@article{Booysen,
abstract = {SARS-CoV-2 and Mycobacterium tuberculosis (Mtb) are major infectious causes of death, with meta-analyses and population-based studies finding increased mortality in coinfected patients simultaneously diagnosed with COVID-19 and tuberculosis. There is a need to understand the immune interaction between SARS-CoV-2 and Mtb which impacts poor outcomes for those co-infected. We performed a PubMed and preprint search using keywords [SARS-CoV-2] AND [tuberculosis] AND [Immune response], including publications after January 2020, excluding reviews or opinions. Abstracts were evaluated by authors for inclusion of data specifically investigating the innate and/or acquired immune responses to SARS-CoV-2 and Mtb in humans and animal models, immunopathological responses in co-infection and both trials and investigations of potential protection against SARS-CoV-2 by Bacille Calmette Gu{\'{e}}rin (BCG). Of the 248 articles identified, 39 were included. Incidence of co-infection is discussed, considering in areas with a high burden of tuberculosis, where reported coinfection is likely underestimated. We evaluated evidence of the clinical association between COVID-19 and tuberculosis, discuss differences and similarities in immune responses in humans and in murine studies, and the implications of co-infection. SARS-CoV-2 and tuberculosis have both been shown to modulate immune responses, particularly of monocytes, macrophages, neutrophils, and T cells. Coinfection may result in impaired immunity to SARS-CoV-2, with an exacerbated inflammatory response, while T cell responses to Mtb may be modulated by SARS-CoV-2. Furthermore, there has been no proven potential clinical benefit of BCG despite numerous large-scale clinical trials.},
author = {Booysen, Petro and Wilkinson, Katalin A and Sheerin, Dylan and Waters, Robyn and Coussens, Anna K and Wilkinson, Robert J},
doi = {10.3389/FIMMU.2023.1254206},
issn = {1664-3224},
journal = {Frontiers in Immunology},
keywords = {Bacille Calmette-Gu{\'{e}}rin,COVID-19,Coinfection,LTBI,Mycobacterium tuberculosis,OA,OA{\_}PMC,T cells,Transcriptomics,immune response,review},
mendeley-tags = {OA,OA{\_}PMC,review},
pages = {1254206},
pmid = {37841282},
publisher = {Frontiers},
title = {{Immune interaction between SARS-CoV-2 and Mycobacterium tuberculosis}},
volume = {14}
}

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Abstracts were evaluated by authors for inclusion of data specifically investigating the innate and/or acquired immune responses to SARS-CoV-2 and Mtb in humans and animal models, immunopathological responses in co-infection and both trials and investigations of potential protection against SARS-CoV-2 by Bacille Calmette Guérin (BCG). Of the 248 articles identified, 39 were included. Incidence of co-infection is discussed, considering in areas with a high burden of tuberculosis, where reported coinfection is likely underestimated. We evaluated evidence of the clinical association between COVID-19 and tuberculosis, discuss differences and similarities in immune responses in humans and in murine studies, and the implications of co-infection. SARS-CoV-2 and tuberculosis have both been shown to modulate immune responses, particularly of monocytes, macrophages, neutrophils, and T cells. 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There is a need to understand the immune interaction between SARS-CoV-2 and Mtb which impacts poor outcomes for those co-infected. We performed a PubMed and preprint search using keywords [SARS-CoV-2] AND [tuberculosis] AND [Immune response], including publications after January 2020, excluding reviews or opinions. Abstracts were evaluated by authors for inclusion of data specifically investigating the innate and/or acquired immune responses to SARS-CoV-2 and Mtb in humans and animal models, immunopathological responses in co-infection and both trials and investigations of potential protection against SARS-CoV-2 by Bacille Calmette Gu{\\'{e}}rin (BCG). Of the 248 articles identified, 39 were included. Incidence of co-infection is discussed, considering in areas with a high burden of tuberculosis, where reported coinfection is likely underestimated. 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