Kwame and Morovatdar, Negar and Morsy, Mahmoud M. and Morze, Jakub and Mossialos, Prof Elias and Motaharinezhad, Fatemeh and Motappa, Rohith and Motavvef, Maha and Motiei, Mahsa and Mousavi, Parsa and Khaneghah, Amin Mousavi and Sadegh Mousavi Kiasary, Seyed Mohamad and Mowafy, Hagar and Mozafar, Mehrdad and MozafaryBazargany, Mohammadhossein and Yousefi, Kimia Mozahheb and Mubarik, Sumaira and Muccioli, Lorenzo and Mueller, Ulrich Otto and Mukherjee, Sumoni and Mukoro, George Duke and Mulatu, Sileshi and Mulita, Admir and Mulita, Francesk and Mulu, Getaneh Baye and Muneer, Muneeb Ahmad and Muniyandi, Malaisamy and Munjal, Kavita and Munkhsaikhan, Yanjinlkham and Munshi, Anjana and Murillo-Zamora, Efren and Musa, Abbas and Musa, Sani and Mushtaq, Ali and Mustafa, Ahmad and Mustafa, Ghulam and Muthu, Sathish and Muthupandian, Saravanan and Muvunyi, Claude Mambo and Muzaffar, Muhammad and Mwita, Julius C. and Myung, Woojae and Nafei, Ayoub and Nagarajan, Ahamarshan Jayaraman and Naghavi, Pirouz and Naghshbandi, Mobin and Naik, Ganesh R. and Naik, Gurudatta and Naik, Hiten and Nainu, Firzan and Nair, Sanjeev and Najafi, Mohammad Sadeq and Rashid Najmuldeen, Hastyar Hama and Nakhostin Ansari, Noureddin and Nambi, Gopal and Nanavaty, Dhairya P. and Nangia, Vinay and Naqvi, Atta Abbas and Swamy, Sreenivas Narasimha and Nargus, Shumaila and Nascimento, Bruno Ramos and Nascimento, Gustavo G. and Naser, Mohammad and Nashwan, Abdulqadir J. and Nasrollahizadeh, Ali and Nasrollahizadeh, Amir and Nassar, Mahmoud and Natto, Zuhair S. and Nauman, Javaid and Naureen, Zakira and Kumari Navaratna, Samidi Nirasha and Nayak, Biswa Prakash and Ganesh Nayak, Shalini Ganesh and Shahariar Nayon, Md Fahad and Nchanji, G Takop and Ndejjo, Rawlance and Ndungu, Anthony Wainaina and Neal, Bruce and Nega, Amanuel Tebabal and Negahdary, Masoud and Negash, Wubshet D. and Negru, Alina Gabriela and Nejjari, Chakib and Nekouei, Omid and Nematollahi, Mohammad Hadi and Nepal, Gaurav and Netsere, Henok Biresaw and Nezameslami, Ahmadreza and Ng, Marie and Ngunjiri, Josephine W. and Nguyen, Cuong Tat and Nguyen, Dang and Hien Nguyen, Hau Thi and Nguyen, Hien Quang and Nhi Nguyen, Kieu Viet and Nguyen, Long and Nguyen, The Phuong and Nguyen, Van Thanh and Niazi, Robina Khan and Nieddu, Luciano and Nikoobar, Ali and Nikravangolsefid, Nasrin and Niranjan, Vikram and Niroomand, Behnaz and Vianney Niyonsenga, Jean Marie and Nizam, Muhammad A. and Afia Nkrumah-Boateng, Princess Afia and Nnaji, Chukwudi A. and Nomura, Shuhei and Ahmed Noor, Syed Toukir and Noormohammadpour, Pardis and Noreen, Mamoona and Noroozi, Masoud and Noubiap, Jean Jacques and Nouri, Mehran and Nriagu, Valentine C. and Nri-Ezedi, Chisom Adaobi and Ntsekhe, Mpiko and Nugen, Fred and Nuh, Abdulkadir Mohamed and Nurchis, Mario Cesare and Dodzi Nyadanu, Sylvester Dodzi and Nyande, Felix Kwasi and Oancea, Bogdan and Odat, Ramez M. and Oddi, Fabio Massimo and Odukoya, Oluwakemi Ololade and Oduro, Michael Safo and Oghenetega, Onome Bright and Ogundeko-Olugbami, Oluwafunmilayo Tosin and Oguta, James Odhiambo and Oh, Sarah and O'Hagan, Edel T. and Ojedoyin, Olusegun Olatunji and Ojo-Akosile, Tolulope R. and Okati-Aliabad, Hassan and Okeke, Sylvester Reuben and Okekunle, Akinkunmi Paul and Okesanya, Olalekan John and Okonji, Osaretin Christabel and Okwute, Patrick Godwin and Olabisi, Oluwaseyi Isaiah and Olagunju, Andrew T. and Olalusi, Oladotun Victor and Olanrewaju, Timothy Olusegun and Olatubi, Matthew Idowu and Oliveira, Arão Belitardo and Moraes Oliveira, Gláucia Maria and Olorukooba, Abdulhakeem Abayomi and Oludoye, Oluseye Olalekan and Olum, Ronald and Oluwole, Oluwafemi G. and Omage, Folorunsho Bright and Omer, Goran Latif and Omonisi, Abidemi E. and Ong, Sok King and Onyeaghala, Chizaram A. and Oommen, Anu Mary and Opitz, Marcel and Ordak, Michal and Orscelik, Atakan and Ortiz, Alberto and Ortiz-Prado, Esteban and Osborne, Augustus and Osman, Alaa A.M. and Osman, Wael M.S. and Ostrominski, John W. and Osuagwu, Uchechukwu Levi and Othman, Elham H. and Otorkpa, Oche Joseph and Oumer, Abdu and Ouyahia, Amel and Owolabi, Mayowa O. and Owusu, Irene Amoakoh and Oyebanji, Oladayo Ayobami and Oyebola, Kolapo and Oyelade, Tope and A, Mahesh P. and Padda, Inderbir and Padron-Monedero, Alicia and Padubidri, Jagadish Rao and Palladino, Raffaele and Pan, Hai-Feng and Panda, Sujogya Kumar and Panda-Jonas, Songhomitra and Katare, Deepshikha Pande and Pandey, Ashok and Able Panelo, Carlo Irwin and Pang, Ke and Pani, Paola and Panigrahi, Sunil Kumar and Panos, Georgios D. and Panos, Leonidas D. and Pant, Suman and Pantazopoulos, Ioannis and Stoian, Anca Pantea and Papadimopoulos, Ilias and Papadopoulou, Paraskevi and Parekh, Utsav and Roudsari, Peyvand Parhizkar and Parikh, Romil R. and Park, Chulwoo and Park, Seoyeon and Parmar, Arpit Jashwantbhai and Parvandi, Ava and Pashaei, Ava and Passera, Roberto and Patel, Hemal M. and Patel, Jay and Patel, Riya Jayesh and Patel, Sangram Kishor and Patil, Prof Shankargouda and Patoulias, Dimitrios and Pattnaik, Snigdha and Paudel, Deepak and Paudel, Susan and Pawar, Shrikant and Pawar, Shubhadarshini and Toroudi, Hamidreza Pazoki and Pedersini, Paolo and Pekarcikova, Jarmila and Pensato, Umberto and Filipino Pepito, Veincent Christian and Peprah, Emmanuel K. and Peprah, Prince and Pereira, Gavin and Pereira, Maria Odete and Perico, Norberto and Perna, Simone and Peter, Olumuyiwa James and Pham, Hoang Nhat and Pham, Hoang Tran and Pham, Tung Thanh and Phillips, Michael R. and Piradov, Michael A. and Pirera, Edoardo and Pisoni, Enrico and Plotnikov, Evgenii and Poddighe, Dimitri and Polibin, Roman V. and Pollner, Peter and Poluru, Ramesh and Avudaiappan, Arjun Pon and Porntaveetus, Thantrira and Pourbabaki, Reza and Pourghazi, Farzad and Pourkand, Donya and Poursadeqiyan, Mohsen and Pourshams, Akram and Prabhu, Ravindra Attur and Pradhan, Jalandhar and Singh Pradhan, Pranil Man and Prakash, Prem and Prakash, V. and Prasad, Ananya and Prashant, Akila and Angga Pribadi, Dimas Ria and Purohit, Jyotirekha and Puvvula, Jagadeesh and Qanash, Husam and Qasim, Nameer Hashim and Qattea, Ibrahim and Qi, Xiang and Qi, Zhipeng and Qian, Gangzhen and Qiu, Jia-Yong and Rabiee, Navid and Radhakrishnan, Venkatraman and Radojčić, Maja R. and Radpour, Negar and Rafiei, Deniz and Raghuveer, Pracheth and Rahim, Fakher and Mohammed-Amin Rahim, Hawbash and Rahimi, Mehran and Rahimian, Zahra and Rahimifard, Mahban and Rahman, Fryad Majeed and Ur Rahman, Mohammad Hifz and Rahman, Mohammad Meshbahur and Rahman, Mosiur and Rahman, Muhammad Aziz and Rahmani, Amir Masoud and Rahmani, Saeed and Rahmanian, Nazanin and Rahmati, Masoud and Rahmawaty, Setyaningrum and Rahmoune, Hakim and Rai, Pramila and Raina, Sunil Kumar and Raj, Jeffrey Pradeep and Raja, Sandesh and Rajaa, Sathish and Rajabi, Erta and Rajendran, Gunaseelan and Rajendran, Judah and Rajendran, Vinoth and Rajpurohit, Siddheesh and Rajput, Prashant and Ramadan, Mahmoud Mohammed and Ramadan, Majed and Ramadhan, Kadar and Ramasamy, Chitra and Ramasamy, Shakthi Kumaran and Ramírez-Vélez, Robinson and Ramphul, Kamleshun and Rana, Kritika and Rana, Rishabh Kumar and Ranabhat, Chhabi Lal and Rancic, Nemanja and Rao, Mithun and Rao, Sowmya J. and Rashedi, Sina and Rashedi, Vahid and Rashid, Mamunur and Rashidi, Mohammad-Mahdi and Rashidian, Pegah and Rasouli, Mohammad Aziz and Rasouli-Saravani, Ashkan and Rauniyar, Santosh Kumar and Rautalin, Ilari and Rawaf, David Laith and Rawaf, Salman and Rawassizadeh, Reza and Rawlley, Bharat and Rayati, Mohammad and Razo, Christian and Rebelo, Artur and Rama Krishna Reddy, Murali Mohan and Redwan, Elrashdy and Rege, Sanika and Rehman, Aqeeb Ur and Rehman, Wajiha and Reifels, Lennart and Reis-Mendes, Ana and Remuzzi, Giuseppe and Rengasamy, Kannan Rr. and Rezaei, Nazila and Rezaeian, Mohsen and Eidgahi, Donya Rezazadeh and Rhee, Taeho Gregory and Rias, Yohanes Andy and Riaz, Mavra A. and P Ribeiro, Antonio Luiz and Rizvi, Moattar Raza and Lima Rocha, Hermano Alexandre and Rocha-Gomes, João Rocha and Rodrigues Da Silva, Thales Philipe and Buendia Rodriguez, Jefferson Antonio and Roever, Leonardo and Rojas-Rueda, David and Romadlon, Debby Syahru and Ronfani, Luca and Rong, Jian and Roshandel, Gholamreza and Roshanshad, Amirhossein and Rotimi, Kunle and Sekhar Rout, Prof Himanshu and Rouzbahani, Shiva and Roy, Adrija and Roy, Bedanta and Roy, Nitai and Roy, Poulami and Roy, Sharmistha and Roy, Shubhanjali and Roy, Simanta and Russo, Michele and Rwegerera, Godfrey M. and N, Chandan S. and Eddin, Adnan Saad and Saadatian, Zahra and Saber, Korosh and Saber-Ayad, Maha Mohamed and Sabet, Cameron John and Sabour, Siamak and Sachdev, Perminder S. and Sachdeva, Rajesh and Sadarangani, Kabir P. and Saddik, Basema Ahmad and Sadee, Bashdar Abuzed and Sadegh, Tarannom and Sadeghi-Ghyassi, Fatemeh and Saeed, Umar and Safari, Mehdi and Sagar, Rajesh and Saghafi, Alireza and Saghazadeh, Amene and Sagoe, Dominic and Saha, Nondo and Sharif-Askari, Fatemeh Saheb and Sharif-Askari, Narjes Saheb and Sahebkar, Amirhossein and Sahiledengle, Biniyam and Sahoo, Pragyan Monalisa and Sahu, Kirti Sundar and Sahu, Monalisha and Sajadi, S Mohammad and Uz Zaman Sajib, Md Refat and Sajid, Mirza Rizwan and Salabat, Dorsa and Salami, Afeez Abolarinwa and Salarabedi, Mohammad-Mahdi and Salau, Ibrahim Layi and Saleh, Mohamed A. and Salehi, Mahdi and Salehi, Sana and Salehi, Sara and Omran, Hossein Salehi and Salem, Marwa Rashad and Y Salem, Mohammed Z. and Salimi, Sohrab and Samadzadeh, Sara and Samargandy, Saad and Samimisedeh, Parham and Samodra, Yoseph Leonardo and Samuel, Nahom Samuel and Samuel, Vijaya Paul and Samy, Abdallah M. and Sanabria, Juan and Sangle, Sandeep G. and Sanjari, Elaheh and Sanjeev, Rama Krishna and Santos, Itamar S. and Santos, Lucas H.C. C. and Santric-Milicevic, Milena M. and Sao Jose, Bruno Piassi and Sapkota, Krishna Prasad and Sarami, Marjan and Sarasmita, Made Ary and Saravanan, Aswini and Saravi, Babak and Sarikhani, Mahshad and Sarikhani, Yaser and Sarkar, Tanmay and Sarlak, Hamid and Sarma, Hemen and Sarmadi, Mohammad and Sarode, Gargi Sachin and Sarode, Sachin C. and Sarrafzadegan, Nizal and Sassano, Michele and Sathian, Brijesh and Sathya Narayanan, Mukesh Kumar and Satpathy, Maheswar and Sattarpour, Reza and Saulam, Jennifer and Far, Mehrdad Savabi and Saxena, Sangeeta Gopal and Saya, Ganesh Kumar and Sayeed, Abu and Schaarschmidt, Benedikt Michael and Schinckus, Christophe and Schmidt, Maria Inês and Schuermans, Art and Schumacher, Austin E. and Schutte, Aletta Elisabeth and Schwebel, David C. and Schwendicke, Falk and Sebastian, Sneha Annie and Seboka, Binyam Tariku and Semreen, Mohammad H. and Sendekie, Ashenafi Kibret and Sengupta, Pallav and Senol, Yigit Can and Senthilkumaran, Subramanian and Sepanlou, Sadaf G. and Serban, Andreea Claudia and Serban, Dragos and Sethi, Yashendra and Sewor, Christian and Seyed Alshohadaei, Seyed Mohammad and Seylani, Allen and Seyoum, Abebaw B. and Sha'aban, Abubakar and Shafie, Mahan and Shahab, Muhammad and Shaharudin, Shazlin and Shahid, Izza and Shahid, Samiah and Ahsan Shahid, Syed Ahsan and Shahid, Wajeehah and Shahkarami, Farshad and Shahrahmani, Fatemeh and Shahsavari, Hamid R. and Shahwan, Moyad Jamal and Shaikh, Masood Ali and Shaikh, Nafhat and Shamim, Muhammad Aaqib and Shams-Beyranvand, Mehran and Shamshad, Hina and Shamsi, Anas and Shamsutdinova, Alfiya and Shan, Dan and Shanawaz, Mohd and Shanmugasundaram, Devika and Sharath, Medha and Sharew, Nigussie Tadesse and Hassan Sharif, Muhammad Junaid and Sharifan, Amin and Sharma, Avimanu and Sharma, Bunty and Sharma, Prof Kamal and Sharma, Prof Manoj and Sharma, Ujjawal and Sharma, Vishal and Shastry, Shamee and Shawahna, Ramzi and Shawel, Samrawit and Shayan, Amir Mehdi and Bappah, Babangida Shehu and Sheida, Fateme and Sheidaei, Ali and Shekhar, Shashank and Shen, Jiabin and Shenoy, Rekha Raghuveer and Shetty, Pavanchand H. and Shi, Hui-Zhong and Shi, Wenming and Shibuya, Prof Kenji and Shiferaw, Desalegn and Shimaponda-Mataa, Nzooma Munkwangu and Shimels, Tariku and Hossain Shimul, Md Monir and Shin, Min-Jeong and Shiri, Rahman and Shittu, Aminu and Shivarov, Velizar and Shlobin, Nathan A. and Shoaib, Ambreen and Shojaie, Shima and Eshkiki, Zahra Shokati and Shool, Sina and Shorofi, Seyed Afshin and Shrestha, Sunil and Shuval, Kerem and Si, Lei and Si, Yafei and Sibuyi, Nicole R.S. and Siddig, Emmanuel Edwar and Siddiqi, Ahmed Kamal and Sidiq, Mohammad and Siegel, Martin and Sikdar, Mithun and Manuel Lopes Rodrigues Silva, Prof Luís and Simegn, Gizeaddis Lamesgin and Simkhada, Padam Prasad and Singh, Abhinav and Singh, Ambrish and Singh, Baljinder and Singh, Bhim Pratap and Singh, Harmanjit and Singh, Harpreet and Singh, Jasvinder A. and Singh, Lucky and Singh, Paramdeep and Singh, Poornima Suryanath and Singh, Puneetpal and Singh, Surendra and Singh, Surjit and Sinha, Mukesh Kumar and Sinha, Ratnesh and Sivaramakrishnan, Gowri and Siwal, Samarjeet Singh and Skhvitaridze, Natia and Sleet, David A. and Sliwa, Karen and Sohal, Aalam and Sohrabi, Somaye and Sokhal, Balamrit Singh and Solanki, Shipra and Solikhah, Solikhah and Soliman, Ahmed M. and Soliman, Sameh S.M. and Howyzeh, Mehdi Soltani and Song, Weiyi and Soni, Mansi and Soni, Suha and Sood, Aayushi and Sood, Prashant and Soraneh, Soroush and Soriano, Joan B. and Sorrentino, Michele and Sousa, Marco Aurelio and Souza, Tamires C.M. and Soyiri, Ireneous N. and Spartalis, Michael and Spearman, Sandra and Chandrashekhar T Sreeramareddy, Prof and Srichawla, Bahadar S. and Srinivasamurthy, Suresh Kumar and Stachteas, Panagiotis and Stafford, Lauryn K. and Stanaway, Jeffrey D. and Stanikzai, Muhammad Haroon and Starodubova, Antonina V. and Steckling-Muschack, Nadine and Steiropoulos, Paschalis and Maree Stephan, Blossom Christa and Stevanović, Aleksandar and Stockfelt, Leo and Stortecky, Stefan and Stubbs, Peter and Subedi, Narayan and Sukaew, Thitiporn and Kamilu Sulaiman, Surajo Kamilu and Suleiman, Auwal Garba and Suleiman Odidi, Muritala Odidi and Suleman, Muhammad and Sulistiyorini, Desy and M Sullman, Mark J. and Meo, Anusha Sultan and Sun, Jing and Sun, Xiaohui and Sun, Zhong and Sundaram, Shanthosh Priyan and Sundström, Johan and Sunny, Sumam and Sunuwar, Dev Ram and Susianti, Hani and Swain, Chandan Kumar and Swami Vetha, Berwin Singh and Szarpak, Prof Lukasz and Damavandi, Payam Tabaee and Tabarés-Seisdedos, Rafael and Tabatabaei, Seyyed Mohammad and Tabche, Celine and Tabibi, Ramin and Tabish, Mohammad and Tabuchi, Takahiro and Tadesse, Getu Ferenji and Tafida, Buhari Abdullahi and Arashlow, Farzin Tahmasbi and Taiba, Jabeen and Tajabadi, Shima and Takele, Wubet Worku and Talaat, Iman M. and Talic, Stella and Tampa, Mircea and Tamuzi, Jacques Lukenze and Tanashat, Mohammad and Tang, Haosu and Tantisattamo, Ekamol and Tarekegn, Gebrekidan Ewnetu and Tariq, Saba and Tavakoli, Kiarash and Tavangar, Seyed Mohammad and Tavasol, Arian and Tekola, Abainash and Temesgen, Worku Animaw and Temsah, Mohamad-Hani and Teramoto, Masayuki and Tewari, Jay and Teye-Kwadjo, Enoch and Teymourzadeh, Azin and Raman Thankappan, Prof Kavumpurathu and Thapa, Rajshree and Thapar, Rekha and Thavamani, Aravind and Sundaram, Mahalakshmi Thayumana and Thiruvengadam, Muthu and Thomas, Joe and Tian, Wei and Vera Ticoalu, Jansje Henny and Tilakaratne, Pramitha Gishan and Tiwari, Krishna and Tleshev, Madi and Tomo, Sojit and Tonelli, Prof Marcello and Topor-Madry, Roman and Touvier, Mathilde and Tovani-Palone, Marcos Roberto and Trabelsi, Khaled and Tran, Nghia Minh and Tran, Ngoc Ha and Huong Tran, Quynh Thuy and Minh Tran, Tam Quoc and Tran, Thang Huu and Minh Duc, Nguyen Tran and Trico, Domenico and Trihandini, Indang and Tripathi, Manjari and Tripathi, Tulika and Tripathy, Jaya Prasad and Tromans, Samuel Joseph and Nguyen Truong, Quynh Xuan and Tri Tai Truyen, Thien Tan and Hsiang-Te Tsai, Daniel and Tse, Gary and Tsermpini, Evangelia Eirini and Tuglo, Lawrence Sena and Tumkur Narayanappa, Santhosh Kumar and Tumurkhuu, Munkhtuya and Tusa, Biruk Shalmeno and Tye, Sok Cin and Tyrovolas, Stefanos and Udoakang, Aniefiok John and Ulhaq, Inam and Ullah, Atta and Ullah, Saeed and Ullah, Shahid and Umair, Muhammad and Onozasi Umar, Hauwa Onozasi and Umar, Lawan and Umar, Muhammad and Unim, Brigid and Unnikrishnan, Bhaskaran and Upadhya, Dinesh and Upadhyay, Era and Uppal, Dipan and Urmey, Jeba Mahiad and Urso, Daniele and Usman, Jibrin Sammani and Ussai, Silvia and Ustunsoz, Damla and Ozsahin, Dilber Uzun and Uzunçıbuk, Hande and Uzzaman, Nazim and Vadagam, Pratyusha and Vahdati, Sanaz and Vaithinathan, Asokan Govindaraj and Vakilian, Alireza and Vakilpour, Azin and Valizadeh, Gelareh and Van Daalen, Kim Robin and Den Eynde, Jef Van and Varghese, Joe and Varma, Ravi Prasad and Varthya, Shoban Babu and Varughese, Santosh and Vasankari, Tommi Juhani and Vasudevan, Srivatsa Surya and Vellingiri, Balachandar and Venketasubramanian, Narayanaswamy and Venkidasamy, Baskar and Verras, Georgios-Ioannis and Vervoort, Dominique and Vijayageetha, Mathavaswami and Villafañe, Jorge Hugo and Villani, Leonardo and Vipparthy, Sharath Chaitanya and Vishwakarma, Mukesh and Vlassov, Vasily and Volovat, Simona Ruxandra and Vosoughi, Mehdi and Vounzoulaki, Elpida and Vujcic, Isidora S. and Wada, Abubakar Sadiq and Wadhwa, Medha and Wafula, Solomon T. and Waheed, Yasir and Wahidin, Mugi and Wahiduzzaman, Mohammad and Wahood, Samer and Wan, Jin-Yi and Wang, Kongjia and Wang, Liang and Wang, Minmin and Wang, Nelson and Wang, Shu and Wang, Wei and Wang, Yanzhong and Wang, Yuan-Pang and Wanjau, Mary Njeri and Bilal Waqar, Ahmed and Waqas, Muhammad and Wassie, Gizachew Tadesse and Gayan Weerakoon, Kosala and Weerasekara, Ishanka and Weintraub, Robert G. and Westerman, Ronny and Wiangkham, Taweewat and Wibowo, Yohanes Cakrapradipta and Wicaksana, Anggi Lukman and Wickramasinghe, Dakshitha Praneeth and Darshana Wickramasinghe, Nuwan Darshana and Wijarnpreecha, Karn and Wijayanto, Matthew Aldo and Wilandika, Angga and Willeit, Prof Peter and Wireko, Andrew Awuah and Wirtu, Gemechu Kumera and Wojewodzic, Marcin W. and Wojtyniak, Bogdan and Wonde, Tewodros Eshete and Wondmeneh, Yohannes Chemere and Wongnaah, Florence Gyembuzie and Chanie Worku, Minichil Chanie and Wu, Prof Felicia and Wu, James Fan and Wu, Jiayuan and Wu, Junhui and Wu, Zenghong and Miskir Wubie, Yihun Miskir and Xiao, Lishun and Xie, Wanqing and Xu, Site and Xu, Wanqing and Xu, Xiaoyue and Xue, Mingyang and Yadav, Vikas and Yadollahi, Mahnaz and Yaghoubi, Sajad and Yahoo (Syed), Saba and Yahya, Galal and Yang, Xinxin and Yano, Yuichiro and Yao, Haiqiang and Yao, Laiang and Yarahmadi, Amir and Melesse, Debas Yaregal and Yasufuku, Yuichi and Yavari, Mohammadjavad and Yaya, Sanni and Yayeh, Melesse Belayneh and Ye, Pengpeng and Yeganeh, Meghdad and Yekdeş, Ali Cem and Yesodharan, Renjulal and Yesuf, Subah Abderehim and Yezengaw, Telksew Yelma and Yezli, Saber and Yi, Siyan and Yin, Dehui and Keon Yon, Dong and Yonemoto, Naohiro and Youm, Yoosik and Yousefi, Zabihollah and Yousefzadeh-Chabok, Shahrokh and Yu, Chuanhua and Yu, Hairui and Yu, Yong and Yuce, Deniz and Yunusa, Ismaeel and Yunusa, Umar and Zaghampour, Manijeh and Abidin, Emilia Zainal and Zairov, Dilmurat and Zakham, Fathiah and Zamagni, Giulia and Zanghì, Aurora and Zare, Iman and Zaresharifi, Shirin and Zarinfar, Yasaman and Zastrozhin, Michael and Zawiah, Mohammed and Ali Zazouli, Mohammad and Zeariya, Mohammed G.M. and Birara Zemariam, Alemu Birara and Zensen, Sebastian and Zhan, Tiansong and Zhang, Casper J.P. and Zhang, Haijun and Zhang, Jinpeng and Zhang, Lin and Zhang, Liqun and Zhang, Xiaoyi and Zhang, Yunquan and Zhang, Zhiqiang and Zhao, Hanqing and Zhao, Zhenping and Zheng, David X. and Zheng, Jinxin and Zheng, Ming-Hua and Zhong, Anthony and Zhou, Jiayan and Zhou, Juexiao and Zhou, Shuduo and Zhou, Xianghong and Zhou, Xiao-Dong and Zhu, Bin and Zhu, Wei and Zhumagaliuly, Abzal and Ziegelmayer, Sebastian and Zielińska, Magdalena and Zoghi, Ghazal and Ali Zoromba, Mohamed Ali and Zou, Prof Zhiyong and Zuber, Mohammed and Zyoud, Ahed H. and Zyoud, Sa'ed H. and Zyoud, Shaher H. and L Murray, Christopher J. and Mensah, George A. and Roth, Gregory A.},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {2167--2243},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Global guideline for the diagnosis and management of candidiasis: an initiative of the ECMM in cooperation with ISHAM and ASM.\n \n \n \n \n\n\n \n Cornely, O. A; Sprute, R.; Bassetti, M.; Chen, S. C.; Groll, A. H; Kurzai, O.; Lass-Flörl, C.; Ostrosky-Zeichner, L.; Rautemaa-Richardson, R.; Revathi, G.; Santolaya, M. E; White, P L.; Alastruey-Izquierdo, A.; Arendrup, M. C; Baddley, J.; Barac, A.; Ben-Ami, R.; Brink, A. J; Grothe, J. H; Guinea, J.; Hagen, F.; Hochhegger, B.; Hoenigl, M.; Husain, S.; Jabeen, K.; Jensen, H. E; Kanj, S. S; Koehler, P.; Lehrnbecher, T.; Lewis, R. E; Meis, J. F; Nguyen, M H.; Pana, Z. D; Rath, P.; Reinhold, I.; Seidel, D.; Takazono, T.; Vinh, D. C; Zhang, S. X; Afeltra, J.; Al-Hatmi, A. M S; Arastehfar, A.; Arikan-Akdagli, S.; Bongomin, F.; Carlesse, F.; Chayakulkeeree, M.; Chai, L. Y A; Chamani-Tabriz, L.; Chiller, T.; Chowdhary, A.; Clancy, C. J; Colombo, A. L; Cortegiani, A.; Corzo Leon, D. E; Drgona, L.; Dudakova, A.; Farooqi, J.; Gago, S.; Ilkit, M.; Jenks, J. D; Klimko, N.; Krause, R.; Kumar, A.; Lagrou, K.; Lionakis, M. S; Lmimouni, B. E; Mansour, M. K; Meletiadis, J.; Mellinghoff, S. C; Mer, M.; Mikulska, M.; Montravers, P.; Neoh, C. F.; Ozenci, V.; Pagano, L.; Pappas, P.; Patterson, T. F; Puerta-Alcalde, P.; Rahimli, L.; Rahn, S.; Roilides, E.; Rotstein, C.; Ruegamer, T.; Sabino, R.; Salmanton-García, J.; Schwartz, I. S; Segal, E.; Sidharthan, N.; Singhal, T.; Sinko, J.; Soman, R.; Spec, A.; Steinmann, J.; Stemler, J.; Taj-Aldeen, S. J; Talento, A. F.; Thompson, G. R; Toebben, C.; Villanueva-Lozano, H.; Wahyuningsih, R.; Weinbergerová, B.; Wiederhold, N.; Willinger, B.; Woo, P. C Y; and Zhu, L.\n\n\n \n\n\n\n The Lancet Infectious Diseases, 25(5): e280–e293. May 2025.\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

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@article{cornely_global_2025,\n\ttitle = {Global guideline for the diagnosis and management of candidiasis: an initiative of the {ECMM} in cooperation with {ISHAM} and {ASM}},\n\tvolume = {25},\n\tissn = {14733099},\n\tshorttitle = {Global guideline for the diagnosis and management of candidiasis},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1473309924007497},\n\tdoi = {10.1016/S1473-3099(24)00749-7},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet Infectious Diseases},\n\tauthor = {Cornely, Oliver A and Sprute, Rosanne and Bassetti, Matteo and Chen, Sharon C-A and Groll, Andreas H and Kurzai, Oliver and Lass-Flörl, Cornelia and Ostrosky-Zeichner, Luis and Rautemaa-Richardson, Riina and Revathi, Gunturu and Santolaya, Maria E and White, P Lewis and Alastruey-Izquierdo, Ana and Arendrup, Maiken C and Baddley, John and Barac, Aleksandra and Ben-Ami, Ronen and Brink, Adrian J and Grothe, Jan H and Guinea, Jesus and Hagen, Ferry and Hochhegger, Bruno and Hoenigl, Martin and Husain, Shahid and Jabeen, Kauser and Jensen, Henrik E and Kanj, Souha S and Koehler, Philipp and Lehrnbecher, Thomas and Lewis, Russell E and Meis, Jacques F and Nguyen, M Hong and Pana, Zoi D and Rath, Peter-Michael and Reinhold, Ilana and Seidel, Danila and Takazono, Takahiro and Vinh, Donald C and Zhang, Sean X and Afeltra, Javier and Al-Hatmi, Abdullah M S and Arastehfar, Amir and Arikan-Akdagli, Sevtap and Bongomin, Felix and Carlesse, Fabianne and Chayakulkeeree, Methee and Chai, Louis Y A and Chamani-Tabriz, Leili and Chiller, Tom and Chowdhary, Anuradha and Clancy, Cornelius J and Colombo, Arnaldo L and Cortegiani, Andrea and Corzo Leon, Dora E and Drgona, Lubos and Dudakova, Anna and Farooqi, Joveria and Gago, Sara and Ilkit, Macit and Jenks, Jeffrey D and Klimko, Nikolai and Krause, Robert and Kumar, Anil and Lagrou, Katrien and Lionakis, Michail S and Lmimouni, Badre E and Mansour, Michael K and Meletiadis, Joseph and Mellinghoff, Sibylle C and Mer, Mervyn and Mikulska, Malgorzata and Montravers, Philippe and Neoh, Chin Fen and Ozenci, Volkan and Pagano, Livio and Pappas, Peter and Patterson, Thomas F and Puerta-Alcalde, Pedro and Rahimli, Laman and Rahn, Sebastian and Roilides, Emmanuel and Rotstein, Coleman and Ruegamer, Tamara and Sabino, Raquel and Salmanton-García, Jon and Schwartz, Ilan S and Segal, Esther and Sidharthan, Neeraj and Singhal, Tanu and Sinko, Janos and Soman, Rajeev and Spec, Andrej and Steinmann, Joerg and Stemler, Jannik and Taj-Aldeen, Saad J and Talento, Alida Fe and Thompson, George R and Toebben, Christina and Villanueva-Lozano, Hiram and Wahyuningsih, Retno and Weinbergerová, Barbora and Wiederhold, Nathan and Willinger, Birgit and Woo, Patrick C Y and Zhu, Li-Ping},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {e280--e293},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Workforce Development in Genomic Data Science for Health: A Worldview.\n \n \n \n \n\n\n \n Lukhele, S. T.; Ras, V.; and Mulder, N.\n\n\n \n\n\n\n Annual Review of Genomics and Human Genetics, 26(1): 449–471. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Workforce$ Paper\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{lukhele_workforce_2025,\n\ttitle = {Workforce {Development} in {Genomic} {Data} {Science} for {Health}: {A} {Worldview}},\n\tvolume = {26},\n\tcopyright = {http://creativecommons.org/licenses/by/4.0/},\n\tissn = {1527-8204, 1545-293X},\n\tshorttitle = {Workforce {Development} in {Genomic} {Data} {Science} for {Health}},\n\turl = {https://www.annualreviews.org/content/journals/10.1146/annurev-genom-012224-122440},\n\tdoi = {10.1146/annurev-genom-012224-122440},\n\tabstract = {Genomics has the potential to transform human health, biomedical research, and life sciences by providing deep insights into genetic variation and disease mechanisms. However, fully realizing these benefits requires a well-trained workforce equipped to handle, analyze, and interpret increasingly complex genomic and linked datasets. The rapid evolution of sequencing technologies, machine learning, and data science tools has heightened the demand for professionals proficient in bioinformatics, high-performance computing, and genomic data governance. This review presents a global perspective on workforce development in genomic data science, detailing key competencies necessary for both research and clinical applications. We discuss some of the existing training programs, competency frameworks, and regional approaches to skills development while identifying gaps in education, infrastructure, and accessibility. Additionally, we explore the integration of genomic data science into healthcare, addressing challenges such as equitable access to training and the need for cross-disciplinary expertise. Tackling these challenges is essential for cultivating a diverse, skilled workforce capable of driving advancements in genomic research, precision medicine, and public health.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Annual Review of Genomics and Human Genetics},\n\tauthor = {Lukhele, Sindiswa T. and Ras, Verena and Mulder, Nicola},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {449--471},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Exploring penetrance of clinically relevant variants in over 800,000 humans from the Genome Aggregation Database.\n \n \n \n \n\n\n \n Gudmundsson, S.; Singer-Berk, M.; Stenton, S. L.; Goodrich, J. K.; Wilson, M. W.; Einson, J.; Watts, N. A.; Genome Aggregation Database Consortium; Abreu, M.; Abubakar, A.; Adolfsson, R.; Aguilar Salinas, C. A.; Ahmad, T.; Albert, C. M.; Alföldi, J.; Allez, M.; López, C. A.; Ardissino, D.; Armean, I. M.; Atkinson, E. G.; Atzmon, G.; Banks, E.; Barnard, J.; Baxter, S. M.; Beaugerie, L.; Benjamin, D.; Benjamin, E. J.; Bergelson, L.; Bernstein, C.; Blackwood, D.; Boehnke, M.; Bonnycastle, L. L.; Bottinger, E. P.; Bowden, D. W.; Bown, M. J.; Brand, H.; Brant, S.; Brookings, T.; Bryant, S.; Callier, S. L.; Campos, H.; Chambers, J. C.; Chan, J. C.; Chao, K. R.; Chapman, S.; Chasman, D. I.; Chen, L. A.; Chen, S.; Chisholm, R.; Cho, J.; Chowdhury, R.; Chung, M. K.; Chung, W. K.; Cibulskis, K.; Cohen, B.; Collins, R. L.; Connolly, K. M.; Correa, A.; Corvin, A.; Covarrubias, M.; Craddock, N.; Cummings, B. B.; Dabelea, D.; Daly, M. J.; Danesh, J.; Darbar, D.; Darnowsky, P.; Denny, J. C.; Donnelly, S.; Duerr, R. H.; Duggirala, R.; Dupuis, J.; Ellinor, P. T.; Elosua, R.; Emery, J.; England, E.; Erdmann, J.; Esko, T.; Evangelista, E.; Farjoun, Y.; Fatkin, D.; Faubion, W.; Ferriera, S.; Figtree, G.; Flannagan, K.; Florez, J.; Francioli, L.; Franke, A.; Frankish, A.; Fu, J.; Färkkilä, M.; Gabriel, S.; Garimella, K.; Gauthier, L. D.; Gentry, J.; Georges, M.; Getz, G.; Glahn, D. C.; Glaser, B.; Glatt, S. J.; Goes, F. S.; Goldstein, D.; Gonzalez, C.; Goodrich, J.; Grant, R. H.; Groop, L.; Gudmundsson, S.; Gupta, N.; Haessly, A.; Haiman, C.; Hall, I.; Hanis, C. L.; Hanyok, J.; Harms, M.; He, Q.; Hiltunen, M.; Holi, M. M.; Hultman, C. M.; Jahl, S.; Jalas, C.; Jeandet, T.; Kallela, M.; Kaplan, D.; Kaprio, J.; Karczewski, K. J.; Karlson, E. W.; Kathiresan, S.; Kenny, E. E.; Kim, B.; Kim, Y. J.; King, D.; Kirov, G.; Koenig, Z.; Kooner, J.; Koskinen, S.; Krumholz, H. M.; Kugathasan, S.; Kupcinskas, J.; Kwak, S. H.; Laakso, M.; Lake, N.; Landén, M.; Langsford, T.; Laricchia, K. M.; Lehtimäki, T.; Lek, M.; Lewis, J.; Lindgren, C. M.; Lipscomb, E.; Llanwarne, C.; Loos, R. J. F.; Louis, E.; Lowther, C.; Lu, W.; Lubitz, S. A.; Lyons, T.; Ma, R. C. W.; MacArthur, D. G.; Manoach, D. S.; Marcus, G. M.; Marrugat, J.; Marston, N.; Marten, D. M.; Martin, A. R.; Mattila, K. M.; McCarroll, S.; McCarthy, M. I.; McCauley, J. L.; McGovern, D.; McPherson, R.; MacQuillin, A.; Meigs, J. B.; Melander, O.; Metspalu, A.; Meyers, D.; Minikel, E. V.; Mitchell, B. D.; Moayyedi, P.; Mohanty, S.; Estrada, A. M.; Mulder, N. J.; Munshi, R.; Naheed, A.; Natale, A.; Nazarian, S.; Neale, B. M.; Newton, C.; Nilsson, P. M.; Novod, S.; O’Donnell-Luria, A. H.; O’Donovan, M. C.; Okada, Y.; Ongur, D.; Ophoff, R.; Orozco, L.; Ouwehand, W.; Owen, M. J.; Owen, N.; Palmer, C.; Palmer, N. D.; Palotie, A.; Parellada, M.; Park, K. S.; Pato, C.; Pedersen, N. L.; Pesaran, T.; Petrillo, N.; Phu, W.; Plon, S.; Posthuma, D.; Poterba, T.; Pulver, A. E.; Quinlan, A.; Rader, D.; Rahman, N.; Rehm, H.; Reif, A.; Reiner, A.; Remes, A. M.; Rhodes, D.; Rich, S.; Rioux, J. D.; Ripatti, S.; Roazen, D.; Roberts, J.; Robinson, E.; Roden, D. M.; Rotter, J. I.; Rouleau, G.; Ruano-Rubio, V.; Ruff, C. T.; Runz, H.; Sabatine, M. S.; Sahakian, N.; Saleheen, D.; Salomaa, V.; Saltzman, A.; Samani, N. J.; Samocha, K. E.; Sanchis-Juan, A.; Sawa, A.; Scharf, J.; Schleicher, M.; Schultz, P.; Schunkert, H.; Schönherr, S.; Seaby, E. G.; Seed, C.; Shah, S. H.; Shand, M.; Sharpe, T.; Shoemaker, M. B.; Shyong, T.; Silverman, E. K.; Skieceviciene, J.; Sklar, P.; Smith, J. G.; Smith, J. T.; Smoller, J.; Soininen, H.; Sokol, H.; Solomonson, M.; Son, R. G.; Soto, J.; Spector, T.; Clair, D. S.; Stevens, C.; Stitziel, N. O.; Sullivan, P. F.; Suvisaari, J.; Tai, E. S.; Talkowski, M. E.; Tarasova, Y.; Taylor, K. D.; Teo, Y. Y.; Tiao, G.; Tibbetts, K.; Tolonen, C.; Tsuang, M.; Tuomi, T.; Turner, D.; Tusie-Luna, T.; Vartiainen, E.; Vawter, M.; Vermeire, S.; Vilella, E.; Vittal, C.; Wade, G.; Walker, M.; Wang, A.; Wang, L.; Wang, Q.; Ware, J. S.; Watkins, H.; Watts, N. A.; Weersma, R. K.; Weisburd, B.; Wessman, M.; Whelan, C.; Whiffin, N.; Wilson, J. G.; Witzgall, L.; Xavier, R. J.; Yohannes, M. T.; Yolken, R.; Zhao, X.; Lappalainen, T.; Rehm, H. L.; MacArthur, D. G.; and O’Donnell-Luria, A.\n\n\n \n\n\n\n Nature Communications, 16(1): 9623. October 2025.\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{gudmundsson_exploring_2025,\n\ttitle = {Exploring penetrance of clinically relevant variants in over 800,000 humans from the {Genome} {Aggregation} {Database}},\n\tvolume = {16},\n\tissn = {2041-1723},\n\turl = {https://www.nature.com/articles/s41467-025-61698-x},\n\tdoi = {10.1038/s41467-025-61698-x},\n\tabstract = {Abstract \n Incomplete penetrance, or absence of disease phenotype in an individual with a disease-associated variant, is a major challenge in variant interpretation. Studying individuals with apparent incomplete penetrance can shed light on underlying drivers of altered phenotype penetrance. Here, we investigate clinically relevant variants from ClinVar in 807,162 individuals from the Genome Aggregation Database (gnomAD), demonstrating improved representation in gnomAD version 4. We then conduct a comprehensive case-by-case assessment of 734 predicted loss of function variants in 77 genes associated with severe, early-onset, highly penetrant haploinsufficient disease. Here, we identify explanations for the presumed lack of disease manifestation in 701 of 734 variants (95\\%). Individuals with unexplained lack of disease manifestation in this set of disorders are rare, underscoring the need and power of deep case-by-case assessment presented here to minimize false assignments of disease risk, particularly in unaffected individuals with higher rates of secondary properties that result in rescue.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Nature Communications},\n\tauthor = {Gudmundsson, Sanna and Singer-Berk, Moriel and Stenton, Sarah L. and Goodrich, Julia K. and Wilson, Michael W. and Einson, Jonah and Watts, Nicholas A. and {Genome Aggregation Database Consortium} and Abreu, Maria and Abubakar, Amina and Adolfsson, Rolf and Aguilar Salinas, Carlos A. and Ahmad, Tariq and Albert, Christine M. and Alföldi, Jessica and Allez, Matthieu and López, Celso Arango and Ardissino, Diego and Armean, Irina M. and Atkinson, Elizabeth G. and Atzmon, Gil and Banks, Eric and Barnard, John and Baxter, Samantha M. and Beaugerie, Laurent and Benjamin, David and Benjamin, Emelia J. and Bergelson, Louis and Bernstein, Charles and Blackwood, Douglas and Boehnke, Michael and Bonnycastle, Lori L. and Bottinger, Erwin P. and Bowden, Donald W. and Bown, Matthew J. and Brand, Harrison and Brant, Steven and Brookings, Ted and Bryant, Sam and Callier, Shawneequa L. and Campos, Hannia and Chambers, John C. and Chan, Juliana C. and Chao, Katherine R. and Chapman, Sinéad and Chasman, Daniel I. and Chen, Lea A. and Chen, Siwei and Chisholm, Rex and Cho, Judy and Chowdhury, Rajiv and Chung, Mina K. and Chung, Wendy K. and Cibulskis, Kristian and Cohen, Bruce and Collins, Ryan L. and Connolly, Kristen M. and Correa, Adolfo and Corvin, Aiden and Covarrubias, Miguel and Craddock, Nick and Cummings, Beryl B. and Dabelea, Dana and Daly, Mark J. and Danesh, John and Darbar, Dawood and Darnowsky, Phil and Denny, Joshua C. and Donnelly, Stacey and Duerr, Richard H. and Duggirala, Ravindranath and Dupuis, Josée and Ellinor, Patrick T. and Elosua, Roberto and Emery, James and England, Eleina and Erdmann, Jeanette and Esko, Tõnu and Evangelista, Emily and Farjoun, Yossi and Fatkin, Diane and Faubion, William and Ferriera, Steven and Figtree, Gemma and Flannagan, Kelly and Florez, Jose and Francioli, Laurent and Franke, Andre and Frankish, Adam and Fu, Jack and Färkkilä, Martti and Gabriel, Stacey and Garimella, Kiran and Gauthier, Laura D. and Gentry, Jeff and Georges, Michel and Getz, Gad and Glahn, David C. and Glaser, Benjamin and Glatt, Stephen J. and Goes, Fernando S. and Goldstein, David and Gonzalez, Clicerio and Goodrich, Julia and Grant, Riley H. and Groop, Leif and Gudmundsson, Sanna and Gupta, Namrata and Haessly, Andrea and Haiman, Christopher and Hall, Ira and Hanis, Craig L. and Hanyok, James and Harms, Matthew and He, Qin and Hiltunen, Mikko and Holi, Matti M. and Hultman, Christina M. and Jahl, Steve and Jalas, Chaim and Jeandet, Thibault and Kallela, Mikko and Kaplan, Diane and Kaprio, Jaakko and Karczewski, Konrad J. and Karlson, Elizabeth W. and Kathiresan, Sekar and Kenny, Eimear E. and Kim, Bong-Jo and Kim, Young Jin and King, Daniel and Kirov, George and Koenig, Zan and Kooner, Jaspal and Koskinen, Seppo and Krumholz, Harlan M. and Kugathasan, Subra and Kupcinskas, Juozas and Kwak, Soo Heon and Laakso, Markku and Lake, Nicole and Landén, Mikael and Langsford, Trevyn and Laricchia, Kristen M. and Lehtimäki, Terho and Lek, Monkol and Lewis, James and Lindgren, Cecilia M. and Lipscomb, Emily and Llanwarne, Christopher and Loos, Ruth J. F. and Louis, Edouard and Lowther, Chelsea and Lu, Wenhan and Lubitz, Steven A. and Lyons, Tom and Ma, Ronald C. W. and MacArthur, Daniel G. and Manoach, Dara S. and Marcus, Gregory M. and Marrugat, Jaume and Marston, Nicholas and Marten, Daniel M. and Martin, Alicia R. and Mattila, Kari M. and McCarroll, Steven and McCarthy, Mark I. and McCauley, Jacob L. and McGovern, Dermot and McPherson, Ruth and MacQuillin, Andrew and Meigs, James B. and Melander, Olle and Metspalu, Andres and Meyers, Deborah and Minikel, Eric V. and Mitchell, Braxton D. and Moayyedi, Paul and Mohanty, Sanghamitra and Estrada, Andrés Moreno and Mulder, Nicola J. and Munshi, Ruchi and Naheed, Aliya and Natale, Andrea and Nazarian, Saman and Neale, Benjamin M. and Newton, Charles and Nilsson, Peter M. and Novod, Sam and O’Donnell-Luria, Anne H. and O’Donovan, Michael C. and Okada, Yukinori and Ongur, Dost and Ophoff, Roel and Orozco, Lorena and Ouwehand, Willem and Owen, Michael J. and Owen, Nick and Palmer, Colin and Palmer, Nicholette D. and Palotie, Aarno and Parellada, Mara and Park, Kyong Soo and Pato, Carlos and Pedersen, Nancy L. and Pesaran, Tina and Petrillo, Nikelle and Phu, William and Plon, Sharon and Posthuma, Danielle and Poterba, Timothy and Pulver, Ann E. and Quinlan, Aaron and Rader, Dan and Rahman, Nazneen and Rehm, Heidi and Reif, Andreas and Reiner, Alex and Remes, Anne M. and Rhodes, Dan and Rich, Stephen and Rioux, John D. and Ripatti, Samuli and Roazen, David and Roberts, Jason and Robinson, Elise and Roden, Dan M. and Rotter, Jerome I. and Rouleau, Guy and Ruano-Rubio, Valentin and Ruff, Christian T. and Runz, Heiko and Sabatine, Marc S. and Sahakian, Nareh and Saleheen, Danish and Salomaa, Veikko and Saltzman, Andrea and Samani, Nilesh J. and Samocha, Kaitlin E. and Sanchis-Juan, Alba and Sawa, Akira and Scharf, Jeremiah and Schleicher, Molly and Schultz, Patrick and Schunkert, Heribert and Schönherr, Sebastian and Seaby, Eleanor G. and Seed, Cotton and Shah, Svati H. and Shand, Megan and Sharpe, Ted and Shoemaker, Moore B. and Shyong, Tai and Silverman, Edwin K. and Skieceviciene, Jurgita and Sklar, Pamela and Smith, J. Gustav and Smith, Jonathan T. and Smoller, Jordan and Soininen, Hilkka and Sokol, Harry and Solomonson, Matthew and Son, Rachel G. and Soto, Jose and Spector, Tim and Clair, David St and Stevens, Christine and Stitziel, Nathan O. and Sullivan, Patrick F. and Suvisaari, Jaana and Tai, E. Shyong and Talkowski, Michael E. and Tarasova, Yekaterina and Taylor, Kent D. and Teo, Yik Ying and Tiao, Grace and Tibbetts, Kathleen and Tolonen, Charlotte and Tsuang, Ming and Tuomi, Tiinamaija and Turner, Dan and Tusie-Luna, Teresa and Vartiainen, Erkki and Vawter, Marquis and Vermeire, Severine and Vilella, Elisabet and Vittal, Christopher and Wade, Gordon and Walker, Mark and Wang, Arcturus and Wang, Lily and Wang, Qingbo and Ware, James S. and Watkins, Hugh and Watts, Nicholas A. and Weersma, Rinse K. and Weisburd, Ben and Wessman, Maija and Whelan, Christopher and Whiffin, Nicola and Wilson, James G. and Witzgall, Lauren and Xavier, Ramnik J. and Yohannes, Mary T. and Yolken, Robert and Zhao, Xuefang and Lappalainen, Tuuli and Rehm, Heidi L. and MacArthur, Daniel G. and O’Donnell-Luria, Anne},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {9623},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Natural immunity and protection against variants in South African children through five COVID-19 waves: A prospective study.\n \n \n \n \n\n\n \n Zar, H. J.; Workman, L.; MacGinty, R.; Botha, M.; Johnson, M.; Hunt, A.; Burd, T.; Nicol, M. P.; Flasche, S.; Quilty, B. J.; and Goldblatt, D.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 150: 107300. January 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{zar_natural_2025,\n\ttitle = {Natural immunity and protection against variants in {South} {African} children through five {COVID}-19 waves: {A} prospective study},\n\tvolume = {150},\n\tissn = {12019712},\n\tshorttitle = {Natural immunity and protection against variants in {South} {African} children through five {COVID}-19 waves},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S120197122400376X},\n\tdoi = {10.1016/j.ijid.2024.107300},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Zar, Heather J. and Workman, Lesley and MacGinty, Rae and Botha, Maresa and Johnson, Marina and Hunt, Adam and Burd, Tiffany and Nicol, Mark P. and Flasche, Stefan and Quilty, Billy J. and Goldblatt, David},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {107300},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Injectable Contraceptives Differentially Affect Select CD4+ HIV‐1 Target Cells in the Genital Tract but Not Systemically: Implications for HIV‐1 Acquisition.\n \n \n \n \n\n\n \n Avenant, C.; Bick, A. J.; Moliki, J. M.; Dlamini, S.; Tomasicchio, M.; Hofmeyr, G. J.; Morrison, C.; Chen, P.; and Hapgood, J. P.\n\n\n \n\n\n\n American Journal of Reproductive Immunology, 93(5): e70093. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Injectable$ Paper\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{avenant_injectable_2025,\n\ttitle = {Injectable {Contraceptives} {Differentially} {Affect} {Select} {CD4}+ {HIV}‐1 {Target} {Cells} in the {Genital} {Tract} but {Not} {Systemically}: {Implications} for {HIV}‐1 {Acquisition}},\n\tvolume = {93},\n\tissn = {1046-7408, 1600-0897},\n\tshorttitle = {Injectable {Contraceptives} {Differentially} {Affect} {Select} {CD4}+ {HIV}‐1 {Target} {Cells} in the {Genital} {Tract} but {Not} {Systemically}},\n\turl = {https://onlinelibrary.wiley.com/doi/10.1111/aji.70093},\n\tdoi = {10.1111/aji.70093},\n\tabstract = {ABSTRACT \n             \n              Problem \n              Observational data suggest lower HIV susceptibility in women using the injectable contraceptive norethisterone enanthate (NET‐EN) versus intramuscular depo medroxyprogesterone acetate (DMPA‐IM). Clinical data investigating the effects of injectables on HIV target cells are inconsistent or limited. No data on HIV target cells are available from head‐to‐head randomized trials comparing DMPA‐IM and NET‐EN, nor at peak progestin concentrations. \n             \n             \n              Method of Study \n               \n                The women's health, injectable contraception, and HIV (WHICH) trial randomized women to DMPA‐IM or NET‐EN at two South African sites (2018–2019). Cells from blood and cytobrushes from women at one site, taken at baseline and 1 week post the 24‐week injection (at peak progestin levels), were analyzed by flow cytometry for select HIV‐1 target cells (CD4 \n                + \n                cells expressing HIV‐1 co‐receptors, an integrin and/or activation markers). \n               \n             \n             \n              Results \n               \n                Systemically, DMPA‐IM and NET‐EN similarly reduced the frequency and number of some CD4 \n                + \n                cells and expression of some CD4 \n                + \n                cell surface markers. In contrast, female genital tract (FGT) results showed significantly different cell numbers between contraceptives for most cell populations; DMPA‐IM tended to increase, but NET‐EN tended to decrease cell numbers. Excluding for non‐study progestin use revealed significant increases in frequency and/or number of several FGT cell populations from baseline to 25 weeks, within the DMPA‐IM arm. \n               \n             \n             \n              Conclusions \n               \n                Both contraceptives exert minimal effects on systemic CD4 \n                + \n                cells but have differential effects in the FGT. The changes in frequency and numbers of HIV‐1 target cells investigated, particularly after exclusion for non‐study progestin use, suggest that DMPA‐IM use may increase HIV‐1 acquisition in the FGT compared to NET‐EN use.},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-19},\n\tjournal = {American Journal of Reproductive Immunology},\n\tauthor = {Avenant, Chanel and Bick, Alexis J. and Moliki, Johnson M. and Dlamini, Sigcinile and Tomasicchio, Michele and Hofmeyr, G. Justus and Morrison, Charles and Chen, Pai‐Lien and Hapgood, Janet P.},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {e70093},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n ‘Marburg virus disease outbreak in Rwanda, 2024’–author's response.\n \n \n \n \n\n\n \n Grobusch, M. P.; Pellejero-Sagastizábal, G.; Jokelainen, P.; Lescure, F.; Mora-Rillo, M.; and Gupta, N.\n\n\n \n\n\n\n Clinical Microbiology and Infection, 31(5): 876–877. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"‘Marburg$ Paper\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{grobusch_marburg_2025,\n\ttitle = {‘{Marburg} virus disease outbreak in {Rwanda}, 2024’–author's response},\n\tvolume = {31},\n\tissn = {1198743X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1198743X25000710},\n\tdoi = {10.1016/j.cmi.2025.02.012},\n\tlanguage = {en},\n\tnumber = {5},\n\turldate = {2026-05-19},\n\tjournal = {Clinical Microbiology and Infection},\n\tauthor = {Grobusch, Martin P. and Pellejero-Sagastizábal, Galadriel and Jokelainen, Pikka and Lescure, F-Xavier and Mora-Rillo, Marta and Gupta, Nitin},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {876--877},\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, 78(12): 848–854. December 2025.\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_2025,\n\ttitle = {Investigating somatic variants and pathways in mismatch repair-deficient ({dMMR}) colorectal carcinoma in {South} {Africa}},\n\tvolume = {78},\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\tnumber = {12},\n\turldate = {2026-05-19},\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 = dec,\n\tyear = {2025},\n\tpages = {848--854},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n AIDS-related mycoses: advances, challenges, and future directions.\n \n \n \n \n\n\n \n Dangarembizi, R.; Hoving, J. C.; Boulware, D. R.; Colombo, A. L.; Govender, N. P.; Oladele, R.; Dat, V. Q.; Schwartz, I. S.; and Brown, G. D.\n\n\n \n\n\n\n Trends in Microbiology, 33(2): 141–144. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"AIDS-related$ Paper\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{dangarembizi_aids-related_2025,\n\ttitle = {{AIDS}-related mycoses: advances, challenges, and future directions},\n\tvolume = {33},\n\tissn = {0966842X},\n\tshorttitle = {{AIDS}-related mycoses},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0966842X24003196},\n\tdoi = {10.1016/j.tim.2024.12.004},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {Trends in Microbiology},\n\tauthor = {Dangarembizi, Rachael and Hoving, Jennifer Claire and Boulware, David R. and Colombo, Arnaldo Lopes and Govender, Nelesh P. and Oladele, Rita and Dat, Vu Quoc and Schwartz, Ilan S. and Brown, Gordon D.},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {141--144},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Production and immunogenicity of a plant-produced beak and feather disease virus vaccine in Japanese quails.\n \n \n \n \n\n\n \n Mulondo, G.; Buyse, M. L. R.; Labuschagne, K.; Jarvis, D.; Van Zyl, A.; Rybicki, E. P.; Hitzeroth, I. I.; and Mbewana, S.\n\n\n \n\n\n\n Archives of Virology, 170(7): 163. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Production$ Paper\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{mulondo_production_2025,\n\ttitle = {Production and immunogenicity of a plant-produced beak and feather disease virus vaccine in {Japanese} quails},\n\tvolume = {170},\n\tissn = {0304-8608, 1432-8798},\n\turl = {https://link.springer.com/10.1007/s00705-025-06352-z},\n\tdoi = {10.1007/s00705-025-06352-z},\n\tabstract = {Abstract \n            Beak and feather disease virus (BFDV), a single-stranded DNA virus, infects endangered psittacine species, including the South African Cape parrot. The disease is highly contagious and can be transmitted through contact with contaminated faeces, crop secretions, and feather and skin dander. To date, there is no vaccine or cure available for BFDV. The production of an effective vaccine depends on having a production platform and methods that are both easy to use and capable of yielding a significant amount of protein that will induce a sufficient immune response. Therefore, the aim of this study was to produce a plant-based BFDV vaccine candidate and to evaluate its ability to elicit an immune response in birds. \n             \n              Recombinant BFDV capsid protein (CP) was transiently expressed in \n              Nicotiana benthamiana \n              and purified using density gradient ultracentrifugation. Japanese quails were immunized with purified BFDV CP. Yolk-derived IgY was purified by water dilution and salt precipitation, and its specificity was verified by western blot analysis. The expression levels of the coat protein increased from non-detectable to an average accumulation of 1.58 mg/kg of fresh plant tissue biomass, and antibodies against BFDV CP were detected in both the blood and eggs of immunized quails, indicating that vaccination with BFDV CP successfully elicited a humoral immune response. \n             \n            This study demonstrates that heterologous expression in plants is a viable method for producing BFDV CP. To the best of our knowledge, this is the first study to show the antibody response to a plant-produced BFDV antigen in a quail model. Given that the presence of anti-CP antibodies in infected birds is associated with immunity, this system can potentially be used to produce a vaccine against BFDV.},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-19},\n\tjournal = {Archives of Virology},\n\tauthor = {Mulondo, Goodman and Buyse, Mélie L. R. and Labuschagne, Kimberley and Jarvis, David and Van Zyl, Albertha and Rybicki, Edward P. and Hitzeroth, Inga I. and Mbewana, Sandiswa},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {163},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Cell-Based Progression of Spiroindoline Phenotypic Hits Leads to the Identification of Compounds with Diverging Parasitological Profiles against the Human Malaria Parasite Plasmodium falciparum.\n \n \n \n \n\n\n \n Dam, J.; Boyle, G. A.; Horatscheck, A.; Woodland, J. G.; Le Manach, C.; Kaur, G.; Taylor, D.; Krugmann, L.; Njoroge, M.; Lawrence, N.; Brunschwig, C.; Zdorichenko, V.; Cox, B.; Wittlin, S.; Von Geldern, T. W.; Smith, D.; Duffy, J.; Basarab, G. S.; and Chibale, K.\n\n\n \n\n\n\n Journal of Medicinal Chemistry, 68(10): 10156–10172. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Cell-Based$ 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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{dam_cell-based_2025,\n\ttitle = {Cell-{Based} {Progression} of {Spiroindoline} {Phenotypic} {Hits} {Leads} to the {Identification} of {Compounds} with {Diverging} {Parasitological} {Profiles} against the {Human} {Malaria} {Parasite} \\textit{{Plasmodium} falciparum}},\n\tvolume = {68},\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.5c00302},\n\tdoi = {10.1021/acs.jmedchem.5c00302},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-19},\n\tjournal = {Journal of Medicinal Chemistry},\n\tauthor = {Dam, Jean and Boyle, Grant A. and Horatscheck, André and Woodland, John G. and Le Manach, Claire and Kaur, Gurminder and Taylor, Dale and Krugmann, Liezl and Njoroge, Mathew and Lawrence, Nina and Brunschwig, Christel and Zdorichenko, Victor and Cox, Brian and Wittlin, Sergio and Von Geldern, Thomas W. and Smith, Dennis and Duffy, James and Basarab, Gregory S. and Chibale, Kelly},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {10156--10172},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A human YEATS4 variant confers resistance to TST and IGRA conversion despite Mycobacterium tuberculosis exposure.\n \n \n \n \n\n\n \n Conil, C.; Bohlen, J.; Kroon, E. E.; Jean-Juste, M. A.; Manry, J.; Chaldebas, M.; Bean, J. M.; Walsh, K. F.; Dallmann-Sauer, M.; Rotival, M.; Seeleuthner, Y.; Marchal, A.; Mourelatos, H.; Fava, V. M.; Zhang, P.; Kerner, G.; Skhoun, H.; Abid, A.; El Ouazzani, H.; Rafik, A.; Bousfiha, A. A.; El Baghdadi, J.; Wilkinson, R. J.; Boisson-Dupuis, S.; Fitzgerald, D. W.; Pape, J. W.; Möller, M.; Hoal, E. G.; Casanova, J.; Abel, L.; Schurr, E.; and Cobat, A.\n\n\n \n\n\n\n Genome Medicine, 17(1): 121. October 2025.\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{conil_human_2025,\n\ttitle = {A human {YEATS4} variant confers resistance to {TST} and {IGRA} conversion despite {Mycobacterium} tuberculosis exposure},\n\tvolume = {17},\n\tissn = {1756-994X},\n\turl = {https://genomemedicine.biomedcentral.com/articles/10.1186/s13073-025-01547-0},\n\tdoi = {10.1186/s13073-025-01547-0},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Genome Medicine},\n\tauthor = {Conil, Clément and Bohlen, Jonathan and Kroon, Elouise E. and Jean-Juste, Marc. A. and Manry, Jérémy and Chaldebas, Matthieu and Bean, James M. and Walsh, Kathleen F. and Dallmann-Sauer, Monica and Rotival, Maxime and Seeleuthner, Yoann and Marchal, Astrid and Mourelatos, Haralambos and Fava, Vinicius M. and Zhang, Peng and Kerner, Gaspard and Skhoun, Hanaa and Abid, Ahmed and El Ouazzani, Hanane and Rafik, Aniss and Bousfiha, Ahmed Aziz and El Baghdadi, Jamila and Wilkinson, Robert J. and Boisson-Dupuis, Stéphanie and Fitzgerald, Daniel W. and Pape, Jean W. and Möller, Marlo and Hoal, Eileen G. and Casanova, Jean-Laurent and Abel, Laurent and Schurr, Erwin and Cobat, Aurélie},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {121},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n How to sustain a public-health genomics and bioinformatics workforce in Africa.\n \n \n \n \n\n\n \n Onywera, H.; Mulder, N.; Kebede, Y.; and Tessema, S. K.\n\n\n \n\n\n\n Nature Medicine, 31(8): 2480–2484. August 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"How$ Paper\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_how_2025,\n\ttitle = {How to sustain a public-health genomics and bioinformatics workforce in {Africa}},\n\tvolume = {31},\n\tissn = {1078-8956, 1546-170X},\n\turl = {https://www.nature.com/articles/s41591-025-03720-9},\n\tdoi = {10.1038/s41591-025-03720-9},\n\tlanguage = {en},\n\tnumber = {8},\n\turldate = {2026-05-19},\n\tjournal = {Nature Medicine},\n\tauthor = {Onywera, Harris and Mulder, Nicola and Kebede, Yenew and Tessema, Sofonias K.},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {2480--2484},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Humoral, T cell and immune gene expression responses to SARS-CoV-2 vaccination in a small group of children with previous MIS-C.\n \n \n \n \n\n\n \n Spracklen, T. F.; Day, J.; Van Der Ross, H.; Butters, C.; Benede, N.; Walters, A.; Bunjun, R.; Moyo-Gwete, T.; Madzivhandila, M.; Mendelsohn, S. C.; Scriba, T. J.; Shey, M.; Burgers, W. A.; Moore, P. L.; Zühlke, L. J.; Keeton, R. S.; and Webb, K.\n\n\n \n\n\n\n Vaccine, 62: 127461. August 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n

@article{spracklen_humoral_2025,\n\ttitle = {Humoral, {T} cell and immune gene expression responses to {SARS}-{CoV}-2 vaccination in a small group of children with previous {MIS}-{C}},\n\tvolume = {62},\n\tissn = {0264410X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S0264410X25007583},\n\tdoi = {10.1016/j.vaccine.2025.127461},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {Vaccine},\n\tauthor = {Spracklen, Timothy F. and Day, Jonathan and Van Der Ross, Hamza and Butters, Claire and Benede, Ntombi and Walters, Avril and Bunjun, Rubina and Moyo-Gwete, Thandeka and Madzivhandila, Mashudu and Mendelsohn, Simon C. and Scriba, Thomas J. and Shey, Muki and Burgers, Wendy A. and Moore, Penny L. and Zühlke, Liesl J. and Keeton, Roanne S. and Webb, Kate},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {127461},\n}\n\n\n\n

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\n\n\n\n

\n \n\n \n \n \n \n \n \n Weekly azithromycin for 48 weeks impacts nasopharyngeal microbial prevalence and Streptococcus pneumoniae serotypes in children with HIV-associated chronic lung disease.\n \n \n \n \n\n\n \n Mushunje, P. K.; Sovershaeva, E.; Olwagen, C. P.; Madhi, S.; Odland, J. Ø.; Ferrand, R. A.; Nicol, M. P.; Abotsi, R. E.; and Dube, F. S.\n\n\n \n\n\n\n Scientific Reports, 15(1): 39175. November 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Weekly$ Paper\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{mushunje_weekly_2025,\n\ttitle = {Weekly azithromycin for 48 weeks impacts nasopharyngeal microbial prevalence and {Streptococcus} pneumoniae serotypes in children with {HIV}-associated chronic lung disease},\n\tvolume = {15},\n\tissn = {2045-2322},\n\turl = {https://www.nature.com/articles/s41598-025-23693-6},\n\tdoi = {10.1038/s41598-025-23693-6},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Scientific Reports},\n\tauthor = {Mushunje, Prince K. and Sovershaeva, Evgeniya and Olwagen, Courtney P. and Madhi, Shabir and Odland, Jon Ø. and Ferrand, Rashida A. and Nicol, Mark P. and Abotsi, Regina E. and Dube, Felix S.},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {39175},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n One-year mortality among adults with advanced HIV in sub-Saharan Africa: a systematic review and meta-analysis.\n \n \n \n \n\n\n \n Scheier, T. C.; De Gouveia, K.; Engel, M. E.; Hohlfeld, A. S.; Cen, A.; Berhe, A.; Fan, S.; Li, J.; Elliott, S.; Ford, N.; Meintjes, G.; Mertz, D.; Eikelboom, J.; and Wasserman, S.\n\n\n \n\n\n\n AIDS. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"One-year$ Paper\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{scheier_one-year_2025,\n\ttitle = {One-year mortality among adults with advanced {HIV} in sub-{Saharan} {Africa}: a systematic review and meta-analysis},\n\tissn = {0269-9370, 1473-5571},\n\tshorttitle = {One-year mortality among adults with advanced {HIV} in sub-{Saharan} {Africa}},\n\turl = {https://journals.lww.com/10.1097/QAD.0000000000004431},\n\tdoi = {10.1097/QAD.0000000000004431},\n\tabstract = {Background: \n              In sub-Saharan Africa (SSA), people with HIV continue to present with advanced HIV disease (AHD), putting them at high risk of life-threatening opportunistic diseases. We aimed to estimate mortality among this population. \n             \n             \n              Methods: \n               \n                We conducted a systematic review and meta-analysis of studies reporting one-year mortality among adults living with HIV and presenting to care with CD4 counts ≤200 cells/mm \n                3 \n                in SSA. MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched for studies (comprising {\\textgreater}500 participants) published between January 1, 2016, and March 21, 2025. Screening and data extraction were done in duplicate. Pooled mortality proportions across CD4 count and time strata were calculated using a generalised linear mixed model. Risk of bias was assessed using a modified Newcastle-Ottawa scale. The protocol is registered with PROSPERO, CRD42023451498. \n               \n             \n             \n              Results: \n               \n                Thirty-six studies with 313,362 participants were included. The weighted median age was 35 years, 64\\% were female, and 98.9\\% were antiretroviral therapy-naive. One-year mortality was 12\\% (95\\% CI 8 – 16) among people with CD4 count ≤200 cells/mm \n                3 \n                and increased with lower CD4 counts (≤100 cells/mm \n                3 \n                , 15\\% (95\\% CI 11 – 19); ≤50 cells/mm \n                3 \n                , 20\\% (95\\% CI 12 – 31)). Most deaths occurred within the first three months after AHD presentation. Heterogeneity was substantial. Risk of bias was high in 18 (50\\%) of 36 included studies. \n               \n             \n             \n              Discussion: \n              There is high one-year mortality among people presenting with AHD in SSA. It is a priority to identify AHD with CD4 testing, improve retention in care, and evaluate additional interventions to reduce mortality in this population.},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {AIDS},\n\tauthor = {Scheier, Thomas C. and De Gouveia, Keisha and Engel, Mark E. and Hohlfeld, Ameer S.-.J. and Cen, Alex and Berhe, Anne and Fan, Sabrina and Li, Jeffery and Elliott, Shakeap and Ford, Nathan and Meintjes, Graeme and Mertz, Dominik and Eikelboom, John and Wasserman, Sean},\n\tmonth = dec,\n\tyear = {2025},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n BCG Revaccination for the Prevention of Mycobacterium tuberculosis Infection.\n \n \n \n \n\n\n \n Schmidt, A. C.; Fairlie, L.; Hellström, E.; Luabeya Kany Kany, A.; Middelkoop, K.; Naidoo, K.; Nair, G.; Gela, A.; Nemes, E.; Scriba, T. J.; Cinar, A.; Frahm, N.; Mogg, R.; Kaufman, D.; Dunne, M. W.; and Hatherill, M.\n\n\n \n\n\n\n New England Journal of Medicine, 392(18): 1789–1800. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"BCG$ Paper\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{schmidt_bcg_2025,\n\ttitle = {{BCG} {Revaccination} for the {Prevention} of \\textit{{Mycobacterium} tuberculosis} {Infection}},\n\tvolume = {392},\n\tissn = {0028-4793, 1533-4406},\n\turl = {http://www.nejm.org/doi/10.1056/NEJMoa2412381},\n\tdoi = {10.1056/NEJMoa2412381},\n\tlanguage = {en},\n\tnumber = {18},\n\turldate = {2026-05-19},\n\tjournal = {New England Journal of Medicine},\n\tauthor = {Schmidt, Alexander C. and Fairlie, Lee and Hellström, Elizabeth and Luabeya Kany Kany, Angelique and Middelkoop, Keren and Naidoo, Kogieleum and Nair, Gonasagrie and Gela, Anele and Nemes, Elisa and Scriba, Thomas J. and Cinar, Amy and Frahm, Nicole and Mogg, Robin and Kaufman, David and Dunne, Michael W. and Hatherill, Mark},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {1789--1800},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A Case of Persistent KSHV Viremia in the Context of HIV, SARS-CoV-2, and Other Co-Infections.\n \n \n \n \n\n\n \n Lambarey, H.; Blumenthal, M. J.; Chinna, P.; Naude, V. N.; Jennings, L.; Orrell, C.; and Schäfer, G.\n\n\n \n\n\n\n Tropical Medicine and Infectious Disease, 10(2): 53. February 2025.\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{lambarey_case_2025,\n\ttitle = {A {Case} of {Persistent} {KSHV} {Viremia} in the {Context} of {HIV}, {SARS}-{CoV}-2, and {Other} {Co}-{Infections}},\n\tvolume = {10},\n\tissn = {2414-6366},\n\turl = {https://www.mdpi.com/2414-6366/10/2/53},\n\tdoi = {10.3390/tropicalmed10020053},\n\tabstract = {Despite the high prevalence of latent Kaposi’s sarcoma-associated herpesvirus (KSHV) infections in patients from endemic areas with a high human immunodeficiency virus (HIV) prevalence, KSHV lytic reactivation in the context of other co-infections is not well understood. Lytic KSHV infections can contribute to severe inflammatory symptoms and KSHV-associated pathogenesis. We have previously reported on KSHV reactivation upon severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exposure in a non-hospitalised cohort of people living with HIV (PLWH). From this cohort, we identified a 34-year-old male who presented for routine HIV care in May 2021 with an unusually high KSHV viral load (VL) of 189,946.3 copies/106 cells, before SARS-CoV-2 infection. The patient was invited into a 2-year follow-up study where his peripheral blood was analysed for selected virological, clinical, and inflammatory parameters every 6 months. He remained highly viremic for KSHV throughout the 2-year study period, during which he was infected with SARS-CoV-2 and developed disseminated tuberculosis, with steadily increasing levels of the inflammatory markers C-reactive protein (CRP), and interleukin-6 (IL-6). His HIV VL remained controlled ({\\textless}1000 copies/mL) and his CD4 count bordered immunosuppression (±200 cells/µL), suggesting some responsiveness to antiretroviral treatment (ART). However, the patient’s uncontrolled lytic KSHV infection may increase his risk for developing a KSHV-associated pathology manifesting with inflammation which should be closely monitored beyond the study period.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {Tropical Medicine and Infectious Disease},\n\tauthor = {Lambarey, Humaira and Blumenthal, Melissa J. and Chinna, Prishanta and Naude, Vincent N. and Jennings, Lauren and Orrell, Catherine and Schäfer, Georgia},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {53},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Neutrophil proteins as potential biomarkers for a sputum-based tuberculosis screening test.\n \n \n \n \n\n\n \n Chambers, M.; Karim, F.; Mazibuko, M.; Mhlane, Z.; Madziwa, L.; Moosa, Y.; Moodley, S.; Hoque, M.; Wong, E. B.; Hiemstra, A.; Malherbe, S. T.; Kriel, B.; Stanley, K.; Van Rensburg, I. C.; Shabangu, A.; Smith, B.; Walzl, G.; Plessis, N. D.; Sterling, T. R; Hatherill, M.; and Leslie, A.\n\n\n \n\n\n\n Frontiers in Immunology, 16: 1636909. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Neutrophil$ Paper\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_neutrophil_2025,\n\ttitle = {Neutrophil proteins as potential biomarkers for a sputum-based tuberculosis screening test},\n\tvolume = {16},\n\tissn = {1664-3224},\n\turl = {https://www.frontiersin.org/articles/10.3389/fimmu.2025.1636909/full},\n\tdoi = {10.3389/fimmu.2025.1636909},\n\tabstract = {Introduction \n              The development of a rapid and affordable assay to screen participants for Q12 additional testing could streamline TB screening in resource-limited settings and for community-wide health screens. Sputum remains the primary testing sample, making it potentially ideal for a screening testing. Neutrophils are highly expanded in sputum from individuals with pulmonary TB with high specificity and have potential as a biomarker for TB. \n             \n             \n              Methods \n              Three neutrophil associated proteins, neutrophil gelatinase associated-lipocalin (NGAL), the protein heterodimer S100A8/A9 and the protein death ligand-1 (PDL-1), were measured in presumptive TB cases from participants attending a primary healthcare clinic in Durban, South Africa, using commercially available ELISAs on a total of 79 participants from a 109-participant cohort. Participants with microbiologically confirmed TB were sampled after 1 month of treatment. Proteins were also measured in tongue swab samples in participants from this cohort at baseline. Baseline results were confirmed in a second TB cohort which recruited a total of 51 participants with presumptive TB from the Western Cape. Finally, we investigate sputum neutrophil protein levels in individuals with community diagnosed asymptomatic TB. \n             \n             \n              Results and discussion \n              Significant increases in all proteins were detectable in sputum from clinic-diagnosed TB participants relative to symptomatic controls. Performance approached the WHO target product profile for a TB triage test, with ROC AUCs reaching 0.866 (with a 95\\% confidence interval of 0.7683 – 0.9633) in the case of S100A8/A9. Sputum protein levels did not correlate with bacterial burden and did not consistently decrease following one month of drug therapy. Only PDL-1 was detectable in mouth swab samples. Sputum neutrophil proteins tended to be elevated in participants with asymptomatic community diagnosed TB, as compared to asymptomatic community controls within the Vukuzazi cohort using a sample size of 42 participants, although this was not significant. This study provides a proof of principle that neutrophil proteins can be easily measured in standard sputum samples and have potential as a screening test for TB. However, more work is needed to explore whether this approach, using these three neutrophil proteins, can meet the WHO target product profile for a triage test worth developing further.},\n\turldate = {2026-05-19},\n\tjournal = {Frontiers in Immunology},\n\tauthor = {Chambers, Mark and Karim, Farina and Mazibuko, Matilda and Mhlane, Zoey and Madziwa, Lindiwe and Moosa, Yunus and Moodley, Sashen and Hoque, Monjurul and Wong, Emily Beth and Hiemstra, Andriette and Malherbe, Stephanus Theron and Kriel, Belinda and Stanley, Kim and Van Rensburg, Ilana Claudia and Shabangu, Ayanda and Smith, Bronwyn and Walzl, Gerhard and Plessis, Nelita Du and Sterling, Timothy R and Hatherill, Mark and Leslie, Alasdair},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {1636909},\n}\n\n\n\n

\n

\n\n\n

\n Introduction The development of a rapid and affordable assay to screen participants for Q12 additional testing could streamline TB screening in resource-limited settings and for community-wide health screens. Sputum remains the primary testing sample, making it potentially ideal for a screening testing. Neutrophils are highly expanded in sputum from individuals with pulmonary TB with high specificity and have potential as a biomarker for TB. Methods Three neutrophil associated proteins, neutrophil gelatinase associated-lipocalin (NGAL), the protein heterodimer S100A8/A9 and the protein death ligand-1 (PDL-1), were measured in presumptive TB cases from participants attending a primary healthcare clinic in Durban, South Africa, using commercially available ELISAs on a total of 79 participants from a 109-participant cohort. Participants with microbiologically confirmed TB were sampled after 1 month of treatment. Proteins were also measured in tongue swab samples in participants from this cohort at baseline. Baseline results were confirmed in a second TB cohort which recruited a total of 51 participants with presumptive TB from the Western Cape. Finally, we investigate sputum neutrophil protein levels in individuals with community diagnosed asymptomatic TB. Results and discussion Significant increases in all proteins were detectable in sputum from clinic-diagnosed TB participants relative to symptomatic controls. Performance approached the WHO target product profile for a TB triage test, with ROC AUCs reaching 0.866 (with a 95% confidence interval of 0.7683 – 0.9633) in the case of S100A8/A9. Sputum protein levels did not correlate with bacterial burden and did not consistently decrease following one month of drug therapy. Only PDL-1 was detectable in mouth swab samples. Sputum neutrophil proteins tended to be elevated in participants with asymptomatic community diagnosed TB, as compared to asymptomatic community controls within the Vukuzazi cohort using a sample size of 42 participants, although this was not significant. This study provides a proof of principle that neutrophil proteins can be easily measured in standard sputum samples and have potential as a screening test for TB. However, more work is needed to explore whether this approach, using these three neutrophil proteins, can meet the WHO target product profile for a triage test worth developing further.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Heterologous Immunization with Improved HIV-1 Subtype C Vaccines Elicit Autologous Tier 2 Neutralizing Antibodies with Rapid Viral Replication Control After SHIV Challenge.\n \n \n \n \n\n\n \n Chege, G. K.; Chapman, R. E.; Keyser, A. T.; Adams, C. H.; Benn, K.; Van Diepen, M. T.; Douglass, N.; Lambson, B.; Hermanus, T.; Moore, P. L.; and Williamson, A.\n\n\n \n\n\n\n Viruses, 17(2): 277. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Heterologous$ Paper\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{chege_heterologous_2025,\n\ttitle = {Heterologous {Immunization} with {Improved} {HIV}-1 {Subtype} {C} {Vaccines} {Elicit} {Autologous} {Tier} 2 {Neutralizing} {Antibodies} with {Rapid} {Viral} {Replication} {Control} {After} {SHIV} {Challenge}},\n\tvolume = {17},\n\tissn = {1999-4915},\n\turl = {https://www.mdpi.com/1999-4915/17/2/277},\n\tdoi = {10.3390/v17020277},\n\tabstract = {We previously reported on HIV vaccines that elicited autologous Tier 2 neutralizing antibodies (nAbs) in rabbits. In the current study, we sought to establish a proof of concept that HIV vaccines using identical designs elicit Tier 2 nAbs in arhesus macaque (RM) model. DNA and MVA vaccines expressing SIV Gag and HIV-1 Env antigens were constructed, and in vitro expression was confirmed. A soluble envelope protein (gp140 Env) was expressed from a stable HEK293 cell line and purified using lectin affinity and size exclusion chromatography. The expression and secretion of SIV Gag and HIV-1 Env by the DNA and MVA vaccines was verified in vitro. Five RMs were inoculated with two DNA, followed by two MVA, and finally with two gp140 Env vaccines at weeks 0, 4, 8, 12, 20 and 28. Vaccine-induced T cell immunity was measured by IFN-γ ELISpot while nAbs were evaluated against MW965 (Tier 1A), 6644 (Tier 1B), autologous ZM109.5A and a closely-related ZM109.B4 (Tier 2) pseudovirions. Vaccinated RMs were challenged intrarectally with simian-human immunodeficiency virus (SHIV), four weeks after the final vaccination, as was an unvaccinated control group (n = 4). Following vaccination, all the animals developed moderate IFN-γ ELISpot responses after the DNA vaccinations which were boosted by the MVA vaccine. After the gp140 Env boost, all animals developed nAbs with peak median titres at 762 (MW965) and 263 (ZM109.5A). The vaccinated animals became infected after a similar number of challenges to the unvaccinated controls, and the resultant number of viral copies in the blood and the lymphoid tissues were similar. However, the duration of detectable viraemia in the vaccinated animals (median: 2 weeks) was shorter than the controls (median: 8.5 weeks). These data show that the vaccines elicited robust cellular and functional humoral immune responses that resulted in a quicker control of viraemia.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {Viruses},\n\tauthor = {Chege, Gerald K. and Chapman, Rosamund E. and Keyser, Alana T. and Adams, Craig H. and Benn, Kealan and Van Diepen, Michiel T. and Douglass, Nicola and Lambson, Bronwen and Hermanus, Tandile and Moore, Penny L. and Williamson, Anna-Lise},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {277},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Balancing safety and efficacy: new insights on primaquine for malaria transmission blocking.\n \n \n \n \n\n\n \n Hänscheid, T.; and Grobusch, M. P\n\n\n \n\n\n\n The Lancet Infectious Diseases, 25(9): 948–949. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Balancing$ Paper\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{hanscheid_balancing_2025,\n\ttitle = {Balancing safety and efficacy: new insights on primaquine for malaria transmission blocking},\n\tvolume = {25},\n\tissn = {14733099},\n\tshorttitle = {Balancing safety and efficacy},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1473309925001173},\n\tdoi = {10.1016/S1473-3099(25)00117-3},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet Infectious Diseases},\n\tauthor = {Hänscheid, Thomas and Grobusch, Martin P},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {948--949},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Peptidyl-dipeptidase A/angiotensin I-converting enzyme.\n \n \n \n \n\n\n \n Sturrock, E. D.; Lubbe, L.; and Danilov, S. M.\n\n\n \n\n\n\n In Handbook of Proteolytic Enzymes, pages 231–242. Elsevier, 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Peptidyl-dipeptidase$ Paper\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{sturrock_peptidyl-dipeptidase_2025,\n\ttitle = {Peptidyl-dipeptidase {A}/angiotensin {I}-converting enzyme},\n\tcopyright = {https://www.elsevier.com/tdm/userlicense/1.0/},\n\tisbn = {9780443288494},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/B9780443288494000254},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tbooktitle = {Handbook of {Proteolytic} {Enzymes}},\n\tpublisher = {Elsevier},\n\tauthor = {Sturrock, Edward D. and Lubbe, Lizelle and Danilov, Sergei M.},\n\tyear = {2025},\n\tdoi = {10.1016/B978-0-443-28849-4.00025-4},\n\tpages = {231--242},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Screening for asymptomatic tuberculosis among adults with household exposure to pulmonary tuberculosis: a prospective observational cohort study.\n \n \n \n \n\n\n \n Mendelsohn, S. C; Mulenga, H.; Tameris, M.; Moloantoa, T.; Malherbe, S. T; Katona, A.; Maruri, F.; Noor, F.; Panchia, R.; Hlongwane, K.; Stanley, K.; Van Der Heijden, Y. F; Hadley, K.; Ariefdien, D. T; Chegou, N. N; Walzl, G.; Scriba, T. J; Sterling, T. R; and Hatherill, M.\n\n\n \n\n\n\n The Lancet Global Health, 13(11): e1869–e1879. November 2025.\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\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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@article{mendelsohn_screening_2025,\n\ttitle = {Screening for asymptomatic tuberculosis among adults with household exposure to pulmonary tuberculosis: a prospective observational cohort study},\n\tvolume = {13},\n\tissn = {2214109X},\n\tshorttitle = {Screening for asymptomatic tuberculosis among adults with household exposure to pulmonary tuberculosis},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X25002761},\n\tdoi = {10.1016/S2214-109X(25)00276-1},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet Global Health},\n\tauthor = {Mendelsohn, Simon C and Mulenga, Humphrey and Tameris, Michele and Moloantoa, Tumelo and Malherbe, Stephanus T and Katona, Austin and Maruri, Fernanda and Noor, Firdows and Panchia, Ravindre and Hlongwane, Khuthadzo and Stanley, Kim and Van Der Heijden, Yuri F and Hadley, Katie and Ariefdien, Dominique T and Chegou, Novel N and Walzl, Gerhard and Scriba, Thomas J and Sterling, Timothy R and Hatherill, Mark},\n\tmonth = nov,\n\tyear = {2025},\n\tpages = {e1869--e1879},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Development of an African horse sickness VP6 DIVA diagnostic ELISA.\n \n \n \n \n\n\n \n Tinarwo, M.; Dennis, S. J.; Hitzeroth, I. I.; Meyers, A. E.; Rybicki, E. P.; and Mbewana, S.\n\n\n \n\n\n\n Virology Journal, 22(1): 276. August 2025.\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{tinarwo_development_2025,\n\ttitle = {Development of an {African} horse sickness {VP6} {DIVA} diagnostic {ELISA}},\n\tvolume = {22},\n\tissn = {1743-422X},\n\turl = {https://virologyj.biomedcentral.com/articles/10.1186/s12985-025-02898-1},\n\tdoi = {10.1186/s12985-025-02898-1},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Virology Journal},\n\tauthor = {Tinarwo, Munyaradzi and Dennis, Susan J. and Hitzeroth, Inga I. and Meyers, Ann E. and Rybicki, Edward P. and Mbewana, Sandiswa},\n\tmonth = aug,\n\tyear = {2025},\n\tpages = {276},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Whole-Exome Sequencing for Molecular Diagnosis of Paediatric Nephrotic Syndrome in Africa: A Call for Implementation.\n \n \n \n \n\n\n \n Gcobo, T.; Katsukunya, J. N.; Lamola, L.; Awany, D.; Ndadza, A.; Dandara, C.; and Mnika, K.\n\n\n \n\n\n\n Genes, 16(11): 1295. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Whole-Exome$ Paper\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{gcobo_whole-exome_2025,\n\ttitle = {Whole-{Exome} {Sequencing} for {Molecular} {Diagnosis} of {Paediatric} {Nephrotic} {Syndrome} in {Africa}: {A} {Call} for {Implementation}},\n\tvolume = {16},\n\tissn = {2073-4425},\n\tshorttitle = {Whole-{Exome} {Sequencing} for {Molecular} {Diagnosis} of {Paediatric} {Nephrotic} {Syndrome} in {Africa}},\n\turl = {https://www.mdpi.com/2073-4425/16/11/1295},\n\tdoi = {10.3390/genes16111295},\n\tabstract = {Nephrotic syndrome (NS) is a common type of kidney disease in children, marked by protein loss in urine, swelling, and low blood protein levels. It is more severe and prevalent in children of African descent, particularly in steroid-resistant forms. Many cases are primary and linked to mutations in genes such as NPHS1, NPHS2, and WT1. While whole-exome sequencing (WES) has advanced the identification of genetic causes globally, its application in African settings remains limited, leaving many cases undiagnosed. This review explores the potential of WES in improving NS diagnosis among African paediatric populations. A literature search was conducted using PubMed, Scopus, and Medline for studies published between 2015 and 2025 focusing on the application of WES in paediatric NS among individuals of African descent. From the 12 articles retrieved, three met the inclusion criteria. These publications reported variants in NPHS1, NPHS2, WT1, PLCE1, COL4A3, COL4A5, TRPC6, and LAMB2 among South African and Egyptian cohorts. WES remains underutilised in African NS research, hindered by limited resources, cost, and underrepresentation in genomic databases. Nonetheless, preliminary evidence suggests WES may contribute to improving diagnosis and guiding treatment through the identification of population-specific pathogenic variants. Increased investment in genomic infrastructure is important for maximising potential benefits and improving diagnostic capabilities.},\n\tlanguage = {en},\n\tnumber = {11},\n\turldate = {2026-05-19},\n\tjournal = {Genes},\n\tauthor = {Gcobo, Thina and Katsukunya, Jonathan N. and Lamola, Lindie and Awany, Denis and Ndadza, Arinao and Dandara, Collet and Mnika, Khuthala},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {1295},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Tunnel sign on magnetic resonance imaging in neuromelioidosis: A systematic literature review.\n \n \n \n \n\n\n \n Gupta, N.; Singh, S.; Kumar, T. P.; Malla, S.; Sethi, A.; Boodman, C.; Van Den Broucke, S.; Vlieghe, E.; Bottieau, E.; Grobusch, M. P.; and Mukhopadhyay, C.\n\n\n \n\n\n\n New Microbes and New Infections, 68: 101639. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Tunnel$ Paper\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{gupta_tunnel_2025,\n\ttitle = {Tunnel sign on magnetic resonance imaging in neuromelioidosis: {A} systematic literature review},\n\tvolume = {68},\n\tissn = {20522975},\n\tshorttitle = {Tunnel sign on magnetic resonance imaging in neuromelioidosis},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2052297525000782},\n\tdoi = {10.1016/j.nmni.2025.101639},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {New Microbes and New Infections},\n\tauthor = {Gupta, Nitin and Singh, Sonali and Kumar, Tirlangi Praveen and Malla, Sundeep and Sethi, Astha and Boodman, Carl and Van Den Broucke, Steven and Vlieghe, Erika and Bottieau, Emmanuel and Grobusch, Martin Peter and Mukhopadhyay, Chiranjay},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {101639},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Equitable access to diagnostic resources means one Xpert-Ultra cartridge for all inpatients with HIV being investigated for tuberculosis.\n \n \n \n \n\n\n \n Boyles, T; Sossen, B; Omar, S V; Meintjes, G; and Taljaard, J\n\n\n \n\n\n\n South African Medical Journal,e3102. May 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Equitable$ Paper\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{boyles_equitable_2025,\n\ttitle = {Equitable access to diagnostic resources means one {Xpert}-{Ultra} cartridge for all inpatients with {HIV} being investigated for tuberculosis},\n\tcopyright = {https://creativecommons.org/licenses/by-nc/4.0},\n\tissn = {2078-5135, 0256-9574},\n\turl = {https://samajournals.co.za/index.php/samj/article/view/3102},\n\tdoi = {10.7196/SAMJ.2025.v115i4.3102},\n\tabstract = {-},\n\turldate = {2026-05-19},\n\tjournal = {South African Medical Journal},\n\tauthor = {Boyles, T and Sossen, B and Omar, S V and Meintjes, G and Taljaard, J},\n\tmonth = may,\n\tyear = {2025},\n\tpages = {e3102},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Approaches to Next-Generation Capripoxvirus and Monkeypox Virus Vaccines.\n \n \n \n \n\n\n \n Williamson, A.\n\n\n \n\n\n\n Viruses, 17(2): 186. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Approaches$ Paper\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{williamson_approaches_2025,\n\ttitle = {Approaches to {Next}-{Generation} {Capripoxvirus} and {Monkeypox} {Virus} {Vaccines}},\n\tvolume = {17},\n\tissn = {1999-4915},\n\turl = {https://www.mdpi.com/1999-4915/17/2/186},\n\tdoi = {10.3390/v17020186},\n\tabstract = {Globally, there are two major poxvirus outbreaks: mpox, caused by the monkeypox virus, and lumpy skin disease, caused by the lumpy skin disease virus. While vaccines for both diseases exist, there is a need for improved vaccines. The original vaccines used to eradicate smallpox, which also protect from the disease now known as mpox, are no longer acceptable. This is mainly due to the risk of serious adverse events, particularly in HIV-positive people. The next-generation vaccine for mpox prevention is modified vaccinia Ankara, which does not complete the viral replication cycle in humans and, therefore, has a better safety profile. However, two modified vaccinia Ankara immunizations are needed to give good but often incomplete protection, and there are indications that the immune response will wane over time. A better vaccine that induces a long-lived response with only one immunization is desirable. Another recently available smallpox vaccine is LC16m8. While LC16m8 contains replicating vaccinia virus, it is a more attenuated vaccine than the original vaccines and has limited side effects. The commonly used lumpy skin disease vaccines are based on attenuated lumpy skin disease virus. However, an inactivated or non-infectious vaccine is desirable as the disease spreads into new territories. This article reviews novel vaccine approaches, including mRNA and subunit vaccines, to protect from poxvirus infection.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {Viruses},\n\tauthor = {Williamson, Anna-Lise},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {186},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n PrEPared to choose: the protocol for an implementation study of the delivery of cabotegravir long-acting injectable pre-exposure prophylaxis (PrEP) as an HIV prevention product option within a real world PrEP choice context in cape town.\n \n \n \n \n\n\n \n Pike, C.; Rousseau, E.; Macdonald, P.; Mapukata, P.; Lebelo, K.; Joseph-Davey, D.; Little, F.; and Bekker, L. G.\n\n\n \n\n\n\n BMC Public Health, 25(1): 3109. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"PrEPared$ Paper\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{pike_prepared_2025,\n\ttitle = {{PrEPared} to choose: the protocol for an implementation study of the delivery of cabotegravir long-acting injectable pre-exposure prophylaxis ({PrEP}) as an {HIV} prevention product option within a real world {PrEP} choice context in cape town},\n\tvolume = {25},\n\tissn = {1471-2458},\n\tshorttitle = {{PrEPared} to choose},\n\turl = {https://bmcpublichealth.biomedcentral.com/articles/10.1186/s12889-025-24370-z},\n\tdoi = {10.1186/s12889-025-24370-z},\n\tabstract = {Abstract \n             \n              Background \n              Increasing choice among HIV pre-exposure prophylaxis (PrEP) products bears potential to increase uptake, persistence, and coverage amongst those at risk of HIV acquisition. Few studies have evaluated PrEP persistence during real-world delivery of multiple PrEP products from community-based sites to adolescents and young people. \n             \n             \n              Methods \n              The PrEPared to Choose (PtC) study delivers PrEP choice across oral, injectable, and vaginal ring options to adolescents and young people (15–29 years) and their potential male partners in Cape Town, South Africa. This phase 3B clinical trial utilizes a type 2 hybrid implementation design with co-primary clinical and implementation aims that include an analysis of PrEP persistence (defined as sustained use of PrEP product as intended with {\\textless} 7 vs. {\\textless} 28 day gap in dosing as scheduled) over the short term (7 months) and long term (18 months), and the identification of implementation strategies that best support PrEP adoption and persistence. PtC is delivered from a mobile clinic and a public health primary care clinic, staffed by trained nurses, HIV counsellors, and peer-navigators. PrEP selection is guided by a co-created PrEP choice counselling intervention, with allowance for product switching at subsequent visits, but no reimbursement for PrEP uptake or return. \n             \n             \n              Discussion \n              PrEPared to Choose will provide an early report of real-world PrEP choice delivery, including all three currently available and approved modalities. The protocol is designed to simulate a real-world environment that provides insight into likely PrEP persistence patterns and practical challenges to PrEP choice implementation in a high HIV burden setting (South Africa) and within high HIV incidence populations (adolescents and young people). The results will be used to inform PrEP choice delivery in South Africa and build a framework into which future, emerging PrEP modalities can be incorporated. \n             \n             \n              Trial approvals and registration \n              This is a phase 3B clinical trial registered with the South African Health Products Regulatory Authority (20230904). Ethical approval was granted by the Human Research Ethics Committee (Faculty of Health Sciences, University of Cape Town, 567/2023). It is registered with the South African National Clinical Trial Registry (DOH-27-012024-5189, 26 January 2024) and ClinicalTrials.gov (NCT06807736, retrospectively registered on 4 February 2025).},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {BMC Public Health},\n\tauthor = {Pike, C. and Rousseau, E. and Macdonald, P. and Mapukata, P. and Lebelo, K. and Joseph-Davey, D. and Little, F. and Bekker, L. G.},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {3109},\n}\n\n\n\n

\n

\n\n\n

\n Abstract Background Increasing choice among HIV pre-exposure prophylaxis (PrEP) products bears potential to increase uptake, persistence, and coverage amongst those at risk of HIV acquisition. Few studies have evaluated PrEP persistence during real-world delivery of multiple PrEP products from community-based sites to adolescents and young people. Methods The PrEPared to Choose (PtC) study delivers PrEP choice across oral, injectable, and vaginal ring options to adolescents and young people (15–29 years) and their potential male partners in Cape Town, South Africa. This phase 3B clinical trial utilizes a type 2 hybrid implementation design with co-primary clinical and implementation aims that include an analysis of PrEP persistence (defined as sustained use of PrEP product as intended with \\textless 7 vs. \\textless 28 day gap in dosing as scheduled) over the short term (7 months) and long term (18 months), and the identification of implementation strategies that best support PrEP adoption and persistence. PtC is delivered from a mobile clinic and a public health primary care clinic, staffed by trained nurses, HIV counsellors, and peer-navigators. PrEP selection is guided by a co-created PrEP choice counselling intervention, with allowance for product switching at subsequent visits, but no reimbursement for PrEP uptake or return. Discussion PrEPared to Choose will provide an early report of real-world PrEP choice delivery, including all three currently available and approved modalities. The protocol is designed to simulate a real-world environment that provides insight into likely PrEP persistence patterns and practical challenges to PrEP choice implementation in a high HIV burden setting (South Africa) and within high HIV incidence populations (adolescents and young people). The results will be used to inform PrEP choice delivery in South Africa and build a framework into which future, emerging PrEP modalities can be incorporated. Trial approvals and registration This is a phase 3B clinical trial registered with the South African Health Products Regulatory Authority (20230904). Ethical approval was granted by the Human Research Ethics Committee (Faculty of Health Sciences, University of Cape Town, 567/2023). It is registered with the South African National Clinical Trial Registry (DOH-27-012024-5189, 26 January 2024) and ClinicalTrials.gov (NCT06807736, retrospectively registered on 4 February 2025).\n

\n\n\n

\n \n\n \n \n \n \n \n \n High burden of variants of uncertain significance in early-onset colorectal cancer among indigenous African patients: a call for global research equity in cancer genetics.\n \n \n \n \n\n\n \n Yildiz, S.; Chambuso, R.; Rebello, G.; and Ramesar, R.\n\n\n \n\n\n\n Molecular Biology Reports, 52(1): 684. December 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"High$ Paper\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{yildiz_high_2025,\n\ttitle = {High burden of variants of uncertain significance in early-onset colorectal cancer among indigenous {African} patients: a call for global research equity in cancer genetics},\n\tvolume = {52},\n\tissn = {0301-4851, 1573-4978},\n\tshorttitle = {High burden of variants of uncertain significance in early-onset colorectal cancer among indigenous {African} patients},\n\turl = {https://link.springer.com/10.1007/s11033-025-10750-6},\n\tdoi = {10.1007/s11033-025-10750-6},\n\tabstract = {Abstract \n             \n              Background \n              Colorectal cancer (CRC) remains a significant global health challenge, with rising incidence among early-onset cases in low- and middle-income countries, including South Africa. However, comprehensive germline genetic data from indigenous African populations remain scarce. This study aimed to explore germline genetic factors contributing to early-onset CRC (eoCRC) in Indigenous African patients using whole exome sequencing (WES). \n             \n             \n              Methods and results \n               \n                We performed WES on blood-derived genomic DNA from 32 Indigenous African patients diagnosed with eoCRC ({\\textless} 50 years), who previously tested negative on a multigene CRC panel. While preliminary but definitive, pathogenic variants were identified in only 5 patients (16\\%) across genes such as \n                C6 \n                , \n                FAT1 \n                , \n                LZTR1 \n                , \n                PYCR1 \n                , and \n                UGT1A7 \n                . A substantial proportion (47\\%, \n                n \n                 = 15) carried variants of uncertain significance (VUS) with strong pathogenic potential (“leaning pathogenic”) in genes \n                ASXL1 \n                , \n                CHEK2 \n                , \n                ERBB2 \n                , \n                ERCC4 \n                , \n                INSR \n                , \n                KIT \n                , \n                MITF \n                , \n                NOTCH1 \n                , \n                NOTCH2 \n                , \n                PDGFRA \n                , \n                RAD51B \n                , \n                RAD54L \n                , \n                RASA1 \n                , \n                RECQL \n                , \n                SUFU \n                , \n                VEGFA \n                , and \n                WT1 \n                . Comparative analysis with public datasets and recurrent findings suggests these leaning pathogenic VUSs may represent true disease-associated variants, currently may be misclassified due to limited representation of African genomes in reference databases. \n               \n             \n             \n              Conclusions \n              Our findings reveal a high burden of potentially pathogenic VUSs in indigenous African patients with eoCRC, reflecting both unique genetic architecture and a critical gap in global genomic equity. These variants may contribute to future variant reclassification and improved understanding of CRC predisposition in African populations. This study underscores the urgent need for population-specific genomic research and the development of inclusive variant databases to support accurate diagnosis and personalised care.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Molecular Biology Reports},\n\tauthor = {Yildiz, Safiye and Chambuso, Ramadhani and Rebello, George and Ramesar, Raj},\n\tmonth = dec,\n\tyear = {2025},\n\tpages = {684},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Resolving the CD4-testing crisis to help end AIDS-related deaths.\n \n \n \n \n\n\n \n Syarif, O.; Oladele, R.; Gils, T.; Rajasingham, R.; Falconer, J.; Achii, P.; Tembo, E.; Tobaiwa, D. D.; Mwehonge, K.; Schutz, C.; Govender, N. P; Meintjes, G.; Meya, D. B; and Loyse, A.\n\n\n \n\n\n\n The Lancet Global Health, 13(1): e16–e18. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Resolving$ Paper\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{syarif_resolving_2025,\n\ttitle = {Resolving the {CD4}-testing crisis to help end {AIDS}-related deaths},\n\tvolume = {13},\n\tissn = {2214109X},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X24004443},\n\tdoi = {10.1016/S2214-109X(24)00444-3},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet Global Health},\n\tauthor = {Syarif, Omar and Oladele, Rita and Gils, Tinne and Rajasingham, Radha and Falconer, Jonathan and Achii, Pamela and Tembo, Edna and Tobaiwa, Donald Denis and Mwehonge, Kenneth and Schutz, Charlotte and Govender, Nelesh P and Meintjes, Graeme and Meya, David B and Loyse, Angela},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {e16--e18},\n}\n\n\n\n

\n

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\n \n\n \n \n \n \n \n \n Bayesian estimation of HIV acquisition dates for prevention trials.\n \n \n \n \n\n\n \n Rossenkhan, R.; Giorgi, E. E.; Shao, D.; Ludwig, J.; Labuschagne, P.; Magaret, C. A.; Ndung'u, T.; Muema, D.; Gounder, K.; Dong, K. L.; Walker, B. D.; Rolland, M.; Robb, M. L.; Eller, L. A.; Sawe, F.; Nitayaphan, S.; Grebe, E.; Busch, M. P.; Delaney, K. P.; Facente, S.; Carpp, L. N.; deCamp , A. C.; Huang, Y.; Korber, B.; Juraska, M.; Rudnicki, E.; Kosmider, E.; Reeves, D. B.; Mayer, B. T.; Hural, J.; Deng, W.; Westfall, D. H.; Yssel, A.; Matten, D.; Bhattacharya, T.; Corey, L.; Gilbert, P. B.; Williamson, C.; Mullins, J. I.; and Edlefsen, P. T.\n\n\n \n\n\n\n mBio, 16(10): e01881–25. October 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Bayesian$ Paper\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{rossenkhan_bayesian_2025,\n\ttitle = {Bayesian estimation of {HIV} acquisition dates for prevention trials},\n\tvolume = {16},\n\tissn = {2150-7511},\n\turl = {https://journals.asm.org/doi/10.1128/mbio.01881-25},\n\tdoi = {10.1128/mbio.01881-25},\n\tabstract = {ABSTRACT \n             \n               \n              Accurate timing estimates of when participants acquire HIV in HIV prevention trials are necessary for determining antibody levels at acquisition. The Antibody-Mediated Prevention (AMP) Studies showed that a passively administered broadly neutralizing antibody can prevent the acquisition of HIV from a neutralization-sensitive virus. We developed a pipeline for estimating the date of detectable HIV acquisition (DDA) in AMP Study participants using diagnostic and viral sequence data. Using a Bayesian strategy that combines three streams of data (REN [rev/vpu/env/Δnef] sequence, GP [gag/Δpol] sequence, and diagnostic) where their 95\\% credible intervals overlap based on pre-specified criteria and decision rules. We evaluated the performance of our AMP pipeline using PacBio viral sequence data from 41 participants across two prospective acute HIV acquisition cohort studies, FRESH and RV217, with twice-weekly sampling. These cohort studies enrolled young women in South Africa and men and women in Kenya and Thailand, respectively, with a high likelihood of HIV acquisition. In evaluating performance, “true DDA” was the center of bounds between last-negative and first-positive RNA diagnostic tests (median time 4 days, range 2–7 days); bias was the mean difference between estimated and true DDA. Using diagnostic data alone yielded timing estimates with a bias of 2.4 days and root mean square error (RMSE) of 7.9 days. These results were improved using sequence + diagnostic data (bias 1.5 days, RMSE 6.9 days), as well as by restricting sequence-based estimation to samples from ≤5 weeks post-DDA (bias 0.2 days, RMSE 7.8 days). \n               \n                IMPORTANCE \n                In HIV prevention trials, accurate timing estimates of when individual participants acquire HIV can be used to estimate antibody levels at the time of acquisition, which is useful for projecting antibody levels needed for prevention. The results we report here suggest that if sequence-based estimation of acquisition timing is used in future clinical trials of combination broadly neutralizing antibody (bnAb) regimens or multispecific bnAbs for HIV prevention, a sampling frequency of at least monthly is needed. Moreover, in the samples analyzed here, we observed less bias in sequence-based timing estimation for samples taken {\\textless}5 weeks post-DDA. This observation is consistent with the timing of immune-driven selective pressures that may negatively impact the power to detect acquisition sieve effects. \n               \n             \n          ,  \n            In HIV prevention trials, accurate timing estimates of when individual participants acquire HIV can be used to estimate antibody levels at the time of acquisition, which is useful for projecting antibody levels needed for prevention. The results we report here suggest that if sequence-based estimation of acquisition timing is used in future clinical trials of combination broadly neutralizing antibody (bnAb) regimens or multispecific bnAbs for HIV prevention, a sampling frequency of at least monthly is needed. Moreover, in the samples analyzed here, we observed less bias in sequence-based timing estimation for samples taken {\\textless}5 weeks post-DDA. This observation is consistent with the timing of immune-driven selective pressures that may negatively impact the power to detect acquisition sieve effects.},\n\tlanguage = {en},\n\tnumber = {10},\n\turldate = {2026-05-19},\n\tjournal = {mBio},\n\tauthor = {Rossenkhan, Raabya and Giorgi, Elena E. and Shao, Danica and Ludwig, James and Labuschagne, Phillip and Magaret, Craig A. and Ndung'u, Thumbi and Muema, Daniel and Gounder, Kamini and Dong, Krista L. and Walker, Bruce D. and Rolland, Morgane and Robb, Merlin L. and Eller, Leigh Anne and Sawe, Fredrick and Nitayaphan, Sorachai and Grebe, Eduard and Busch, Michael P. and Delaney, Kevin P. and Facente, Shelley and Carpp, Lindsay N. and deCamp, Allan C. and Huang, Yunda and Korber, Bette and Juraska, Michal and Rudnicki, Erika and Kosmider, Ewelina and Reeves, Daniel B. and Mayer, Bryan T. and Hural, John and Deng, Wenjie and Westfall, Dylan H. and Yssel, Anna and Matten, David and Bhattacharya, Tanmoy and Corey, Lawrence and Gilbert, Peter B. and Williamson, Carolyn and Mullins, James I. and Edlefsen, Paul T.},\n\teditor = {Mahalingam, Suresh},\n\tmonth = oct,\n\tyear = {2025},\n\tpages = {e01881--25},\n}\n\n\n\n

\n

\n\n\n

\n ABSTRACT Accurate timing estimates of when participants acquire HIV in HIV prevention trials are necessary for determining antibody levels at acquisition. The Antibody-Mediated Prevention (AMP) Studies showed that a passively administered broadly neutralizing antibody can prevent the acquisition of HIV from a neutralization-sensitive virus. We developed a pipeline for estimating the date of detectable HIV acquisition (DDA) in AMP Study participants using diagnostic and viral sequence data. Using a Bayesian strategy that combines three streams of data (REN [rev/vpu/env/Δnef] sequence, GP [gag/Δpol] sequence, and diagnostic) where their 95% credible intervals overlap based on pre-specified criteria and decision rules. We evaluated the performance of our AMP pipeline using PacBio viral sequence data from 41 participants across two prospective acute HIV acquisition cohort studies, FRESH and RV217, with twice-weekly sampling. These cohort studies enrolled young women in South Africa and men and women in Kenya and Thailand, respectively, with a high likelihood of HIV acquisition. In evaluating performance, “true DDA” was the center of bounds between last-negative and first-positive RNA diagnostic tests (median time 4 days, range 2–7 days); bias was the mean difference between estimated and true DDA. Using diagnostic data alone yielded timing estimates with a bias of 2.4 days and root mean square error (RMSE) of 7.9 days. These results were improved using sequence + diagnostic data (bias 1.5 days, RMSE 6.9 days), as well as by restricting sequence-based estimation to samples from ≤5 weeks post-DDA (bias 0.2 days, RMSE 7.8 days). IMPORTANCE In HIV prevention trials, accurate timing estimates of when individual participants acquire HIV can be used to estimate antibody levels at the time of acquisition, which is useful for projecting antibody levels needed for prevention. The results we report here suggest that if sequence-based estimation of acquisition timing is used in future clinical trials of combination broadly neutralizing antibody (bnAb) regimens or multispecific bnAbs for HIV prevention, a sampling frequency of at least monthly is needed. Moreover, in the samples analyzed here, we observed less bias in sequence-based timing estimation for samples taken \\textless5 weeks post-DDA. This observation is consistent with the timing of immune-driven selective pressures that may negatively impact the power to detect acquisition sieve effects. , In HIV prevention trials, accurate timing estimates of when individual participants acquire HIV can be used to estimate antibody levels at the time of acquisition, which is useful for projecting antibody levels needed for prevention. The results we report here suggest that if sequence-based estimation of acquisition timing is used in future clinical trials of combination broadly neutralizing antibody (bnAb) regimens or multispecific bnAbs for HIV prevention, a sampling frequency of at least monthly is needed. Moreover, in the samples analyzed here, we observed less bias in sequence-based timing estimation for samples taken \\textless5 weeks post-DDA. This observation is consistent with the timing of immune-driven selective pressures that may negatively impact the power to detect acquisition sieve effects.\n

\n\n\n

\n \n\n \n \n \n \n \n \n A 3D In Vitro Blood-Brain Barrier Model to Study Pathogen and Drug Effects on the BBB.\n \n \n \n \n\n\n \n Proust, A.; and Wilkinson, R. J.\n\n\n \n\n\n\n In Iovino, F., editor(s), In Vitro and In Vivo Models to Study Infections of the Central Nervous System, volume 2950, pages 61–69. Springer US, New York, NY, 2025.\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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@incollection{iovino_3d_2025,\n\taddress = {New York, NY},\n\ttitle = {A {3D} {In} {Vitro} {Blood}-{Brain} {Barrier} {Model} to {Study} {Pathogen} and {Drug} {Effects} on the {BBB}},\n\tvolume = {2950},\n\tisbn = {9781071646731 9781071646748},\n\turl = {https://link.springer.com/10.1007/978-1-0716-4674-8_5},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tbooktitle = {In {Vitro} and {In} {Vivo} {Models} to {Study} {Infections} of the {Central} {Nervous} {System}},\n\tpublisher = {Springer US},\n\tauthor = {Proust, Alizé and Wilkinson, Robert J.},\n\teditor = {Iovino, Federico},\n\tyear = {2025},\n\tdoi = {10.1007/978-1-0716-4674-8_5},\n\tpages = {61--69},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n ‘Unravelling the shared genetic architecture between suicidality and subcortical brain volume: a genome-wide association study’.\n \n \n \n \n\n\n \n Defo, J.; and Ramesar, R.\n\n\n \n\n\n\n Acta Neuropsychiatrica, 37: e58. 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"‘Unravelling$ Paper\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{defo_unravelling_2025,\n\ttitle = {‘{Unravelling} the shared genetic architecture between suicidality and subcortical brain volume: a genome-wide association study’},\n\tvolume = {37},\n\tissn = {0924-2708, 1601-5215},\n\tshorttitle = {‘{Unravelling} the shared genetic architecture between suicidality and subcortical brain volume},\n\turl = {https://www.cambridge.org/core/product/identifier/S0924270825000122/type/journal_article},\n\tdoi = {10.1017/neu.2025.12},\n\tabstract = {Abstract \n             \n              Suicidality is a significant public health concern, with neuroimaging studies revealing abnormalities in the brains of suicidal individuals and post-mortem samples. However, the genetic architecture between suicidality and subcortical brain volumes remains poorly characterized. Using genome-wide association studies (GWAS), we investigated the genetic overlap between suicidality and subcortical brain volume. GWAS summary statistics for suicidal behaviours, including Suicide Attempts, Ever Self-Harmed, and Thoughts of Life Not Worth Living, from the UK Biobank, Suicide from the FinnGen Biobank, and data on seven subcortical brain volumes and Intracranial Volume from the ENIGMA2 study, were used to investigate the genetic correlation between phenotypes as well as potential genetic factors. A common genetic factor was identified, comprising two categories: Suicide Attempt, Ever Self-Harmed, and Thoughts of Life Not Worth Living from the UK Biobank, and Suicide from FinnGen, Intracranial Volume, and subcortical brain volumes. Cross-phenotype GWAS meta-analysis of each category at variant, gene and subnetwork levels unveils a list of significant variants (P-value {\\textless}5 × 10 \n              −8 \n              ), and potential hub genes (P-value {\\textless}0.05) of consideration. Network, pathway, and Gene Ontology analyses of these joint categories highlighted enriched pathways and biological processes related to blood-brain barrier permeability suggesting that the presence and severity of suicidality are associated with an inflammatory signature detectable in both blood and brain tissues. This study underscores the role of brain and peripheral blood inflammation in suicide risk and holds promise for developing targeted interventions and personalized treatment strategies to reduce suicidality in at-risk populations.},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {Acta Neuropsychiatrica},\n\tauthor = {Defo, Joel and Ramesar, Raj},\n\tyear = {2025},\n\tpages = {e58},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n The clinical and economic impact of genotypic resistance testing for people diagnosed with persistent virological non-suppression on tenofovir–lamivudine–dolutegravir in South Africa: a modelling study.\n \n \n \n \n\n\n \n Hyle, E. P; Bekker, L.; McCluskey, S. M; Chen, W.; Sax, P. E; Moosa, M.; Machoko, M.; Bangs, A.; Steegen, K.; Siedner, M. J; Van De Vijver, D. A M C; Resch, S. C; Neilan, A. M; Phillips, A.; Walensky, R. P; Lessells, R. J; Weinstein, M. C; Dugdale, C. M; Wood, R.; and Freedberg, K. A\n\n\n \n\n\n\n The Lancet HIV, 12(9): e627–e637. September 2025.\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{hyle_clinical_2025,\n\ttitle = {The clinical and economic impact of genotypic resistance testing for people diagnosed with persistent virological non-suppression on tenofovir–lamivudine–dolutegravir in {South} {Africa}: a modelling study},\n\tvolume = {12},\n\tissn = {23523018},\n\tshorttitle = {The clinical and economic impact of genotypic resistance testing for people diagnosed with persistent virological non-suppression on tenofovir–lamivudine–dolutegravir in {South} {Africa}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S235230182500164X},\n\tdoi = {10.1016/S2352-3018(25)00164-X},\n\tlanguage = {en},\n\tnumber = {9},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet HIV},\n\tauthor = {Hyle, Emily P and Bekker, Linda-Gail and McCluskey, Suzanne M and Chen, Wanyi and Sax, Paul E and Moosa, Mahomed-Yunus and Machoko, Munashe and Bangs, Audrey and Steegen, Kim and Siedner, Mark J and Van De Vijver, David A M C and Resch, Stephen C and Neilan, Anne M and Phillips, Andrew and Walensky, Rochelle P and Lessells, Richard J and Weinstein, Milton C and Dugdale, Caitlin M and Wood, Robin and Freedberg, Kenneth A},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {e627--e637},\n}\n\n\n\n

\n

\n\n\n\n

\n \n\n \n \n \n \n \n \n Epidemiological and histopathological features of colorectal adenocarcinoma in the Western Cape public health sector between 2018 and 2020.\n \n \n \n \n\n\n \n Naidoo, K; Begg, W; Van Wyk, A.; and Ramesar, R.\n\n\n \n\n\n\n South African Journal of Surgery, 63(3): 187–192. September 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Epidemiological$ Paper\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{naidoo_epidemiological_2025,\n\ttitle = {Epidemiological and histopathological features of colorectal adenocarcinoma in the {Western} {Cape} public health sector between 2018 and 2020},\n\tvolume = {63},\n\tissn = {0038-2361, 2078-5151},\n\turl = {http://journals.co.za/doi/10.36303/SAJS.02652},\n\tdoi = {10.36303/SAJS.02652},\n\tlanguage = {en},\n\tnumber = {3},\n\turldate = {2026-05-19},\n\tjournal = {South African Journal of Surgery},\n\tauthor = {Naidoo, K and Begg, W and Van Wyk, Ac and Ramesar, Rs},\n\tmonth = sep,\n\tyear = {2025},\n\tpages = {187--192},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Cardiometabolic Biomarkers and Systemic Inflammation in US Adolescents and Young Adults With Latent Tuberculosis Infection: A Population-Based Cohort Study.\n \n \n \n \n\n\n \n Magodoro, I. M; Ntusi, N. A B; Jao, J.; Zar, H. J; Claggett, B. L; Siedner, M. J; Wilkinson, K. A; and Wilkinson, R. J\n\n\n \n\n\n\n Open Forum Infectious Diseases, 12(4): ofaf194. March 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Cardiometabolic$ Paper\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_cardiometabolic_2025,\n\ttitle = {Cardiometabolic {Biomarkers} and {Systemic} {Inflammation} in {US} {Adolescents} and {Young} {Adults} {With} {Latent} {Tuberculosis} {Infection}: {A} {Population}-{Based} {Cohort} {Study}},\n\tvolume = {12},\n\tcopyright = {https://creativecommons.org/licenses/by/4.0/},\n\tissn = {2328-8957},\n\tshorttitle = {Cardiometabolic {Biomarkers} and {Systemic} {Inflammation} in {US} {Adolescents} and {Young} {Adults} {With} {Latent} {Tuberculosis} {Infection}},\n\turl = {https://academic.oup.com/ofid/article/doi/10.1093/ofid/ofaf194/8099195},\n\tdoi = {10.1093/ofid/ofaf194},\n\tabstract = {Abstract \n             \n              Background \n              Mycobacterium tuberculosis (Mtb) infection in adults increases incident type 2 diabetes and atherosclerotic cardiovascular disease risk. It is unknown if this cardiometabolic detriment occurs in young people. We investigated whether young persons with latent tuberculosis infection (LTBI) have worse cardiometabolic health than their peers who are uninfected. \n             \n             \n              Methods \n              Peripubescent adolescents (12–15 years old) and older adolescents/young adults (16–30 years old) were assessed for LTBI by tuberculin skin testing (induration ≥10 mm). Outcomes included fasting plasma glucose, hemoglobin A1c, C-peptide, N-terminal prohormone of brain natriuretic peptide, high-sensitivity cardiac troponin T, C-reactive protein, ferritin, diabetes/prediabetes (fasting plasma glucose ≥5.6 mmol/L and/or hemoglobin A1c ≥5.7\\%), and homeostatic model of insulin resistance. LTBI cases were propensity score matched 1:4 with controls who were uninfected with tuberculosis (TB) on sociodemographics to estimate adjusted median, mean difference, and odds ratio of cardiometabolic indices. \n             \n             \n              Results \n              Seventy-five LTBI cases were matched to 300 peers who were TB uninfected. Among older participants, LTBI was associated with higher inflammation (adjusted median [IQR]: C-reactive protein, 0.22 mg/dL [0.05–0.34] vs 0.11 [0.04–0.35], P = .027; ferritin, 55.0 ng/mL [25.1–90.3] vs 41.1 [29.5–136.2], P = .047) but not among peripubescent adolescents. No meaningful differences were observed in fasting plasma glucose (adjusted mean difference [95\\% CI], −0.05 mmol/L [−.22 to .12]; P = .57), hemoglobin A1c (0.0\\% [−.17\\% to .17\\%], P = .98), diabetes/prediabetes prevalence (adjusted odds ratio [95\\% CI], 0.9 [.29–2.29]; P = .85), insulin secretion/resistance, N-terminal prohormone of brain natriuretic peptide, or high-sensitivity cardiac troponin T by LTBI status. \n             \n             \n              Conclusions \n              Older adolescents and young adults with LTBI had higher inflammation than those without LTBI, while cardiometabolic profiles were similar. Unlike that in adults, Mtb infection in young people may not be associated with cardiometabolic derangement, though the long-term consequences of chronic inflammation require further study.},\n\tlanguage = {en},\n\tnumber = {4},\n\turldate = {2026-05-19},\n\tjournal = {Open Forum Infectious Diseases},\n\tauthor = {Magodoro, Itai M and Ntusi, Ntobeko A B and Jao, Jennifer and Zar, Heather J and Claggett, Brian L and Siedner, Mark J and Wilkinson, Katalin A and Wilkinson, Robert J},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {ofaf194},\n}\n\n\n\n

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\n Abstract Background Mycobacterium tuberculosis (Mtb) infection in adults increases incident type 2 diabetes and atherosclerotic cardiovascular disease risk. It is unknown if this cardiometabolic detriment occurs in young people. We investigated whether young persons with latent tuberculosis infection (LTBI) have worse cardiometabolic health than their peers who are uninfected. Methods Peripubescent adolescents (12–15 years old) and older adolescents/young adults (16–30 years old) were assessed for LTBI by tuberculin skin testing (induration ≥10 mm). Outcomes included fasting plasma glucose, hemoglobin A1c, C-peptide, N-terminal prohormone of brain natriuretic peptide, high-sensitivity cardiac troponin T, C-reactive protein, ferritin, diabetes/prediabetes (fasting plasma glucose ≥5.6 mmol/L and/or hemoglobin A1c ≥5.7%), and homeostatic model of insulin resistance. LTBI cases were propensity score matched 1:4 with controls who were uninfected with tuberculosis (TB) on sociodemographics to estimate adjusted median, mean difference, and odds ratio of cardiometabolic indices. Results Seventy-five LTBI cases were matched to 300 peers who were TB uninfected. Among older participants, LTBI was associated with higher inflammation (adjusted median [IQR]: C-reactive protein, 0.22 mg/dL [0.05–0.34] vs 0.11 [0.04–0.35], P = .027; ferritin, 55.0 ng/mL [25.1–90.3] vs 41.1 [29.5–136.2], P = .047) but not among peripubescent adolescents. No meaningful differences were observed in fasting plasma glucose (adjusted mean difference [95% CI], −0.05 mmol/L [−.22 to .12]; P = .57), hemoglobin A1c (0.0% [−.17% to .17%], P = .98), diabetes/prediabetes prevalence (adjusted odds ratio [95% CI], 0.9 [.29–2.29]; P = .85), insulin secretion/resistance, N-terminal prohormone of brain natriuretic peptide, or high-sensitivity cardiac troponin T by LTBI status. Conclusions Older adolescents and young adults with LTBI had higher inflammation than those without LTBI, while cardiometabolic profiles were similar. Unlike that in adults, Mtb infection in young people may not be associated with cardiometabolic derangement, though the long-term consequences of chronic inflammation require further study.\n

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\n \n\n \n \n \n \n \n \n Exposure to Human Immunodeficiency Virus Is Associated With Altered Composition of Maternal Microchimeric T Cells in Infants.\n \n \n \n \n\n\n \n Armistead, B.; Peters, M Q.; Houck, J.; Carlson, M.; Balle, C.; Mulugeta, N.; Gray, C. M; Jaspan, H. B; and Harrington, W. E\n\n\n \n\n\n\n The Journal of Infectious Diseases, 231(2): 435–439. February 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Exposure$ Paper\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{armistead_exposure_2025,\n\ttitle = {Exposure to {Human} {Immunodeficiency} {Virus} {Is} {Associated} {With} {Altered} {Composition} of {Maternal} {Microchimeric} {T} {Cells} in {Infants}},\n\tvolume = {231},\n\tcopyright = {https://academic.oup.com/pages/standard-publication-reuse-rights},\n\tissn = {0022-1899, 1537-6613},\n\turl = {https://academic.oup.com/jid/article/231/2/435/7829605},\n\tdoi = {10.1093/infdis/jiae521},\n\tabstract = {Abstract \n            Human immunodeficiency virus–exposed but uninfected infants (iHEU) display altered immunity and are at increased risk of infection. We previously reported that iHEU have decreased maternal microchimerism (MMc)—maternal cells transferred to the offspring in utero/during breastfeeding. We quantified MMc in T-cell subpopulations in iHEU and HIV-unexposed infants (iHU) to determine whether a selective deficiency in MMc contributes to altered cellular immunity. Across all infants, MMc levels were highest in CD8+ T cells; however, the level of CD8+ T-cell MMc was lower in iHEU versus iHU. In limited functional studies, we did not identify cytomegalovirus-specific MMc during infant primary infection.},\n\tlanguage = {en},\n\tnumber = {2},\n\turldate = {2026-05-19},\n\tjournal = {The Journal of Infectious Diseases},\n\tauthor = {Armistead, Blair and Peters, M Quinn and Houck, John and Carlson, Marc and Balle, Christina and Mulugeta, Nolawit and Gray, Clive M and Jaspan, Heather B and Harrington, Whitney E},\n\tmonth = feb,\n\tyear = {2025},\n\tpages = {435--439},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n A comparative analysis of somatic mutational profiles according to HIV status among women with cervical intraepithelial neoplasia 3 (CIN3): a focus on hotspots in TP53, PIK3CA, PTEN, and EGFR.\n \n \n \n \n\n\n \n Mabizela, N.; Soko, N.; Wu, H.; Naidoo, R.; and Dandara, C.\n\n\n \n\n\n\n Infectious Agents and Cancer, 20(1): 18. March 2025.\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{mabizela_comparative_2025,\n\ttitle = {A comparative analysis of somatic mutational profiles according to {HIV} status among women with cervical intraepithelial neoplasia 3 ({CIN3}): a focus on hotspots in {TP53}, {PIK3CA}, {PTEN}, and {EGFR}},\n\tvolume = {20},\n\tissn = {1750-9378},\n\tshorttitle = {A comparative analysis of somatic mutational profiles according to {HIV} status among women with cervical intraepithelial neoplasia 3 ({CIN3})},\n\turl = {https://infectagentscancer.biomedcentral.com/articles/10.1186/s13027-025-00647-1},\n\tdoi = {10.1186/s13027-025-00647-1},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2026-05-19},\n\tjournal = {Infectious Agents and Cancer},\n\tauthor = {Mabizela, Nosipho and Soko, Nyarai and Wu, Hue-Tsi and Naidoo, Richard and Dandara, Collet},\n\tmonth = mar,\n\tyear = {2025},\n\tpages = {18},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Cost-effective pricing of long-acting injectable HIV pre-exposure prophylaxis for adolescent girls and young women in South Africa: a model-based analysis.\n \n \n \n \n\n\n \n Jin, E. Y; Ahmed, A. R; Bekker, L.; Rousseau, E.; Dugdale, C. M; Flanagan, C. F; Wallace, M.; Freedberg, K. A; Orrell, C.; Reddy, K. P; Paltiel, A D.; Ciaranello, A. L; and Neilan, A. M\n\n\n \n\n\n\n The Lancet Global Health, 13(7): e1230–e1239. July 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Cost-effective$ Paper\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{jin_cost-effective_2025,\n\ttitle = {Cost-effective pricing of long-acting injectable {HIV} pre-exposure prophylaxis for adolescent girls and young women in {South} {Africa}: a model-based analysis},\n\tvolume = {13},\n\tissn = {2214109X},\n\tshorttitle = {Cost-effective pricing of long-acting injectable {HIV} pre-exposure prophylaxis for adolescent girls and young women in {South} {Africa}},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S2214109X25001196},\n\tdoi = {10.1016/S2214-109X(25)00119-6},\n\tlanguage = {en},\n\tnumber = {7},\n\turldate = {2026-05-19},\n\tjournal = {The Lancet Global Health},\n\tauthor = {Jin, Elena Y and Ahmed, Ali R and Bekker, Linda-Gail and Rousseau, Elzette and Dugdale, Caitlin M and Flanagan, Clare F and Wallace, Melissa and Freedberg, Kenneth A and Orrell, Catherine and Reddy, Krishna P and Paltiel, A David and Ciaranello, Andrea L and Neilan, Anne M},\n\tmonth = jul,\n\tyear = {2025},\n\tpages = {e1230--e1239},\n}\n\n\n\n

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\n \n\n \n \n \n \n \n \n Autoantibodies directed against interferon alpha, nuclear antigens, cardiolipin, and beta 2 glycoprotein 1 are not induced by SARS-CoV-2 or associated with long COVID.\n \n \n \n \n\n\n \n Epstein-Shuman, A.; Hunt, J. H.; Caturegli, P.; Winguth, P.; Fernandez, R. E.; Rozek, G. M.; Zhu, X.; DiRico, N. A.; Jamal, A.; Hsieh, Y.; Manabe, Y. C.; Redd, A. D.; Reynolds, S. J.; Antar, A. A.; and Laeyendecker, O.\n\n\n \n\n\n\n International Journal of Infectious Diseases, 150: 107289. January 2025.\n \n\n\n\n
\n\n\n\n \n \n $\"Autoantibodies$ Paper\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{epstein-shuman_autoantibodies_2025,\n\ttitle = {Autoantibodies directed against interferon alpha, nuclear antigens, cardiolipin, and beta 2 glycoprotein 1 are not induced by {SARS}-{CoV}-2 or associated with long {COVID}},\n\tvolume = {150},\n\tissn = {12019712},\n\turl = {https://linkinghub.elsevier.com/retrieve/pii/S1201971224003606},\n\tdoi = {10.1016/j.ijid.2024.107289},\n\tlanguage = {en},\n\turldate = {2026-05-19},\n\tjournal = {International Journal of Infectious Diseases},\n\tauthor = {Epstein-Shuman, Adam and Hunt, Joanne H. and Caturegli, Patrizio and Winguth, Patrick and Fernandez, Reinaldo E. and Rozek, Gracie M. and Zhu, Xianming and DiRico, Nicholas A. and Jamal, Armaan and Hsieh, Yu-Hsiang and Manabe, Yukari C. and Redd, Andrew D. and Reynolds, Steven J. and Antar, Annukka A.R. and Laeyendecker, Oliver},\n\tmonth = jan,\n\tyear = {2025},\n\tpages = {107289},\n}\n

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