Porcine reproductive and respiratory syndrome virus degrades TANK-binding kinase 1 via chaperon-mediated autophagy to suppress type I interferon production and facilitate viral proliferation
文献类型： 外文期刊
作者： Zhao, Shuang-shuang 1 ; Qian, Qisheng 3 ; Wang, Yao 3 ; Qiao, Songlin 3 ; Li, Rui 3 ;
作者机构： 1.Zhejiang A&F Univ, Key Lab Appl Technol Green Eco Healthy Anim Husb Z, Zhejiang Prov Engn Lab Anim Hlth Inspect & Interne, Zhejiang Int Sci & Technol Cooperat Base Vet Med &, Hangzhou 311300, Zhejiang, Peoples R China
2.Zhejiang A&F Univ, Coll Vet Med, Hangzhou 311300, Zhejiang, Peoples R China
3.Henan Acad Agr Sci, Inst Anim Hlth, Key Lab Anim Immunol, Zhengzhou 450002, Henan, Peoples R China
关键词： PRRSV; Nsp2; TBK1; IFN-I; CMA
期刊名称：VETERINARY RESEARCH （ 影响因子：3.5； 五年影响因子：4.0 ）
ISSN： 0928-4249
年卷期： 2024 年 55 卷 1 期
页码：
收录情况： SCI
摘要： Porcine reproductive and respiratory syndrome virus (PRRSV) has led to significant economic losses in the global swine industry. Type I interferon (IFN-I) plays a crucial role in the host's resistance to PRRSV infection. Despite extensive research showing that PRRSV employs multiple strategies to antagonise IFN-I induction, the underlying mechanisms remain to be fully elucidated. In this study, we have discovered that PRRSV inhibits the production of IFN-I by degrading TANK-binding kinase 1 (TBK1) through chaperon-mediated autophagy (CMA). From a mechanistic standpoint, PRRSV nonstructural protein 2 (Nsp2) increases the interaction between the heat shock protein member 8 (HSPA8) and TBK1. This interaction leads to the translocation of TBK1 into lysosomes for degradation, mediated by lysosomal-associated membrane protein 2A (LAMP2A). As a result, the downstream activation of IFN regulatory factor 3 (IRF3) and the production of IFN-I are hindered. Together, these results reveal a new mechanism by which PRRSV suppresses host innate immunity and contribute to the development of new antiviral strategies against the virus.
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