2. Academic Validation
  3. Enhancing MyD88 oligomerization is one important mechanism by which IBDV VP2 induces inflammatory response

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

  • PLoS Pathog. 2025 Mar 11;21(3):e1012985. doi: 10.1371/journal.ppat.1012985.
Mengmeng Huang 1 2,  Mengmeng Xu 1 2 3,  Jingzhe Han 1 2 3,  Erjing Ke 1 2 3,  Xinxin Niu 1 2,  Yulong Zhang 1 2,  Guodong Wang 1 2,  Hangbo Yu 1 2,  Runhang Liu 1 2,  Suyan Wang 1 2 4,  Yongzhen Liu 1 2 4,  Yuntong Chen 1 2 4,  Jinze Han 1 2 3,  Ziwen Wu 1 2,  Hongyu Cui 1 2 4,  Yanping Zhang 1 2 4,  Yulu Duan 1 2 4,  Yulong Gao 1 2 4,  Xiaole Qi 1 2 4
Affiliations

Affiliations

  • 1 Avian Immunosuppressive Diseases Division, State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, the Chinese Academy of Agricultural Sciences, Harbin, China.
  • 2 World Organization for Animal Health (WOAH) Reference Laboratory for Infectious Bursal Disease, Harbin Veterinary Research Institute, the Chinese Academy of Agricultural Sciences, Harbin, China.
  • 3 Tianjin Key Laboratory of Agricultural Animal Breeding and Healthy Husbandry, College of Animal Science and Veterinary Medicine, Tianjin Agricultural University, Tianjin, China.
  • 4 Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Disease and Zoonosis, Yangzhou University, Yangzhou, China.
PMID: 40067802 DOI: 10.1371/journal.ppat.1012985
Abstract

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-κB signaling pathway and then increase IL-1β 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-κB signaling pathway activation and IL-1β 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-κB-IL-1β 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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