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Swine acute diarrhea syndrome coronavirus (SADS-CoV) antagonizes interferon-beta production via blocking IPS-1 and RIG-I #MMPMID31884203
Zhou Z; Sun Y; Yan X; Tang X; Li Q; Tan Y; Lan T; Ma J
Virus Res 2020[Mar]; 278 (ä): 197843 PMID31884203show ga
Swine acute diarrhea syndrome coronavirus (SADS-CoV), a newly emerging enteric coronavirus, is considered to be associated with swine acute diarrhea syndrome (SADS) which has caused significantly economic losses to the porcine industry. Interactions between SADS-CoV and the host innate immune response is unclear yet. In this study, we used IPEC-J2 cells as a model to explore potential evasion strategies employed by SADS-CoV. Our results showed that SADS-CoV infection failed to induce IFN-beta production, and inhibited poly (I:C) and Sendai virus (SeV)-triggered IFN-beta expression. SADS-CoV also blocked poly (I:C)-induced phosphorylation and nuclear translocation of IRF-3 and NF-kappaB. Furthermore, SADS-CoV did not interfere with the activity of IFN-beta promoter stimulated by IRF3, TBK1 and IKKepsilon, but counteracted its activation induced by IPS-1 and RIG-I. Collectively, this study is the first investigation that shows interactions between SADS-CoV and the host innate immunity, which provides information of the molecular mechanisms underlying SASD-CoV infection.