Acta Veterinaria et Zootechnica Sinica ›› 2022, Vol. 53 ›› Issue (9): 3272-3278.doi: 10.11843/j.issn.0366-6964.2022.09.041

• RESEARCH NOTES • Previous Articles    

ASFV MGF360-14L Interacts with MAVS and Inhibit the Expression of Type Ⅰ Interferon

WANG Yang1, CUI Shuai1, XIN Ting1, WANG Xixi2, YU Hainan1, CHEN Shiyu1, JIANG Yajun1, GAO Xintao3, PANG Zhongbao1, JIANG Yitong1, GUO Xiaoyu1, JIA Hong1, ZHU Hongfei1*   

  1. 1. Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China;
    2. Institute of Microbiology, Chinese Academy of Sciences, Beijing 100080, China;
    3. Biotechnology Research Institute, Chinese Academy of Agricultural Sciences, Beijing 100081, China
  • Received:2022-01-10 Online:2022-09-23 Published:2022-09-23

Abstract: This study was conducted to investigate the inhibitory effect of the African swine fever virus (ASFV) MGF360-14L on type Ⅰ interferon (IFN) and its mechanism. The effects of MGF360-14L on MAVS-induced IFN-β promoter activity were detected by dual luciferase assay, and the interaction between MGF360-14L and MAVS was examined by co-immunoprecipitation and indirect immunofluorescence assays. The results showed that the viral non-structural protein MGF360-14L inhibited interferon β (IFN-β) promoter activity induced by MAVS signaling. MGF360-14L interacted with MAVS and inhibited the phosphorylation of TBK1 and IRF3 induced by MAVS and TRIM21. In addition, MGFF360-14L competed with TRIM21 to bind MAVS and inhibit the TRIM21-mediated ubiquitination of MAVS, thereby reducing IFN-β levels. In conclusion, MGF360-14L may inhibit TRIM21-mediated ubiquitination of MAVS by competitively binding MAVS, thus down-regulating the production of type Ⅰ interferon. These findings provide new insights into the mechanisms underlying ASFV immune evasion.

Key words: African swine fever virus, type Ⅰ interferon, MAVS, ubiquitination, immune evasion

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