文献类型： 外文期刊
作者： Li, Zijian 1 ; Yang, Jingjing 1 ; Ma, Ruiyi 1 ; Xie, Shijie 1 ; Wang, Dan 1 ; Quan, Rong 1 ; Wen, Xuexia 2 ; Liu, Jue 3 ; Song, Jiangwei 1 ;
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, Dept Prevent Vet Med, Shenyang, Peoples R China
3.Yangzhou Univ, Coll Vet Med, Dept Prevent Vet Med, Yangzhou, Jiangsu, Peoples R China
关键词： Seneca Valley virus (SVV); HDAC4; 3C protease; cleavage; type I interferon (IFN-I)
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 a newly identified pathogen that poses a notable threat to the global pig industry. SVV has evolved multiple strategies to evade host antiviral innate immune responses. However, the underlying molecular mechanisms have not yet been fully elucidated. Histone deacetylases (HDACs) have been shown to function as host antiviral innate immune factors. In this study, we examined the mechanisms underlying SVV evasion of host innate immunity and found that SVV infection induced degradation and cleavage of HDAC4. Ectopic expression of HDAC4 suppressed SVV replication, whereas siRNA-mediated knockdown of HDAC4 enhanced SVV replication. Further studies showed that the viral 3C protease (3C(pro)) degraded HDAC4 in a protease activity- and caspase pathway-dependent manner. In addition, 3C(pro) cleaved HDAC4 at Q599, which blocked its ability to limit viral replication. We also found that HDAC4 interacted with the SVV viral RNA-dependent RNA polymerase 3D and induced its proteasomal degradation. The cleaved HDAC4 products did not block SVV replication or induce 3D degradation and did not induce type I interferon (IFN) activation and expression of IFN-stimulated genes (ISGs). Collectively, these findings identified HDAC4 as an antiviral factor with effects against SVV infection and provided mechanistic insights into how SVV 3C(pro) antagonizes its function, which has implications for viral evasion of innate immunity.
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