The Seneca Valley virus 3C protease cleaves DCP1A to attenuate its antiviral effects

文献类型： 外文期刊

第一作者： Yang, Jingjing

作者： Yang, Jingjing;Li, Zijian;Wen, Xuexia;Yang, Jingjing;Li, Zijian;Wen, Xuexia;Ma, Ruiyi;Xie, Shijie;Wang, Dan;Quan, Rong;Song, Jiangwei

作者机构：

关键词： Seneca Valley virus (SVV); DCP1A; 3C protease; 3D; cleavage

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： 2025 年 56 卷 1 期

页码：

收录情况： SCI

摘要： Seneca Valley virus (SVV), a new member of Picornaviridae, causes idiopathic vesicular symptoms in pregnant sows and acute death in neonatal piglets, considerably damaging the swine industry. The viral protease 3C (3Cpro) cleaves host immune-related molecules to create a favorable environment for viral replication. In this study, we found that mRNA decapping enzyme 1A (DCP1A) is a novel antiviral effector against SVV infection that targets 3D viral RNA-dependent RNA polymerase for OPTN-mediated autophagic degradation. To counteract this effect, SVV 3Cpro targets DCP1A for cleavage at glutamine 343 (Q343), resulting in the cleaved products DCP1A (1-343) and DCP1A (344-580), which lose the ability to restrict SVV replication. In contrast, the 3C cleavage-resistant DCP1A-Q343A mutant exhibited stronger antiviral effects than the wild-type DCP1A. Additionally, the degradation of the viral 3D protein targeted by DCP1A was abolished after its cleavage by SVV 3Cpro. In conclusion, our study demonstrated that SVV 3Cpro is a pivotal ISG antagonist that cleaves DCP1A. These results offer novel insight into how viruses evade host immunity.

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