2. Academic Validation
  3. miR-17195 promotes infectious bronchitis virus proliferation and macrophage-mediated inflammation via the PLCβ2-TAK1 axis

miR-17195 promotes infectious bronchitis virus proliferation and macrophage-mediated inflammation via the PLCβ2-TAK1 axis

  • Vet Microbiol. 2025 Dec 9:313:110834. doi: 10.1016/j.vetmic.2025.110834.
Zheng Wang 1,  Chi Liu 2,  Xuan Chen 1,  Jianlan Li 2,  Waner Li 2,  Zhaxi Duoji 2,  Qingcheng Yang 1,  Ting Xu 1,  Anyun Zhang 3,  Peng Ma 4,  Hongning Wang 5
Affiliations

Affiliations

  • 1 Animal Disease Prevention and Green Development Key Laboratory of Sichuan Province, College of Life Science, Sichuan University, Chengdu 610000, China.
  • 2 Department of Anatomy and Histology, School of Preclinical Medicine, Chengdu University, Chengdu 610000, China.
  • 3 Animal Disease Prevention and Green Development Key Laboratory of Sichuan Province, College of Life Science, Sichuan University, Chengdu 610000, China. Electronic address: [email protected].
  • 4 Key Laboratory of Cellular Physiology, Ministry of Education, College of Basic Medicine, Shanxi Medical University, Taiyuan 030001, China. Electronic address: [email protected].
  • 5 Animal Disease Prevention and Green Development Key Laboratory of Sichuan Province, College of Life Science, Sichuan University, Chengdu 610000, China. Electronic address: [email protected].
PMID: 41447967 DOI: 10.1016/j.vetmic.2025.110834
Abstract

Infectious Bronchitis virus (IBV) causes Infectious bronchitis (IB) is an acute, highly contagious disease primarily affecting chickens and Other avian species, characterized by respiratory and renal pathologies. MicroRNAs (miRNAs) play pivotal roles in virus-host interactions and regulate diverse physiological and pathological processes during viral Infection. Here, we demonstrate that IBV Infection upregulates host-derived miR-17195 in HD11 cells, which targets and suppresses PLCβ2 to enhance replication. Moreover, miR-17195 promotes TAK1 phosphorylation by suppressing PLCβ2, which subsequently activates JNK/p38/NF-κB signaling to increase the level of pro-inflammatory cytokines. In addition, we uncovered that IBV uniquely employs miR-17195-mediated PLCβ2 downregulation to potentiate cytokine storm-induced tissue damage, which contrasts with the PLCβ2 upregulation observed during NDV, VSV, or H9N2 Infection, revealing a distinct viral pathogenesis mechanism. Overall, these results provide insights into IBV-induced multi-organ damage and highlight the therapeutic potential of modulating miR-17195 to mitigate IBV-associated disease severity.

Keywords

Infectious bronchitis virus; Inflammation; MiR-17195; TAK1.

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