SARS-CoV-2 nsp12 attenuates type I interferon production by inhibiting IRF3 nuclear translocation.
Wenjing Wang,Zhuo Zhou,Xia Xiao,Zhongqin Tian,Xiaojing Dong,Conghui Wang,Li Li,Lili Ren,Xiaobo Lei,Zichun Xiang,Jianwei Wang +10 more
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TLDR
Wang et al. as discussed by the authors reported that SARS-CoV-2 nsp12, the viral RNA-dependent RNA polymerase (RdRp), suppresses host antiviral responses.Abstract:
SARS-CoV-2 is the pathogenic agent of COVID-19, which has evolved into a global pandemic. Compared with some other respiratory RNA viruses, SARS-CoV-2 is a poor inducer of type I interferon (IFN). Here, we report that SARS-CoV-2 nsp12, the viral RNA-dependent RNA polymerase (RdRp), suppresses host antiviral responses. SARS-CoV-2 nsp12 attenuated Sendai virus (SeV)- or poly(I:C)-induced IFN-β promoter activation in a dose-dependent manner. It also inhibited IFN promoter activation triggered by RIG-I, MDA5, MAVS, and IRF3 overexpression. Nsp12 did not impair IRF3 phosphorylation but suppressed the nuclear translocation of IRF3. Mutational analyses suggested that this suppression was not dependent on the polymerase activity of nsp12. Given these findings, our study reveals that SARS-CoV-2 RdRp can antagonize host antiviral innate immunity and thus provides insights into viral pathogenesis.read more
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Mechanisms of Antiviral Immune Evasion of SARS-CoV-2
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SARS-CoV-2 Nsp5 Activates NF-κB Pathway by Upregulating SUMOylation of MAVS.
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TL;DR: Wang et al. as discussed by the authors found that SARS-CoV-2 Nsp5 can induce the expression of cytokines IL-1β, IL-6, TNF-α and IL-2 in Calu-3 and THP1 cells.
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