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10.1038/srep17554 http://scihub22266oqcxt.onion/10.1038/srep17554 C4668369!4668369 !26631542     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26631542 &cmd=llinks): Failed to open stream: HTTP request failed! 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Middle East respiratory syndrome coronavirus ORF4b protein inhibits type I interferon production through both cytoplasmic and nuclear targets |pdf=|usr=}}{{26631542 }} gab.com Text Middle East respiratory syndrome coronavirus ORF4b protein inhibits type I interferon production through both cytoplasmic and nuclear targets JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26631542 #FOAvip Middle East respiratory syndrome coronavirus (MERS-CoV) is a novel and highly pathogenic human coronavirus and has quickly spread to other countries in the Middle East, Europe, North Africa and Asia since 2012. Previous studies have shown that MERS-CoV ORF4b antagonizes the early antiviral alpha/beta interferon (IFN-?/?) response, which may significantly contribute to MERS-CoV pathogenesis; however, the underlying mechanism is poorly understood. Here, we found that ORF4b in the cytoplasm could specifically bind to TANK binding kinase 1 (TBK1) and I?B kinase epsilon (IKK?), suppress the molecular interaction between mitochondrial antiviral signaling protein (MAVS) and IKK?, and inhibit IFN regulatory factor 3 (IRF3) phosphorylation and subsequent IFN-? production. Further analysis showed that ORF4b could also inhibit IRF3 and IRF7-induced production of IFN-?, whereas deletion of the nuclear localization signal of ORF4b abrogated its ability to inhibit IRF3 and IRF7-induced production of IFN-?, but not IFN-? production induced by RIG-I, MDA5, MAVS, IKK?, and TBK-1, suggesting that ORF4b could inhibit the induction of IFN-? in both the cytoplasm and nucleus. Collectively, these results indicate that MERS-CoV ORF4b inhibits the induction of type I IFN through a direct interaction with IKK?/TBK1 in the cytoplasm, and also in the nucleus with unknown mechanism. Viruses have evolved multiple strategies to evade or thwart a host's antiviral responses. A novel human coronavirus (HCoV), Middle East respiratory syndrome coronavirus (MERS-CoV), is distinguished from other coronaviruses by its high pathogenicity and mortality. However, virulence determinants that distinguish MERS-CoV from other HCoVs have yet to be identified. MERS-CoV ORF4b antagonizes the early antiviral response, which may contribute to MERS-CoV pathogenesis. Here, we report the identification of the interferon (IFN) antagonism mechanism of MERS-CoV ORF4b. MERS-CoV ORF4b inhibits the production of type I IFN through a direct interaction with IKK?/TBK1 in the cytoplasm, and also in the nucleus with unknown mechanism. These findings provide a rationale for the novel pathogenesis of MERS-CoV as well as a basis for developing a candidate therapeutic against this virus. Twit Text FOAVip Middle East respiratory syndrome coronavirus ORF4b protein inhibits type I interferon production through both cytoplasmic and nuclear targets ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26631542 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26631542 #FOAvip English Wikipedia <ref>{{Cite pmid|26631542 }}</ref> Middle East respiratory syndrome coronavirus ORF4b protein inhibits type I interferon production through both cytoplasmic and nuclear targets #MMPMID26631542 Yang Y ; Ye F ; Zhu N ; Wang W ; Deng Y ; Zhao Z ; Tan W Sci Rep 2015[Dec]; 5 (ä): 17554 PMID26631542 show ga Middle East respiratory syndrome coronavirus (MERS-CoV) is a novel and highly pathogenic human coronavirus and has quickly spread to other countries in the Middle East, Europe, North Africa and Asia since 2012. Previous studies have shown that MERS-CoV ORF4b antagonizes the early antiviral alpha/beta interferon (IFN-?/?) response, which may significantly contribute to MERS-CoV pathogenesis; however, the underlying mechanism is poorly understood. Here, we found that ORF4b in the cytoplasm could specifically bind to TANK binding kinase 1 (TBK1) and I?B kinase epsilon (IKK?), suppress the molecular interaction between mitochondrial antiviral signaling protein (MAVS) and IKK?, and inhibit IFN regulatory factor 3 (IRF3) phosphorylation and subsequent IFN-? production. Further analysis showed that ORF4b could also inhibit IRF3 and IRF7-induced production of IFN-?, whereas deletion of the nuclear localization signal of ORF4b abrogated its ability to inhibit IRF3 and IRF7-induced production of IFN-?, but not IFN-? production induced by RIG-I, MDA5, MAVS, IKK?, and TBK-1, suggesting that ORF4b could inhibit the induction of IFN-? in both the cytoplasm and nucleus. Collectively, these results indicate that MERS-CoV ORF4b inhibits the induction of type I IFN through a direct interaction with IKK?/TBK1 in the cytoplasm, and also in the nucleus with unknown mechanism. Viruses have evolved multiple strategies to evade or thwart a host's antiviral responses. A novel human coronavirus (HCoV), Middle East respiratory syndrome coronavirus (MERS-CoV), is distinguished from other coronaviruses by its high pathogenicity and mortality. However, virulence determinants that distinguish MERS-CoV from other HCoVs have yet to be identified. MERS-CoV ORF4b antagonizes the early antiviral response, which may contribute to MERS-CoV pathogenesis. Here, we report the identification of the interferon (IFN) antagonism mechanism of MERS-CoV ORF4b. MERS-CoV ORF4b inhibits the production of type I IFN through a direct interaction with IKK?/TBK1 in the cytoplasm, and also in the nucleus with unknown mechanism. These findings provide a rationale for the novel pathogenesis of MERS-CoV as well as a basis for developing a candidate therapeutic against this virus. |Adaptor Proteins, Signal Transducing/metabolism [MESH] |Cell Nucleus/metabolism/*virology [MESH] |Cytoplasm/metabolism/*virology [MESH] |DEAD Box Protein 58/genetics/metabolism [MESH] |HeLa Cells/virology [MESH] |Host-Pathogen Interactions [MESH] |Humans [MESH] |I-kappa B Kinase/metabolism [MESH] |Interferon Regulatory Factor-3/genetics/metabolism [MESH] |Interferon Regulatory Factor-7/metabolism [MESH] |Interferon-Induced Helicase, IFIH1/genetics/metabolism [MESH] |Interferon-beta/genetics/*metabolism [MESH] |Middle East Respiratory Syndrome Coronavirus/*pathogenicity [MESH] |Phosphorylation [MESH] |Protein Serine-Threonine Kinases/metabolism [MESH] |Receptors, Immunologic [MESH]Middle East respiratory syndrome coronavirus ORF4b protein inhibits ty(epmc).pdf DeepDyve Pubget Overpricing