Abstract
Hepatitis B virus (HBV) replication is inhibited in a noncytopathic manner by alpha/beta interferon (IFN-alpha/beta) and IFN-gamma. We demonstrate here that inhibitors of cellular proteasome activity can block this antiviral effect. These results suggest that a critical component of the IFN-induced antiviral response may be the proteasome-dependent degradation of viral or cellular proteins that are required for HBV replication.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Triphosphatases / metabolism*
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Antiviral Agents / pharmacology
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Cell Line
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Cysteine Endopeptidases / metabolism*
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Hepatitis B virus / drug effects*
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Hepatitis B virus / physiology
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Interferon Type I / pharmacology
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Interferons / pharmacology*
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Multienzyme Complexes / metabolism*
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Proteasome Endopeptidase Complex
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Recombinant Proteins
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Virus Replication / drug effects*
Substances
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Antiviral Agents
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Interferon Type I
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Multienzyme Complexes
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Recombinant Proteins
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Interferons
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Cysteine Endopeptidases
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Proteasome Endopeptidase Complex
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Adenosine Triphosphatases