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10.1038/s41586-021-04352-y http://scihub22266oqcxt.onion/10.1038/s41586-021-04352-y 34942634!8850198!34942634     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34942634&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\34942634.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nature 2022 ; 602 (7897): 487-495 Nephropedia Template TP {{tp|p=34942634|t=2022. Evolution of enhanced innate immune evasion by SARS-CoV-2 |pdf=|usr=}}{{34942634}} gab.com Text Evolution of enhanced innate immune evasion by SARS-CoV-2 JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=34942634 #FOAvip The emergence of SARS-CoV-2 variants of concern suggests viral adaptation to enhance human-to-human transmission(1,2). Although much effort has focused on the characterization of changes in the spike protein in variants of concern, mutations outside of spike are likely to contribute to adaptation. Here, using unbiased abundance proteomics, phosphoproteomics, RNA sequencing and viral replication assays, we show that isolates of the Alpha (B.1.1.7) variant(3) suppress innate immune responses in airway epithelial cells more effectively than first-wave isolates. We found that the Alpha variant has markedly increased subgenomic RNA and protein levels of the nucleocapsid protein (N), Orf9b and Orf6-all known innate immune antagonists. Expression of Orf9b alone suppressed the innate immune response through interaction with TOM70, a mitochondrial protein that is required for activation of the RNA-sensing adaptor MAVS. Moreover, the activity of Orf9b and its association with TOM70 was regulated by phosphorylation. We propose that more effective innate immune suppression, through enhanced expression of specific viral antagonist proteins, increases the likelihood of successful transmission of the Alpha variant, and may increase in vivo replication and duration of infection(4). The importance of mutations outside the spike coding region in the adaptation of SARS-CoV-2 to humans is underscored by the observation that similar mutations exist in the N and Orf9b regulatory regions of the Delta and Omicron variants. Twit Text FOAVip Evolution of enhanced innate immune evasion by SARS-CoV-2 ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=34942634 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34942634 #FOAvip English Wikipedia <ref>{{Cite pmid|34942634}}</ref> Evolution of enhanced innate immune evasion by SARS-CoV-2 #MMPMID34942634 Thorne LG; Bouhaddou M; Reuschl AK; Zuliani-Alvarez L; Polacco B; Pelin A; Batra J; Whelan MVX; Hosmillo M; Fossati A; Ragazzini R; Jungreis I; Ummadi M; Rojc A; Turner J; Bischof ML; Obernier K; Braberg H; Soucheray M; Richards A; Chen KH; Harjai B; Memon D; Hiatt J; Rosales R; McGovern BL; Jahun A; Fabius JM; White K; Goodfellow IG; Takeuchi Y; Bonfanti P; Shokat K; Jura N; Verba K; Noursadeghi M; Beltrao P; Kellis M; Swaney DL; Garcia-Sastre A; Jolly C; Towers GJ; Krogan NJ Nature 2022[Feb]; 602 (7897): 487-495 PMID34942634show ga The emergence of SARS-CoV-2 variants of concern suggests viral adaptation to enhance human-to-human transmission(1,2). Although much effort has focused on the characterization of changes in the spike protein in variants of concern, mutations outside of spike are likely to contribute to adaptation. Here, using unbiased abundance proteomics, phosphoproteomics, RNA sequencing and viral replication assays, we show that isolates of the Alpha (B.1.1.7) variant(3) suppress innate immune responses in airway epithelial cells more effectively than first-wave isolates. We found that the Alpha variant has markedly increased subgenomic RNA and protein levels of the nucleocapsid protein (N), Orf9b and Orf6-all known innate immune antagonists. Expression of Orf9b alone suppressed the innate immune response through interaction with TOM70, a mitochondrial protein that is required for activation of the RNA-sensing adaptor MAVS. Moreover, the activity of Orf9b and its association with TOM70 was regulated by phosphorylation. We propose that more effective innate immune suppression, through enhanced expression of specific viral antagonist proteins, increases the likelihood of successful transmission of the Alpha variant, and may increase in vivo replication and duration of infection(4). The importance of mutations outside the spike coding region in the adaptation of SARS-CoV-2 to humans is underscored by the observation that similar mutations exist in the N and Orf9b regulatory regions of the Delta and Omicron variants. |*Evolution, Molecular[MESH] |*Immune Evasion[MESH] |COVID-19/*immunology/transmission/*virology[MESH] |Coronavirus Nucleocapsid Proteins/chemistry/metabolism[MESH] |Humans[MESH] |Immunity, Innate/genetics/*immunology[MESH] |Interferons/immunology[MESH] |Mitochondrial Precursor Protein Import Complex Proteins/metabolism[MESH] |Phosphoproteins/chemistry/metabolism[MESH] |Phosphorylation[MESH] |Proteomics[MESH] |RNA, Viral/genetics[MESH] |RNA-Seq[MESH]Evolution of enhanced innate immune evasion by SARS-CoV-2 (epmc).pdf DeepDyve Pubget Overpricing