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10.1016/j.isci.2022.104464 http://scihub22266oqcxt.onion/10.1016/j.isci.2022.104464 35634577!9130411!35634577     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=35634577&cmd=llinks): Failed to open stream: HTTP request failed! 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Immunopathogenic overlap between COVID-19 and tuberculosis identified from transcriptomic meta-analysis and human macrophage infection |pdf=|usr=}}{{35634577}} gab.com Text Immunopathogenic overlap between COVID-19 and tuberculosis identified from transcriptomic meta-analysis and human macrophage infection JO: iScience http://www.kidney.de/pget.php?&tw=1&pmid=35634577 #FOAvip 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 (p<0.005), in three independent cohorts. Integrative single-cell-RNAseq analysis identified FCN1- 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. Twit Text FOAVip Immunopathogenic overlap between COVID-19 and tuberculosis identified from transcriptomic meta-analysis and human macrophage infection ????iScience http://www.kidney.de/pget.php?&tw=1&pmid=35634577 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35634577 #FOAvip English Wikipedia <ref>{{Cite pmid|35634577}}</ref> Immunopathogenic overlap between COVID-19 and tuberculosis identified from transcriptomic meta-analysis and human macrophage infection #MMPMID35634577 Sheerin D; Abhimanyu; Peton N; Vo W; Allison CC; Wang X; Johnson WE; Coussens AK iScience 2022[Jun]; 25 (6): 104464 PMID35634577show ga 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 (p<0.005), in three independent cohorts. Integrative single-cell-RNAseq analysis identified FCN1- 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. äImmunopathogenic overlap between COVID-19 and tuberculosis identified (epmc).pdf DeepDyve Pubget Overpricing