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Pseudorabies virus tegument protein US2 antagonizes antiviral innate immunity by targeting cGAS-STING signaling pathway

文献类型： 外文期刊

作者： Kong, Zhengjie 1 ; Chen, Xing 2 ; Gong, Lele 2 ; Wang, Lele 2 ; Zhang, Yifeng 1 ; Guan, Kaifeng 1 ; Yao, Wanzi 1 ; Kang, Yu 1 ; Lu, Xinyi 1 ; Zhang, Yuhang 2 ; Du, Yongkun 2 ; Sun, Aijun 2 ; Zhuang, Guoqing 2 ; Zhao, Jianguo 3 ; Wan, Bo 2 ; Zhang, Gaiping 1 ;

作者机构： 1.Peking Univ, Sch Adv Agr Sci, Beijing, Peoples R China

2.Henan Acad Agr Sci, Key Lab Anim Immunol, Zhengzhou, Peoples R China

3.Chinese Acad Sci, State Key Lab Stem Cell & Reprod Biol, Inst Zool, Beijing, Peoples R China

4.Henan Agr Univ, Coll Vet Med, Int Joint Res Ctr Natl Anim Immunol, Zhengzhou, Peoples R China

5.Zhengzhou Univ, Henan Agr Univ, Longhu Lab, Zhengzhou, Peoples R China

关键词： pseudorabies virus; cGAS-STING; tegument protein US2; TRIM21; immune invasion

期刊名称：FRONTIERS IN IMMUNOLOGY （ 影响因子：5.7； 五年影响因子：6.8 ）

ISSN： 1664-3224

年卷期： 2024 年 15 卷

页码：

收录情况： SCI

摘要： Background The cGAS-STING axis-mediated type I interferon pathway is a crucial strategy for host defense against DNA virus infection. Numerous evasion strategies developed by the pseudorabies virus (PRV) counteract host antiviral immunity. To what extent PRV-encoded proteins evade the cGAS-STING signaling pathway is unknown.Methods Using US2 stably expressing cell lines and US2-deficient PRV model, we revealed that the PRV tegument protein US2 reduces STING protein stability and downregulates STING-mediated antiviral signaling.Results To promote K48-linked ubiquitination and STING degradation, US2 interacts with the LBD structural domain of STING and recruits the E3 ligase TRIM21. TRIM21 deficiency consistently strengthens the host antiviral immune response brought on by PRV infection. Additionally, US2-deficient PRV is less harmful in mice.Conclusions Our study implies that PRV US2 inhibits IFN signaling by a new mechanism that selectively targets STING while successfully evading the host antiviral response. As a result, the present study reveals a novel strategy by which PRV evades host defense and offers explanations for why the Bartha-K61 classical vaccine strain failed to offer effective defense against PRV variant strains in China, indicating that US2 may be a key target for developing gene-deficient PRV vaccines.

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