中国兽医科学2025，Vol.55Issue(10)：1310-1318,9.DOI:10.16656/j.issn.1673-4696.2025.0177
塞内卡病毒VP3蛋白诱导宿主细胞翻译阻滞的机制研究
Mechanistic study on host cell translation arrest induced by Senecavirus A VP3 protein
摘要
Abstract
To elucidate the regulatory mechanism of Senecavirus A(SVA)VP3 protein on the host cel-lular translation system,this study initially employed laser confocal immunofluorescence and Wes-tern-blot analysis to confirm that exogenous expression of SVA VP3 induced host cellular translation arrest.Further investigations utilizing luciferase reporter assays,quantitative real-time PCR(qRT-PCR),and Western-blot revealed that SVA VP3-mediated host translation arrest was independent of intracellular protein degradation pathways and transcriptional regulation.Instead,SVA VP3 not only triggers phosphorylation of eIF2α but also suppresses mTOR-S6K signaling pathway activation,eIF4E phosphorylation,and eIF4F complex assembly,thereby severely impairing host cellular protein synthe-sis.Furthermore,proteomics analysis indicated that SVA VP3 played a pivotal role in viral hijacking of host translational machinery to facilitate viral proliferation.Collectively,this study elucidated the underlying mechanisms by which SVA VP3 protein induced host translational arrest,providing novel insights into understanding SVA translational regulation and pathogenesis of infection.关键词
塞内卡病毒/VP3/翻译阻滞/eIF2α磷酸化/mTOR-S6K信号通路Key words
Senecavirus A/VP3/translational arrest/eIF2α phosphorylation/mTOR-S6K signaling path-way分类
农业科技引用本文复制引用
邓小双,李鑫威,万浩成,周梦菡,胡曼,张雨杭,万博,韩世充..塞内卡病毒VP3蛋白诱导宿主细胞翻译阻滞的机制研究[J].中国兽医科学,2025,55(10):1310-1318,9.基金项目
国家自然科学基金面上项目(32373005) （32373005）
河南省优秀青年科学基金项目(252300421156) （252300421156）
