SADS‐CoV nsp1 inhibits the IFN‐β production by preventing TBK1 phosphorylation and inducing CBP degradation

Author:

Xiang Yingjie1,Mou Chunxiao12,Shi Kaichuang3,Chen Xiang4,Meng Xia1,Bao Wenbin5,Chen Zhenhai124

Affiliation:

1. College of Veterinary Medicine Yangzhou University Yangzhou China

2. Joint International Research Laboratory of Agriculture and Agri‐Product Safety,The Ministry of Education of China Yangzhou University Yangzhou China

3. Guangxi Center for Animal Disease Control and Prevention Nanning Guangxi China

4. Jiangsu Co‐Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses Yangzhou University Yangzhou China

5. Key Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design of Jiangsu Province, College of Animal Science and Technology Yangzhou University Yangzhou China

Abstract

AbstractSwine acute diarrhea syndrome (SADS) is first reported in January 2017 in Southern China. It subsequently causes widespread outbreaks in multiple pig farms, leading to economic losses. Therefore, it is an urgent to understand the molecular mechanisms underlying the pathogenesis and immune evasion of Swine acute diarrhea syndrome coronavirus (SADS‐CoV). Our research discovered that SADS‐CoV inhibited the production of interferon‐β (IFN‐β) during viral infection. The nonstructural protein 1 (nsp1) prevented the phosphorylation of TBK1 by obstructing the interaction between TBK1 and Ub protein. Moreover, nsp1 induced the degradation of CREB‐binding protein (CBP) through the proteasome‐dependent pathway, thereby disrupting the IFN‐β enhancer and inhibiting IFN transcription. Finally, we identified nsp1‐Phe39 as the critical amino acid that downregulated IFN production. In conclusion, our findings described two mechanisms in nsp1 that inhibited IFN production and provided new insights into the evasion strategy adopted by SADS‐CoV to evade host antiviral immunity.

Publisher

Wiley

Subject

Infectious Diseases,Virology

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