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10.1038/celldisc.2017.6

http://scihub22266oqcxt.onion/10.1038/celldisc.2017.6
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C5359216!5359216!28373913
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suck abstract from ncbi


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pmid28373913      Cell+Discov 2017 ; 3 (ä): 17006-
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  • 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 (ä): 17006- PMID28373913show 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.
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