期刊
VIRUS GENES
卷 42, 期 1, 页码 37-45出版社
SPRINGER
DOI: 10.1007/s11262-010-0544-x
关键词
SARS-CoV; Nucleocapsid protein; Poly(I:C); IFN-beta
资金
- China National Basic Research Program [2006CB504305, 2010CB911800]
- China National Natural Science Foundation [30925003, 30921001]
Severe acute respiratory syndrome coronavirus (SARS-CoV) encodes a highly basic nucleocapsid (N) protein which can inhibit the synthesis of type I interferon (IFN), but the molecular mechanism of this antagonism remains to be identified. In this study, we demonstrated that the N protein of SARS-CoV could inhibit IFN-beta (IFN-beta) induced by poly(I:C) or Sendai virus. However, we found that N protein could not inhibit IFN-beta production induced by overexpression of downstream signaling molecules of two important IFN-beta induction pathways, toll-like receptor 3 (TLR3)- and RIG-I-like receptors (RLR)-dependent pathways. These results indicate that SARS-CoV N protein targets the initial step, probably the cellular PRRs (pattern recognition receptors)-RNAs-recognition step in the innate immune pathways, to suppress IFN expression responses. In addition, co-immunoprecipitation assays revealed that N protein did not interact with RIG-I or MDA5. Further, an assay using truncated mutants revealed that the C-terminal domain of N protein was critical for its antagonism of IFN induction, and the N deletion mutant impaired for RNA-binding almost completely lost the IFN-beta antagonist activity. These results contribute to our further understanding of the pathogenesis of SARS-CoV.
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