期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 102, 期 28, 页码 9913-9917出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0504273102
关键词
antiviral; beta; interferon gamma
资金
- NCI NIH HHS [R01 CA040489, R37 CA040489, CA 40489] Funding Source: Medline
We have previously shown that IFN-beta inhibits hepatitis B virus (HBV) replication by noncytolytic mechanisms that either destabilize pregenomic (pg)RNA-containing capsids or prevent their assembly. Using immortalized murine hepatocyte cell lines stably transfected with a doxycycline (dox)-inducible HBV replication system, we now show that replication-competent pgRNA-containing capsids are not produced when the cells are pretreated with IFN-beta before HBV expression is induced with dox. Furthermore, the turnover rate of preformed HBV RNA-containing capsids is not changed in the presence of IFN-beta or IFN-gamma under conditions in which further pgRNA synthesis is inhibited by dox removal. in summary, these results demonstrate that types 1 and 2 IFN activate hepatocellular mechanism(s) that prevent the formation of replication-competent HBV capsids and, thereby, inhibit HBV replication.
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