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Enhancing MyD88 oligomerization is one important mechanism by which IBDV VP2 induces inflammatory response

文献类型： 外文期刊

作者： Huang, Mengmeng;Xu, Mengmeng;Han, Jingzhe;Ke, Erjing;Niu, Xinxin;Zhang, Yulong;Wang, Guodong;Yu, Hangbo;Liu, Runhang;Wang, Suyan;Liu, Yongzhen;Chen, Yuntong;Han, Jinze;Wu, Ziwen;Cui, Hongyu;Zhang, Yanping;Duan, Yulu;Gao, Yulong;Qi, Xiaole

作者机构：

期刊名称： PLOS PATHOGENS

ISSN： 1553-7366

年卷期： 2025 年 21 卷 3 期

页码：

收录情况： SCIE（2025版）

摘要： The inflammatory response is an essential component of innate immunity to defense against pathogens. Infectious bursal disease (IBD) is the most important immunosuppressive disease in chickens and is caused by the infectious bursal disease virus (IBDV). Acute inflammation is a typical pathogenic process for IBD, however, the underlying mechanism is not clear. Here, we report that IBDV induces obvious inflammatory response in vivo and in vitro. Furthermore, viral VP2 is identified as an important inflammatory stimulus. It is observed that IBDV VP2 can activate NF-kappa B signaling pathway and then increase IL-1 beta production. In detail, IBDV VP2 interacts with myeloid differentiation primary response gene 88 (MyD88), potentiates the oligomerization of MyD88 and assembly of MyD88 complex, which is one important element leading to NF-kappa B signaling pathway activation and IL-1 beta production increase. More meaningfully, residues 253/284 of viral VP2 are significantly involved in IBDV-induced inflammatory response through modulating the interaction strength between VP2 and MyD88 and the following MyD88-NF-kappa B-IL-1 beta signaling pathway. This study reveals one molecular mechanism that trigger inflammation during IBDV infection, which is of great significance for a deeper understanding of the pathogenic mechanisms of IBDV.

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