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Consistently, G-NSs thus inhibited phosphorylation/activation and nuclear translocation of IFN-regulatory factor 3 (IRF3, the substrate of TBK1), diminishing the IFN induction. Furthermore, G-NSs sequestration of STAT2 blocked phosphorylation/activation and nuclear translocation of STAT2, disabling IFN action and host antiviral state establishment. Collectively, this study shows the robust subversion of the two phases of the IFN antiviral system by GTV and unravels the respective molecular mechanisms, exhibiting some notable difference