African Swine Fever Virus MGF360-14L Negatively Regulates Type I Interferon Signaling by Targeting IRF3

被引：41
|
作者：
Wang, Yang [1 ]
Cui, Shuai [1 ]
Xin, Ting [1 ]
Wang, Xixi [2 ]
Yu, Hainan [1 ]
Chen, Shiyu [1 ]
Jiang, Yajun [1 ]
Gao, Xintao [3 ]
Jiang, Yitong [1 ]
Guo, Xiaoyu [1 ]
Jia, Hong [1 ]
Zhu, Hongfei [1 ]
机构：
[1] Chinese Acad Agr Sci, Inst Anim Sci, Beijing, Peoples R China
[2] Chinese Acad Sci, Inst Microbiol, Beijing, Peoples R China
[3] Chinese Acad Agr Sci CAAS, Biotechnol Res Inst, Beijing, Peoples R China
来源：
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY | 2022年 / 11卷
关键词：
African swine fever virus; interferon; IRF3; ubiquitination; immune evasion; UTILITY;
D O I：
10.3389/fcimb.2021.818969
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
African swine fever (ASF) is a devastating infectious disease caused by African swine fever virus (ASFV). The ASFV genome encodes multiple structural and non-structural proteins that contribute to evasion of host immunity. In this study, we determined that the viral non-structural protein MGF360-14L inhibits interferon-beta (IFN-beta) promoter activity induced by cGAS-STING signaling. MGF360-14L was also found to downregulate expression of the IRF3 protein and promote its degradation through ubiquitin-meditated proteolysis. Moreover, MGF360-14L was shown to interact with and destabilize IRF3 by facilitating E3 ligase TRIM21-mediated K63-linked ubiquitination of IRF3. Overall, our study revealed that MGF360-14L promotes degradation of IRF3 through TRIM21, thereby inhibiting type I interferon production. These findings provide new insights into the mechanisms underlying ASFV immune evasion.
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页数：9
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