Abstract
Hepatitis C virus (HCV) is a global public health problem that mediates a persistent infection in nearly 200 million people. HCV is efficient in establishing chronicity due in part to the inefficiency of the host immune system in controlling and counteracting HCV-mediated evasion strategies. HCV persistence is linked to the ability of the virus to suppress the RIG-I pathway and interferon production from infected hepatocytes, thus evading innate immune defenses within the infected cell. This review describes the virus and host processes that regulate the RIG-I pathway during HCV infection. An understanding of these HCV-host interactions could lead to more effective therapies for HCV designed to reactivate the host immune response following HCV infection.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Enzyme Inhibitors / immunology
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Enzyme Inhibitors / metabolism*
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Gene Expression Regulation
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Hepacivirus / pathogenicity
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Hepacivirus / physiology*
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Hepatitis C / genetics
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Hepatitis C / immunology*
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Hepatitis C / metabolism
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Hepatitis C / virology*
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Humans
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Immunity, Innate*
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Interferons / immunology*
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Intracellular Space / immunology
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Intracellular Space / metabolism
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Receptors, Retinoic Acid / antagonists & inhibitors
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Receptors, Retinoic Acid / immunology
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Signal Transduction / immunology
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Viral Proteins / immunology
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Viral Proteins / metabolism*
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Virulence
Substances
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Enzyme Inhibitors
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PLAAT4 protein, human
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Receptors, Retinoic Acid
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Viral Proteins
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Interferons