Swine acute diarrhea syndrome coronavirus (SADS-CoV), first discovered in 2017, is a porcine enteric coronavirus that can cause acute diarrhea syndrome (SADS) in piglets. Here, we studied the role of SADS-CoV nucleocapsid (N) protein in innate immunity. Our results showed that SADS-CoV N protein could inhibit type I interferon (IFN) production mediated by Sendai virus (Sev) and could block the phosphorylation and nuclear translocation of interferon regulatory factor 3 (IRF3). Simultaneously, the IFN- β promoter activity mediated by TANK binding kinase 1 (TBK1) or its upstream molecules in the RLRs signal pathway was inhibited by SADS-CoV N protein. Further investigations revealed that SADS-CoV N protein could counteract interaction between TNF receptor-associated factor 3 (TRAF3) and TBK1, which led to reduced TBK1 activation and IFN- β production. Our study is the first report of the interaction between SADS-CoV N protein and the host antiviral innate immune responses, and the mechanism utilized by SADS-CoV N protein provides a new insight of coronaviruses evading host antiviral innate immunity.
【저자키워드】 nucleocapsid protein, TANK Binding Kinase 1, interferon beta, TRAF3, SADS-CoV, 【초록키워드】 coronavirus, Antiviral, Innate immunity, type I interferon, Protein, nucleocapsid, N protein, Phosphorylation, pathway, IRF3, IFN, mechanism, binding, TNF, Interaction, acute diarrhea, Activation, interferon regulatory factor, TBK1, nuclear translocation, syndrome, innate immune responses, promoter, upstream, Sendai virus, Host, TANK, inhibit, inhibited, reduced, provide, RLR, 【제목키워드】 Production, TBK1, blocking,