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10.1371/journal.ppat.1009820 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1009820 34807954!8648102!34807954     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2021 ; 17 (11): e1009820 Nephropedia Template TP {{tp|p=34807954|t=2021. TMPRSS2 promotes SARS-CoV-2 evasion from NCOA7-mediated restriction |pdf=|usr=}}{{34807954}} gab.com Text TMPRSS2 promotes SARS-CoV-2 evasion from NCOA7-mediated restriction JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=34807954 #FOAvip Interferons play a critical role in regulating host immune responses to SARS-CoV-2, but the interferon (IFN)-stimulated gene (ISG) effectors that inhibit SARS-CoV-2 are not well characterized. The IFN-inducible short isoform of human nuclear receptor coactivator 7 (NCOA7) inhibits endocytic virus entry, interacts with the vacuolar ATPase, and promotes endo-lysosomal vesicle acidification and lysosomal protease activity. Here, we used ectopic expression and gene knockout to demonstrate that NCOA7 inhibits infection by SARS-CoV-2 as well as by lentivirus particles pseudotyped with SARS-CoV-2 Spike in lung epithelial cells. Infection with the highly pathogenic, SARS-CoV-1 and MERS-CoV, or seasonal, HCoV-229E and HCoV-NL63, coronavirus Spike-pseudotyped viruses was also inhibited by NCOA7. Importantly, either overexpression of TMPRSS2, which promotes plasma membrane fusion versus endosomal fusion of SARS-CoV-2, or removal of Spike's polybasic furin cleavage site rendered SARS-CoV-2 less sensitive to NCOA7 restriction. Collectively, our data indicate that furin cleavage sensitizes SARS-CoV-2 Spike to the antiviral consequences of endosomal acidification by NCOA7, and suggest that the acquisition of furin cleavage may have favoured the co-option of cell surface TMPRSS proteases as a strategy to evade the suppressive effects of IFN-induced endo-lysosomal dysregulation on virus infection. Twit Text FOAVip TMPRSS2 promotes SARS-CoV-2 evasion from NCOA7-mediated restriction ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=34807954 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34807954 #FOAvip English Wikipedia <ref>{{Cite pmid|34807954}}</ref> TMPRSS2 promotes SARS-CoV-2 evasion from NCOA7-mediated restriction #MMPMID34807954 Khan H; Winstone H; Jimenez-Guardeno JM; Graham C; Doores KJ; Goujon C; Matthews DA; Davidson AD; Rihn SJ; Palmarini M; Neil SJD; Malim MH PLoS Pathog 2021[Nov]; 17 (11): e1009820 PMID34807954show ga Interferons play a critical role in regulating host immune responses to SARS-CoV-2, but the interferon (IFN)-stimulated gene (ISG) effectors that inhibit SARS-CoV-2 are not well characterized. The IFN-inducible short isoform of human nuclear receptor coactivator 7 (NCOA7) inhibits endocytic virus entry, interacts with the vacuolar ATPase, and promotes endo-lysosomal vesicle acidification and lysosomal protease activity. Here, we used ectopic expression and gene knockout to demonstrate that NCOA7 inhibits infection by SARS-CoV-2 as well as by lentivirus particles pseudotyped with SARS-CoV-2 Spike in lung epithelial cells. Infection with the highly pathogenic, SARS-CoV-1 and MERS-CoV, or seasonal, HCoV-229E and HCoV-NL63, coronavirus Spike-pseudotyped viruses was also inhibited by NCOA7. Importantly, either overexpression of TMPRSS2, which promotes plasma membrane fusion versus endosomal fusion of SARS-CoV-2, or removal of Spike's polybasic furin cleavage site rendered SARS-CoV-2 less sensitive to NCOA7 restriction. Collectively, our data indicate that furin cleavage sensitizes SARS-CoV-2 Spike to the antiviral consequences of endosomal acidification by NCOA7, and suggest that the acquisition of furin cleavage may have favoured the co-option of cell surface TMPRSS proteases as a strategy to evade the suppressive effects of IFN-induced endo-lysosomal dysregulation on virus infection. |COVID-19/*virology[MESH] |Cell Line[MESH] |Endosomes/metabolism[MESH] |Furin/genetics/*metabolism[MESH] |Gene Expression[MESH] |Humans[MESH] |Immune Evasion[MESH] |Interferons/metabolism[MESH] |Lysosomes/enzymology[MESH] |Nuclear Receptor Coactivators/genetics/*metabolism[MESH] |Protein Isoforms[MESH] |Proteolysis[MESH] |SARS-CoV-2/*physiology[MESH] |Serine Endopeptidases/genetics/*metabolism[MESH] |Spike Glycoprotein, Coronavirus/metabolism[MESH] |Viral Pseudotyping[MESH]TMPRSS2 promotes SARS-CoV-2 evasion from NCOA7-mediated restriction (epmc).pdf DeepDyve Pubget Overpricing