期刊
VIRUS RESEARCH
卷 155, 期 1, 页码 231-239出版社
ELSEVIER
DOI: 10.1016/j.virusres.2010.10.013
关键词
Hepatitis B virus; HBx protein; C-terminal truncations
类别
资金
- NIH [R01AI064844]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI064844] Funding Source: NIH RePORTER
More than 350 million people worldwide are chronically infected with the human hepatitis B virus (HBV). Chronic HBV infections are associated with the development of hepatocellular carcinoma. While the mechanism of HBV-associated carcinoma remains undefined, it is thought to involve a combination of a continuous inflammatory response to HBV-infected hepatocytes and activities of HBV proteins such as the HBV X protein (HBx). HBx stimulates HBV replication; however, the mechanism by which HBx stimulates HBV replication remains incompletely understood. Studies performed with the woodchuck hepatitis virus (WHV) in woodchucks demonstrated that a C-terminally truncated mutant of the WHV X protein could not stimulate WHV replication. However, whether the C-terminus of HBx is important for HBx-stimulation of HBV replication is unclear. We have constructed C-terminal truncation mutants of HBx and have demonstrated that the C-terminus of HBx impacts HBx stability, HBx activation of transcription, and HBx stimulation of HBV replication. These observations highlight the impact of the HBx C-terminus on HBx activities and the importance of directly analyzing HBx expression and functions in HBV-associated tumors that contain chromosomal integrants of HBV with truncations of the HBx gene. (c) 2010 Elsevier B.V. All rights reserved.
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