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Published on: February 22, 2017
miR-17195 promotes infectious bronchitis virus proliferation and macrophage-mediated inflammation via the PLCβ2-TAK1
Zheng Wang1, Chi Liu2, Xuan Chen1
1Animal Disease Prevention and Green Development Key Laboratory of Sichuan Province, College of Life Science, Sichuan University, Chengdu 610000, China.
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.
Insights
Infectious Bronchitis virus (IBV) upregulates miR-17195 in chickens, suppressing PLCβ2 to boost viral replication and inflammation. This distinct mechanism drives IBV-induced tissue damage, offering therapeutic targets.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Infectious Bronchitis virus (IBV) causes acute, contagious respiratory and renal disease in poultry.
- MicroRNAs (miRNAs) are key regulators of host-virus interactions during infection.
- Understanding viral pathogenesis mechanisms is crucial for disease control.
Purpose of the Study:
- To investigate the role of host-derived miRNAs in IBV infection.
- To elucidate the molecular mechanisms by which IBV induces pathogenesis.
- To identify potential therapeutic targets for mitigating IBV-associated disease.
Main Methods:
- HD11 cell culture and IBV infection model.
- Quantitative real-time PCR for miRNA and gene expression analysis.
- Western blotting to assess protein phosphorylation and signaling pathways.
- Comparison of PLCβ2 regulation with other avian viruses (NDV, VSV, H9N2).
Main Results:
- IBV infection upregulates host miR-17195 in HD11 cells.
- miR-17195 targets and suppresses PLCβ2, enhancing IBV replication.
- miR-17195 promotes TAK1 phosphorylation, activating JNK/p38/NF-κB signaling and increasing pro-inflammatory cytokines.
- IBV uniquely uses miR-17195-mediated PLCβ2 downregulation to exacerbate cytokine storm-induced tissue damage.
Conclusions:
- IBV employs a distinct pathogenesis strategy involving miR-17195-mediated suppression of PLCβ2.
- This mechanism contributes to IBV-induced multi-organ damage and inflammation.
- Modulating miR-17195 presents a potential therapeutic avenue for controlling IBV.
