期刊
JOURNAL OF VIROLOGY
卷 79, 期 5, 页码 2689-2699出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.79.5.2689-2699.2005
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资金
- NIAID NIH HHS [AI48235, U19 AI040035, T32 AI 07520, T32 AI007520, AI060389, R56 AI060389, U01 AI048235, R01 AI060389, U19-AI40035] Funding Source: Medline
- NIGMS NIH HHS [T32-GM08203, T32 GM008203] Funding Source: Medline
Virus-responsive signaling pathways that induce alpha/beta interferon production and engage intracellular immune defenses influence the outcome of many viral infections. The processes that trigger these defenses and their effect upon host permissiveness for specific viral pathogens are not well understood. We show that structured hepatitis C virus (HCV) genomic RNA activates interferon regulatory factor 3 (IRF3), thereby inducing interferon in cultured cells. This response is absent in cells selected for permissiveness for HCV RNA replication. Studies including genetic complementation revealed that permissiveness is due to mutational inactivation of RIG-I, an interferon-inducible cellular DExD/H box RNA helicase. Its helicase domain binds HCV RNA and transduces the activation signal for IRF3 by its caspase recruiting domain homolog. RIG-I is thus a pathogen receptor that regulates cellular permissiveness to HCV replication and, as an interferon-responsive gene, may play a key role in interferon-based therapies for the treatment of HCV infection.
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