Seneca Valley Virus 3C(pro) Cleaves Heterogeneous Nuclear Ribonucleoprotein K to Facilitate Viral Replication
文献类型: 外文期刊
作者: Song, Jiangwei 1 ; Quan, Rong 1 ; Wang, Dan 1 ; Liu, Jue 2 ;
作者机构: 1.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing Key Lab Prevent & Control Infect Dis Lives, Beijing, Peoples R China
2.Yangzhou Univ, Coll Vet Med, Yangzhou, Peoples R China
3.Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou, Peoples R China
关键词: seneca valley virus; heterogeneous nuclear ribonucleoprotein K; viral replication; host protein regulation; viral 3C protease
期刊名称:FRONTIERS IN MICROBIOLOGY ( 影响因子:6.064; 五年影响因子:6.843 )
ISSN:
年卷期: 2022 年 13 卷
页码:
收录情况: SCI
摘要: Seneca Valley virus (SVV) has emerged as an important pathogen that is associated with idiopathic vesicular infection in pigs, causing a potential threat to the global swine industry. The heterogeneous nuclear ribonucleoprotein K (hnRNP K) that shuttles between the nucleus and cytoplasm plays an important role in viral infection. In this study, we observed that infection with SVV induced cleavage, degradation, and cytoplasmic redistribution of hnRNP K in cultured cells, which was dependent on the activity of viral 3C(pro) protease. Also, the 3C(pro) induced degradation of hnRNP K via the caspase pathway. Further studies demonstrated that SVV 3C(pro) cleaved hnRNP K at residue Q364, and the expression of the cleavage fragment hnRNP K (aa.365-464) facilitates viral replication, which is similar to full-length hnRNP K, whereas hnRNP K (aa.1-364) inhibits viral replication. Additionally, hnRNP K interacts with the viral 5 ' untranslated region (UTR), and small interfering RNA (siRNA)-mediated knockdown of hnRNP K results in significant inhibition of SVV replication. Overall, our results demonstrated that the hnRNP K positively regulates SVV replication in a protease activity-dependent fashion in which the cleaved C-terminal contributes crucially to the upregulation of SVV replication. This finding of the role of hnRNP K in promoting SVV propagation provides a novel antiviral strategy to utilize hnRNP K as a potential target for therapy.
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