Immune evasion strategies of Seneca Valley virus: mechanisms of host innate immune suppression

Shijie Xie , Jingyu Yan , Bo Jiang , Jue Liu , Jiangwei Song
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引用次数: 0

Abstract

Seneca Valley virus (SVV), an emerging picornavirus, poses a significant threat to the global swine industry. Innate immunity acts as the initial defense mechanism of host cells against viral infection. Upon infection, viruses can be detected by the cellular host's pattern recognition receptors (PRRs), which trigger the activation of signaling cascades and the strong production of type I interferon (IFN-I) to limit viral replication. SVV employs diverse strategies to evade innate immunity, primarily through 3C protease, which targets host antiviral proteins to antagonize IFN-I signaling. Additionally, SVV hijacks autophagy, apoptosis, and pyroptosis to facilitate its own replication. In this review, we summarize recent research on the underlying mechanisms employed by SVV to manipulate host innate immune response and programmed cell death pathways. This review will provide insights for the design of SVV vaccines and contribute to the prevention and control of SVV infection.
塞内卡谷病毒的免疫逃避策略:宿主先天免疫抑制机制
塞内卡谷病毒(SVV)是一种新兴的小核糖核酸病毒,对全球养猪业构成重大威胁。先天免疫是宿主细胞抵御病毒感染的初始防御机制。感染后,病毒可被细胞宿主的模式识别受体(PRRs)检测到,从而触发信号级联反应的激活和I型干扰素(IFN-I)的强烈产生,以限制病毒的复制。SVV采用多种策略逃避先天免疫,主要通过3C蛋白酶,其靶向宿主抗病毒蛋白拮抗IFN-I信号。此外,SVV劫持自噬、凋亡和焦亡以促进自身复制。在这篇综述中,我们总结了SVV操纵宿主先天免疫反应和程序性细胞死亡途径的潜在机制的最新研究。这一综述将为SVV疫苗的设计提供新的思路,并有助于SVV感染的预防和控制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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