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10.1038/celldisc.2017.6 http://scihub22266oqcxt.onion/10.1038/celldisc.2017.6 C5359216!5359216 !28373913     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28373913 &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       Cell+Discov 2017 ; 3 (?): 17006 Nephropedia Template TP {{tp|p=28373913 |t=2017. Zika virus evades interferon-mediated antiviral response through the co-operation of multiple nonstructural proteins in vitro |pdf=|usr=}}{{28373913 }} gab.com Text Zika virus evades interferon-mediated antiviral response through the co-operation of multiple nonstructural proteins in vitro JO: Cell Discov http://www.kidney.de/pget.php?&tw=1&pmid=28373913 #FOAvip Type I interferon (IFN) serves as the first line of defense against invading pathogens. Inhibition of IFN-triggered signaling cascade by Zika virus (ZIKV) plays a critical role for ZIKV to evade antiviral responses from host cells. Here we demonstrate that ZIKV nonstructural proteins NS1, NS4B and NS2B3 inhibit the induction of IFN and downstream IFN-stimulated genes through diverse strategies. NS1 and NS4B of ZIKV inhibit IFN? signaling at TANK-binding kinase 1 level, whereas NS2B-NS3 of ZIKV impairs JAK-STAT signaling pathway by degrading Jak1 and reduces virus-induced apoptotic cell death. Furthermore, co-operation of NS1, NS4B and NS2B3 further enhances viral infection by blocking IFN-induced autophagic degradation of NS2B3. Hence, our study reveals a novel antagonistic system employing multiple ZIKV nonstructural proteins in restricting the innate antiviral responses. Twit Text FOAVip Zika virus evades interferon-mediated antiviral response through the co-operation of multiple nonstructural proteins in vitro ????Cell Discov http://www.kidney.de/pget.php?&tw=1&pmid=28373913 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28373913 #FOAvip English Wikipedia <ref>{{Cite pmid|28373913 }}</ref> Zika virus evades interferon-mediated antiviral response through the co-operation of multiple nonstructural proteins in vitro #MMPMID28373913 Wu Y ; Liu Q ; Zhou J ; Xie W ; Chen C ; Wang Z ; Yang H ; Cui J Cell Discov 2017[]; 3 (?): 17006 PMID28373913 show ga Type I interferon (IFN) serves as the first line of defense against invading pathogens. Inhibition of IFN-triggered signaling cascade by Zika virus (ZIKV) plays a critical role for ZIKV to evade antiviral responses from host cells. Here we demonstrate that ZIKV nonstructural proteins NS1, NS4B and NS2B3 inhibit the induction of IFN and downstream IFN-stimulated genes through diverse strategies. NS1 and NS4B of ZIKV inhibit IFN? signaling at TANK-binding kinase 1 level, whereas NS2B-NS3 of ZIKV impairs JAK-STAT signaling pathway by degrading Jak1 and reduces virus-induced apoptotic cell death. Furthermore, co-operation of NS1, NS4B and NS2B3 further enhances viral infection by blocking IFN-induced autophagic degradation of NS2B3. Hence, our study reveals a novel antagonistic system employing multiple ZIKV nonstructural proteins in restricting the innate antiviral responses. ?Zika virus evades interferon-mediated antiviral response through the c(epmc).pdf DeepDyve Pubget Overpricing