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10.1016/j.jmb.2021.167265 http://scihub22266oqcxt.onion/10.1016/j.jmb.2021.167265 34562466!8457632!34562466     free     free     free Deprecated: Implicit conversion from float 211.6 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\34562466.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Mol+Biol 2022 ; 434 (6): 167265 Nephropedia Template TP {{tp|p=34562466|t=2022. Mechanisms of Antiviral Immune Evasion of SARS-CoV-2 |pdf=|usr=}}{{34562466}} gab.com Text Mechanisms of Antiviral Immune Evasion of SARS-CoV-2 JO: J Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=34562466 #FOAvip Coronavirus disease (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is characterized by a delayed interferon (IFN) response and high levels of proinflammatory cytokine expression. Type I and III IFNs serve as a first line of defense during acute viral infections and are readily antagonized by viruses to establish productive infection. A rapidly growing body of work has interrogated the mechanisms by which SARS-CoV-2 antagonizes both IFN induction and IFN signaling to establish productive infection. Here, we summarize these findings and discuss the molecular interactions that prevent viral RNA recognition, inhibit the induction of IFN gene expression, and block the response to IFN treatment. We also describe the mechanisms by which SARS-CoV-2 viral proteins promote host shutoff. A detailed understanding of the host-pathogen interactions that unbalance the IFN response is critical for the design and deployment of host-targeted therapeutics to manage COVID-19. Twit Text FOAVip Mechanisms of Antiviral Immune Evasion of SARS-CoV-2 ????J Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=34562466 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34562466 #FOAvip English Wikipedia <ref>{{Cite pmid|34562466}}</ref> Mechanisms of Antiviral Immune Evasion of SARS-CoV-2 #MMPMID34562466 Beyer DK; Forero A J Mol Biol 2022[Mar]; 434 (6): 167265 PMID34562466show ga Coronavirus disease (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is characterized by a delayed interferon (IFN) response and high levels of proinflammatory cytokine expression. Type I and III IFNs serve as a first line of defense during acute viral infections and are readily antagonized by viruses to establish productive infection. A rapidly growing body of work has interrogated the mechanisms by which SARS-CoV-2 antagonizes both IFN induction and IFN signaling to establish productive infection. Here, we summarize these findings and discuss the molecular interactions that prevent viral RNA recognition, inhibit the induction of IFN gene expression, and block the response to IFN treatment. We also describe the mechanisms by which SARS-CoV-2 viral proteins promote host shutoff. A detailed understanding of the host-pathogen interactions that unbalance the IFN response is critical for the design and deployment of host-targeted therapeutics to manage COVID-19. |*COVID-19/genetics/immunology[MESH] |*Immune Evasion[MESH] |*Interferons/genetics[MESH] |*SARS-CoV-2/immunology[MESH] |Gene Expression[MESH] |Humans[MESH] |Immunity, Innate[MESH]Mechanisms of Antiviral Immune Evasion of SARS-CoV-2 (epmc).pdf DeepDyve Pubget Overpricing