College of Veterinary Medicine, Sichuan Agricultural University, Cheng Du, China.
Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Cheng Du, China.
Front Immunol. 2022 Aug 15;13:963923. doi: 10.3389/fimmu.2022.963923. eCollection 2022.
IFN is the most potent antiviral cytokine required for the innate and adaptive immune responses, and its expression can help the host defend against viral infection. Arteriviruses have evolved strategies to antagonize the host cell's innate immune responses, interfering with IFN expression by interfering with RIG, blocking PRR, obstructing IRF-3/7, NF-κB, and degrading STAT1 signaling pathways, thereby assisting viral immune evasion. Arteriviruses infect immune cells and may result in persistence in infected hosts. In this article, we reviewed the strategies used by Arteriviruses to antagonize IFN production and thwart IFN-activated antiviral signaling, mainly including structural and nonstructural proteins of Arteriviruses encoding IFN antagonists directly or indirectly to disrupt innate immunity. This review will certainly provide a better insight into the pathogenesis of the arthritis virus and provide a theoretical basis for developing more efficient vaccines.
IFN 是先天和适应性免疫反应所必需的最有效的抗病毒细胞因子，其表达可以帮助宿主抵抗病毒感染。动脉炎病毒已经进化出了拮抗宿主细胞先天免疫反应的策略，通过干扰 RIG、阻断 PRR、阻碍 IRF-3/7、NF-κB 和降解 STAT1 信号通路来干扰 IFN 的表达，从而协助病毒免疫逃逸。动脉炎病毒感染免疫细胞，并可能导致受感染宿主的持续感染。在本文中，我们综述了动脉炎病毒拮抗 IFN 产生和阻断 IFN 激活的抗病毒信号的策略，主要包括动脉炎病毒编码 IFN 拮抗剂的结构蛋白和非结构蛋白，它们直接或间接地破坏先天免疫。本综述必将深入了解关节炎病毒的发病机制，并为开发更有效的疫苗提供理论依据。
