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| 论文摘要： | Although fish possess an effective interferon (IFN) system to defend against viral infection, grass carp reovirus (GCRV) still causes epidemic hemorrhagic disease and tremendous economic loss in grass carp. Therefore, it is necessary to investigate the immune escape strategies employed by GCRV. In this study, we show that the structural protein VP4 of GCRV (encoded by the S6 segment) significantly restricts IFN expression by degrading stimulator of IFN genes (STING) through the autophagy-lyso some-dependent pathway. First, overexpression of VP4 inhibited the expression of IFN induced by GCRV and polyinosinic-polycytidylic acid (poly I:C) at both the promoter and mRNA levels. Second, VP4 was found to associate with STING, and the N-terminal transmembrane domain is essential for this interaction. Additionally, VP4 dramatically blocked STING-induced IFN expression and weakened its antiviral capacity. Further mechanistic studies revealed that VP4 degrades STING via the autophagy-lysosome pathway in a dose-dependent manner. Interestingly, toll-interacting protein (TOLLIP), a selective autophagy receptor, was found to interact with VP4 and reduce VP4-mediated STING degradation after tollip knockdown. Finally, overexpression of VP4 facilitated GCRV proliferation, while its depletion had the opposite effect. These findings indicate that GCRV VP4 recruits TOLLIP to degrade STING and achieve immune escape. This enhances our comprehension of aquatic virus pathogenesis. |
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