Immunopathogenic overlap between COVID-19 and tuberculosis identified from transcriptomic meta-analysis and human macrophage infection. Sheerin, D., Abhimanyu, Peton, N., Vo, W., Allison, C. C., Wang, X., Johnson, W E., & Coussens, A. K iScience, 25(6):104464, Elsevier, jun, 2022. ![Immunopathogenic overlap between COVID-19 and tuberculosis identified from transcriptomic meta-analysis and human macrophage infection [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Summary Current and previous tuberculosis (TB) increase the risk of COVID-19 mortality and severe disease. To identify mechanisms of immunopathogenic interaction between COVID-19 and TB, we performed a systematic review and patient-level meta-analysis of COVID-19 transcriptomic signatures, spanning disease severity, from whole blood, PBMCs, and BALF. 35 eligible signatures were profiled on 1181 RNA-seq samples from 853 individuals across the spectrum of TB infection. Thirteen COVID-19 gene-signatures had significantly higher "COVID-19 risk scores" in active TB and latent TB progressors compared with non-progressors and uninfected controls (pFCN1- and SPP1-expressing macrophages enriched in severe COVID-19 BALF and active TB blood. Gene ontology and protein-protein interaction networks identified 12-gene disease-exacerbation hot spots between COVID-19 and TB. Finally, we in vitro validated that SARS-CoV-2 infection is increased in human macrophages cultured in the inflammatory milieu of Mtb-infected macrophages, correlating with TMPRSS2, IFNA1, IFNB1, IFNG, TNF, and IL1B induction.
@article{Sheerin2022,
abstract = {Summary Current and previous tuberculosis (TB) increase the risk of COVID-19 mortality and severe disease. To identify mechanisms of immunopathogenic interaction between COVID-19 and TB, we performed a systematic review and patient-level meta-analysis of COVID-19 transcriptomic signatures, spanning disease severity, from whole blood, PBMCs, and BALF. 35 eligible signatures were profiled on 1181 RNA-seq samples from 853 individuals across the spectrum of TB infection. Thirteen COVID-19 gene-signatures had significantly higher "COVID-19 risk scores" in active TB and latent TB progressors compared with non-progressors and uninfected controls (pFCN1- and SPP1-expressing macrophages enriched in severe COVID-19 BALF and active TB blood. Gene ontology and protein-protein interaction networks identified 12-gene disease-exacerbation hot spots between COVID-19 and TB. Finally, we in vitro validated that SARS-CoV-2 infection is increased in human macrophages cultured in the inflammatory milieu of Mtb-infected macrophages, correlating with TMPRSS2, IFNA1, IFNB1, IFNG, TNF, and IL1B induction.},
author = {Sheerin, Dylan and Abhimanyu and Peton, Nashied and Vo, William and Allison, Cody Charles and Wang, Xutao and Johnson, W Evan and Coussens, Anna K},
doi = {10.1016/J.ISCI.2022.104464},
file = {:C$\backslash$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Sheerin et al. - 2022 - Immunopathogenic overlap between COVID-19 and tuberculosis identified from transcriptomic meta-analysis and huma.pdf:pdf},
issn = {2589-0042},
journal = {iScience},
keywords = {Immunology,OA,Pathophysiology,Transcriptomics,Virology,fund{\_}not{\_}ack,original},
mendeley-tags = {OA,fund{\_}not{\_}ack,original},
month = {jun},
number = {6},
pages = {104464},
pmid = {35634577},
publisher = {Elsevier},
title = {{Immunopathogenic overlap between COVID-19 and tuberculosis identified from transcriptomic meta-analysis and human macrophage infection}},
url = {http://www.cell.com/article/S2589004222007350/fulltext http://www.cell.com/article/S2589004222007350/abstract https://www.cell.com/iscience/abstract/S2589-0042(22)00735-0},
volume = {25},
year = {2022}
}
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