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10.1002/jmv.27050 http://scihub22266oqcxt.onion/10.1002/jmv.27050 33913550!8242602!33913550     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33913550&cmd=llinks): Failed to open stream: HTTP request failed! 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SARS-CoV-2 ORF9b antagonizes type I and III interferons by targeting multiple components of the RIG-I/MDA-5-MAVS, TLR3-TRIF, and cGAS-STING signaling pathways |pdf=|usr=}}{{33913550}} gab.com Text SARS-CoV-2 ORF9b antagonizes type I and III interferons by targeting multiple components of the RIG-I/MDA-5-MAVS, TLR3-TRIF, and cGAS-STING signaling pathways JO: J Med Virol http://www.kidney.de/pget.php?&tw=1&pmid=33913550 #FOAvip The suppression of types I and III interferon (IFN) responses by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contributes to the pathogenesis of coronavirus disease 2019 (COVID-19). The strategy used by SARS-CoV-2 to evade antiviral immunity needs further investigation. Here, we reported that SARS-CoV-2 ORF9b inhibited types I and III IFN production by targeting multiple molecules of innate antiviral signaling pathways. SARS-CoV-2 ORF9b impaired the induction of types I and III IFNs by Sendai virus and poly (I:C). SARS-CoV-2 ORF9b inhibited the activation of types I and III IFNs induced by the components of cytosolic dsRNA-sensing pathways of RIG-I/MDA5-MAVS signaling, including RIG-I, MDA-5, MAVS, TBK1, and IKKepsilon, rather than IRF3-5D, which is the active form of IRF3. SARS-CoV-2 ORF9b also suppressed the induction of types I and III IFNs by TRIF and STING, which are the adaptor protein of the endosome RNA-sensing pathway of TLR3-TRIF signaling and the adaptor protein of the cytosolic DNA-sensing pathway of cGAS-STING signaling, respectively. A mechanistic analysis revealed that the SARS-CoV-2 ORF9b protein interacted with RIG-I, MDA-5, MAVS, TRIF, STING, and TBK1 and impeded the phosphorylation and nuclear translocation of IRF3. In addition, SARS-CoV-2 ORF9b facilitated the replication of the vesicular stomatitis virus. Therefore, the results showed that SARS-CoV-2 ORF9b negatively regulates antiviral immunity and thus facilitates viral replication. This study contributes to our understanding of the molecular mechanism through which SARS-CoV-2 impairs antiviral immunity and provides an essential clue to the pathogenesis of COVID-19. Twit Text FOAVip SARS-CoV-2 ORF9b antagonizes type I and III interferons by targeting multiple components of the RIG-I/MDA-5-MAVS, TLR3-TRIF, and cGAS-STING signaling pathways ????J Med Virol http://www.kidney.de/pget.php?&tw=1&pmid=33913550 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33913550 #FOAvip English Wikipedia <ref>{{Cite pmid|33913550}}</ref> SARS-CoV-2 ORF9b antagonizes type I and III interferons by targeting multiple components of the RIG-I/MDA-5-MAVS, TLR3-TRIF, and cGAS-STING signaling pathways #MMPMID33913550 Han L; Zhuang MW; Deng J; Zheng Y; Zhang J; Nan ML; Zhang XJ; Gao C; Wang PH J Med Virol 2021[Sep]; 93 (9): 5376-5389 PMID33913550show ga The suppression of types I and III interferon (IFN) responses by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contributes to the pathogenesis of coronavirus disease 2019 (COVID-19). The strategy used by SARS-CoV-2 to evade antiviral immunity needs further investigation. Here, we reported that SARS-CoV-2 ORF9b inhibited types I and III IFN production by targeting multiple molecules of innate antiviral signaling pathways. SARS-CoV-2 ORF9b impaired the induction of types I and III IFNs by Sendai virus and poly (I:C). SARS-CoV-2 ORF9b inhibited the activation of types I and III IFNs induced by the components of cytosolic dsRNA-sensing pathways of RIG-I/MDA5-MAVS signaling, including RIG-I, MDA-5, MAVS, TBK1, and IKKepsilon, rather than IRF3-5D, which is the active form of IRF3. SARS-CoV-2 ORF9b also suppressed the induction of types I and III IFNs by TRIF and STING, which are the adaptor protein of the endosome RNA-sensing pathway of TLR3-TRIF signaling and the adaptor protein of the cytosolic DNA-sensing pathway of cGAS-STING signaling, respectively. A mechanistic analysis revealed that the SARS-CoV-2 ORF9b protein interacted with RIG-I, MDA-5, MAVS, TRIF, STING, and TBK1 and impeded the phosphorylation and nuclear translocation of IRF3. In addition, SARS-CoV-2 ORF9b facilitated the replication of the vesicular stomatitis virus. Therefore, the results showed that SARS-CoV-2 ORF9b negatively regulates antiviral immunity and thus facilitates viral replication. This study contributes to our understanding of the molecular mechanism through which SARS-CoV-2 impairs antiviral immunity and provides an essential clue to the pathogenesis of COVID-19. |Adaptor Proteins, Signal Transducing/genetics/immunology[MESH] |Adaptor Proteins, Vesicular Transport/genetics/immunology[MESH] |Animals[MESH] |Chlorocebus aethiops[MESH] |Coronavirus Nucleocapsid Proteins/genetics/immunology[MESH] |DEAD Box Protein 58/genetics/*immunology[MESH] |Gene Expression Regulation[MESH] |HEK293 Cells[MESH] |HeLa Cells[MESH] |Humans[MESH] |I-kappa B Kinase/genetics/immunology[MESH] |Immune Evasion/*genetics[MESH] |Immunity, Innate[MESH] |Interferon Regulatory Factor-3/genetics/immunology[MESH] |Interferon-Induced Helicase, IFIH1/genetics/immunology[MESH] |Interferons/genetics/*immunology[MESH] |Membrane Proteins/genetics/immunology[MESH] |Nucleotidyltransferases/genetics/*immunology[MESH] |Phosphoproteins/genetics/immunology[MESH] |Plasmids/chemistry/metabolism[MESH] |Protein Serine-Threonine Kinases/genetics/immunology[MESH] |Receptors, Immunologic/genetics/*immunology[MESH] |SARS-CoV-2/genetics/*immunology/pathogenicity[MESH] |Signal Transduction/genetics/immunology[MESH] |Toll-Like Receptor 3/genetics/*immunology[MESH] |Transfection[MESH] |Vero Cells[MESH]SARS-CoV-2 ORF9b antagonizes type I and III interferons by targeting m(epmc).pdf DeepDyve Pubget Overpricing