Popis: |
Highlights • SADS-CoV failed to induce IFN-β expression and inhibited poly (I:C)-or SEV-mediated IFN-β production in IPEC-J2 cells. • SADS-CoV interrupted poly (I:C)-induced phosphorylation and nuclear translocation of IRF3 and NF-κB. • SADS-CoV failed to block IRF3, TBK1 and IKKε activity. • SADS-CoV impeded IFN-β induction mediated by IPS-1 and RIG-I. 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-β production, and inhibited poly (I:C) and Sendai virus (SeV)-triggered IFN-β expression. SADS-CoV also blocked poly (I:C)-induced phosphorylation and nuclear translocation of IRF-3 and NF-κB. Furthermore, SADS-CoV did not interfere with the activity of IFN-β promoter stimulated by IRF3, TBK1 and IKKε, 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. |