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Open Access Green as soon as Postprint is submitted to ZB.
Inhibition of cellular proteasome activities enhances hepadnavirus replication in an HBX-dependent manner.
J. Virol. 78, 4566-4572 (2004)
The X protein (HBX) of the hepatitis B virus (HBV) is not essential for the HBV life cycle in vitro but is important for productive infection in vivo. Our previous study suggests that interaction of HBX with the proteasome complex may underlie the pleiotropic functions of HBX. With the woodchuck model, we demonstrated that the X-deficient mutants of woodchuck hepatitis virus (WHV) are not completely replication defective, possibly behaving like attenuated viruses. In the present study, we analyzed the effects of the proteasome inhibitors on the replication of wild-type and X-negative HBV and WHV. Recombinant adenoviruses or baculoviruses expressing replicating HBV or WHV genomes have been developed as a robust and convenient system to study viral replication in tissue culture. In cells infected with either the recombinant adenovirus-HBV or baculovirus-WHV, the replication level of the X-negative construct was about 10% of that of the wild-type virus. In the presence of proteasome inhibitors, the replication of the wild-type virus was not affected, while the replication of the X-negative virus of either HBV or WHV was enhanced and restored to the wild-type level. Our data suggest that HBX affects hepadnavirus replication through a proteasome-dependent pathway.
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Publication type
Article: Journal article
Document type
Scientific Article
ISSN (print) / ISBN
0022-538X
e-ISSN
1098-5514
Journal
Journal of Virology
Quellenangaben
Volume: 78,
Issue: 9,
Pages: 4566-4572
Publisher
American Society for Microbiology (ASM)
Reviewing status
Peer reviewed
Institute(s)
Institute of Virology (VIRO)