Foot-and-Mouth Virus Capsid Protein VP1 Antagonizes Type I Interferon Signaling via Degradation of Histone Deacetylase 5

文献类型： 外文期刊

第一作者： Gong, Qing

作者： Gong, Qing;Ren, Shanhui;Dou, Yongxi;Tadele, Berihun Afera;Zhou, Luoyi;Wang, Tao;Yao, Kaishen;Xu, Jian;Yin, Xiangping;Sun, Yuefeng;Hu, Tao;Zhou, Luoyi;Wang, Tao

作者机构：

关键词： innate immune response; FMDV infection; VP1; HDAC5; IFN-beta

期刊名称：CELLS （ 影响因子：6.0； 五年影响因子：6.7 ）

ISSN：

年卷期： 2024 年 13 卷 6 期

页码：

收录情况： SCI

摘要： Foot-and-mouth disease (FMD) is a highly contagious and economically important disease of cloven-hoofed animals that hampers trade and production. To ensure effective infection, the foot-and-mouth disease virus (FMDV) evades host antiviral pathways in different ways. Although the effect of histone deacetylase 5 (HDAC5) on the innate immune response has previously been documented, the precise molecular mechanism underlying HDAC5-mediated FMDV infection is not yet clearly understood. In this study, we found that silencing or knockout of HDAC5 promoted FMDV replication, whereas HDAC5 overexpression significantly inhibited FMDV propagation. IFN-beta and IFN-stimulated response element (ISRE) activity was strongly activated through the overexpression of HDAC5. The silencing and knockout of HDAC5 led to an increase in viral replication, which was evident by decreased IFN-beta, ISG15, and ISG56 production, as well as a noticeable reduction in IRF3 phosphorylation. Moreover, the results showed that the FMDV capsid protein VP1 targets HDAC5 and facilitates its degradation via the proteasomal pathway. In conclusion, this study highlights that HDAC5 acts as a positive modulator of IFN-beta production during viral infection, while FMDV capsid protein VP1 antagonizes the HDAC5-mediated antiviral immune response by degrading HDAC5 to facilitate viral replication.

分类号：

  • 相关文献
作者其他论文 更多>>

微信小程序