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Seneca Valley virus infection exploits DNA damage response to facilitate viral replication

文献类型： 外文期刊

作者： Song, Jiangwei 1 ; Li, Zijian 2 ; Yang, Jingjing 2 ; Ma, Ruiyi 1 ; Wang, Dan 1 ; Quan, Rong 1 ; Wen, Xuexia 2 ; Liu, Jue 3 ;

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.Shenyang Agr Univ, Coll Anim Sci & Vet Med, Shenyang, Peoples R China

3.Yangzhou Univ, Coll Vet Med, Yangzhou, Peoples R China

关键词： Seneca Valley virus (SVV); DNA damage response (DDR); DNA repair; DNA double-strand break (DSB); viral replication

期刊名称：JOURNAL OF VIROLOGY （ 影响因子：3.8； 五年影响因子：3.9 ）

ISSN： 0022-538X

年卷期： 2025 年 99 卷 3 期

页码：

收录情况： SCI

摘要： Seneca Valley virus (SVV) is an emerging pathogen that causes severe vesicular diseases in swine, posing a significant threat to the global pork industry. DNA and RNA viruses manipulate the host DNA damage response (DDR) to modulate cellular machinery and facilitate their life cycles. However, the interaction between the host DDR and SVV infection remains unexplored. Here, we aimed to comprehensively investigate the DDR and DNA repair signaling pathways during SVV infection. We found that SVV infection causes DNA damage and triggers distinct DDR signaling pathways, including ataxia telangiectasia-mutated (ATM) kinase, ATM-Rad3-related kinase, and DNA-dependent protein kinase. However, it failed to induce the formation of gamma H2AX and 53BP1 foci, resulting in unrepaired DNA damage. Furthermore, we found that SVV 2B and 2C proteins can activate DDR signaling pathways and impair DNA repair. SVV-induced DDR triggered NF-kappa B signaling accompanied by upregulation of pro-inflammatory cytokines, as evidenced by the inhibition of ATM kinase, abolished SVV-induced NF-kappa B activation. Inhibition of the ATM pathway attenuated SVV replication. These findings expand our understanding of host DDR manipulation during viral infection and provide crucial insights into a novel mechanism exploited by SVV to regulate the inflammatory response for efficient replication.

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