Abstract
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.
Keywords:
DHAV-3; MDA5; RIG-I; TLR7; innate immunity.
© 2025. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.
MeSH terms
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Animals
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DEAD Box Protein 58* / genetics
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DEAD Box Protein 58* / immunology
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Ducks / virology
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Fibroblasts / immunology
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Fibroblasts / virology
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Hepatitis Virus, Duck* / genetics
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Hepatitis Virus, Duck* / immunology
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Hepatitis, Viral, Animal* / immunology
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Hepatitis, Viral, Animal* / virology
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Immunity, Innate*
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Interferon-Induced Helicase, IFIH1* / genetics
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Interferon-Induced Helicase, IFIH1* / immunology
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Interferon-Induced Helicase, IFIH1* / metabolism
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Interferon-beta / genetics
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Interferon-beta / immunology
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Picornaviridae Infections* / immunology
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Picornaviridae Infections* / veterinary
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Picornaviridae Infections* / virology
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Poultry Diseases* / immunology
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Poultry Diseases* / virology
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Toll-Like Receptor 7* / genetics
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Toll-Like Receptor 7* / immunology
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Toll-Like Receptor 7* / metabolism
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Virus Replication
Substances
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Interferon-Induced Helicase, IFIH1
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Toll-Like Receptor 7
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DEAD Box Protein 58
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Interferon-beta