Foot-and-mouth disease virus structural protein VP3 interacts with HDAC8 and promotes its autophagic degradation to facilitate viral replication

文献类型： 外文期刊

第一作者： Zhang, Huijun

作者： Zhang, Huijun;Wang, Xiangwei;Qu, Min;Yin, Xiangping;Liu, Xiangtao;Sun, Yuefeng;Zhang, Huijun;Tang, Lijie;Li, Zhiyong;Sun, Yuefeng

作者机构：

关键词： Autophagy; FMDV; histone deacetylase 8; virus replication; innate immune response; >

期刊名称：AUTOPHAGY （ 影响因子：13.3； 五年影响因子：14.5 ）

ISSN： 1554-8627

年卷期： 2023 年

页码：

收录情况： SCI

摘要： Macroautophagy/autophagy has been utilized by many viruses, including foot-and-mouth disease virus (FMDV), to facilitate replication, while the underlying mechanism of the interplay between autophagy and innate immune responses is still elusive. This study showed that HDAC8 (histone deacetylase 8) inhibits FMDV replication by regulating innate immune signal transduction and antiviral response. To counteract the HDAC8 effect, FMDV utilizes autophagy to promote HDAC8 degradation. Further data showed that FMDV structural protein VP3 promotes autophagy during virus infection and interacts with and degrades HDAC8 in an AKT-MTOR-ATG5-dependent autophagy pathway. Our data demonstrated that FMDV evolved a strategy to counteract host antiviral activity by autophagic degradation of a protein that regulates innate immune response during virus infection.

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