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<p>The roles of RIG-I, MDA5, and TLR7 in duck hepatitis A virus genotype 3 (DHAV-3) infection were investigated using duck embryo fibroblasts (DEFs). DHAV-3 infection induced significant upregulation of RIG-I, MDA5, and TLR7 and high IFN-β, IL-6, and OASL responses. Overexpression and knockdown of RIG-I, MDA5, and TLR7 exerted significant effects on DHAV-3-induced IFN-β, IL-6, and OASL expression and DHAV-3 replication. Overexpression and inhibition of TLR7 altered DHAV-3-induced RIG-I and MDA5 expression. Together, these findings suggest that TLR7 and RIG-I/MDA5 play a coordinated role in detection and initiation of innate immunity against DHAV-3 infection.</p>

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Coordinated role of RIG-I, MDA5, and TLR7 in the innate immune response to duck hepatitis A virus 3

  • 期刊论文

  • 发表日期：

    2025年9月24日

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  • Duo Peng,
  • Xiaoyang Hu,
  • Jingjing Huang,
  • Qiong Li,
  • Yinuo Song,
  • Dabing Zhang

摘要

The roles of RIG-I, MDA5, and TLR7 in duck hepatitis A virus genotype 3 (DHAV-3) infection were investigated using duck embryo fibroblasts (DEFs). DHAV-3 infection induced significant upregulation of RIG-I, MDA5, and TLR7 and high IFN-β, IL-6, and OASL responses. Overexpression and knockdown of RIG-I, MDA5, and TLR7 exerted significant effects on DHAV-3-induced IFN-β, IL-6, and OASL expression and DHAV-3 replication. Overexpression and inhibition of TLR7 altered DHAV-3-induced RIG-I and MDA5 expression. Together, these findings suggest that TLR7 and RIG-I/MDA5 play a coordinated role in detection and initiation of innate immunity against DHAV-3 infection.