Swine acute diarrhea syndrome coronavirus nucleocapsid protein antagonizes the IFN response through inhibiting TRIM25 oligomerization and functional activation of RIG-I/TRIM25

文献类型： 外文期刊

第一作者： Zhang, Jiyu

作者： Zhang, Jiyu;Shi, Hongyan;Zhang, Liaoyuan;Feng, Tingshuai;Chen, Jianfei;Zhang, Xin;Ji, Zhaoyang;Jing, Zhaoyang;Zhu, Xiaoyuan;Liu, Dakai;Yang, Xiaoman;Zeng, Miaomiao;Shi, Da;Feng, Li

作者机构：

关键词： Swine acute diarrhea syndrome coronavirus; nucleocapsid; interferon; RIG-I; TRIM25

期刊名称：VETERINARY RESEARCH （ 影响因子：3.5； 五年影响因子：4.0 ）

ISSN： 0928-4249

年卷期： 2024 年 55 卷 1 期

页码：

收录情况： SCI

摘要： Swine acute diarrhea syndrome coronavirus (SADS-CoV), an emerging Alpha-coronavirus, brings huge economic loss in swine industry. Interferons (IFNs) participate in a frontline antiviral defense mechanism triggering the activation of numerous downstream antiviral genes. Here, we demonstrated that TRIM25 overexpression significantly inhibited SADS-CoV replication, whereas TRIM25 deficiency markedly increased viral yield. We found that SADS-CoV N protein suppressed interferon-beta (IFN-beta) production induced by Sendai virus (SeV) or poly(I:C). Moreover, we determined that SADS-CoV N protein interacted with RIG-I N-terminal two caspase activation and recruitment domains (2CARDs) and TRIM25 coiled-coil dimerization (CCD) domain. The interaction of SADS-CoV N protein with RIG-I and TRIM25 caused TRIM25 multimerization inhibition, the RIG-I-TRIM25 interaction disruption, and consequent the IRF3 and TBK1 phosphorylation impediment. Overexpression of SADS-CoV N protein facilitated the replication of VSV-GFP by suppressing IFN-beta production. Our results demonstrate that SADS-CoV N suppresses the host IFN response, thus highlighting the significant involvement of TRIM25 in regulating antiviral immune defenses.

分类号：

  • 相关文献
作者其他论文 更多>>

微信小程序