Abstract
Clinical data suggest that Hepatitis C virus (HCV) levels are generally lower in Hepatitis B virus (HBV) co-infected patients, but the mechanism is unknown. Here, we show that HBV, but not HCV, activated absent in melanoma-2. This in turn results in inflammasome-mediated cleavage of pro-IL-18, leading to an innate immune activation cascade that results in increased interferon-γ, suppressing both viruses.
Keywords:
AIM2; NK cells; hepatitis B virus; hepatitis C virus; monocytes.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Coinfection* / immunology
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Coinfection* / virology
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DNA-Binding Proteins* / metabolism
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Hepacivirus* / immunology
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Hepatitis B virus* / immunology
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Hepatitis B virus* / physiology
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Hepatitis B* / complications
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Hepatitis B* / immunology
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Hepatitis B* / virology
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Hepatitis C* / complications
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Hepatitis C* / immunology
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Hepatitis C* / virology
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Humans
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Immunity, Innate*
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Inflammasomes / metabolism
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Interferon-gamma / immunology
Substances
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AIM2 protein, human
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DNA-Binding Proteins
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IL18 protein, human
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Inflammasomes
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Interferon-gamma