Inhibition of hepatitis B virus replication by interferon requires proteasome activity.
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.
Robek
Michael D
MD
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.
Wieland
Stefan F
SF
Chisari
Francis V
FV
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000998:Antiviral Agents / Q000494:pharmacology; D002460:Cell Line; D003546:Cysteine Endopeptidases / Q000378:metabolism*; D006515:Hepatitis B virus / Q000187:drug effects* / Q000502:physiology; D007370:Interferon Type I / Q000494:pharmacology; D007372:Interferons / Q000494:pharmacology*; D009097:Multienzyme Complexes / Q000378:metabolism*; D046988:Proteasome Endopeptidase Complex; D011994:Recombinant Proteins; D014779:Virus Replication / Q000187:drug effects*
D000998:Antiviral Agents; D007370:Interferon Type I; D009097:Multienzyme Complexes; D011994:Recombinant Proteins; D007372:Interferons; D003546:Cysteine Endopeptidases; D046988:Proteasome Endopeptidase Complex; D000251:Adenosine Triphosphatases