Chronic ethanol consumption stimulates hepatitis B virus gene expression and replication in transgenic mice
Article first published online: 30 DEC 2003
Copyright © 2001 American Association for the Study of Liver Diseases
Volume 34, Issue 4, pages 792–797, October 2001
How to Cite
Larkin, J., Clayton, M. M., Liu, J. and Feitelson, M. A. (2001), Chronic ethanol consumption stimulates hepatitis B virus gene expression and replication in transgenic mice. Hepatology, 34: 792–797. doi: 10.1053/jhep.2001.27565
- Issue published online: 30 DEC 2003
- Article first published online: 30 DEC 2003
- Manuscript Accepted: 5 JUL 2001
- Manuscript Received: 4 APR 2001
- National Institutes Health. Grant Numbers: AA07186, CA79512, AA07215
- Alcoholic Beverage Medical Research Foundation.
Epidemiologic observations show a higher frequency of hepatitis B virus (HBV) serologic markers in chronic alcoholics compared with the general population. This may be the result of an increased susceptibility of alcoholics to infection and/or to an ethanol-mediated stimulation of HBV gene expression and replication. To test the latter hypothesis, HBV transgenic SCID mice, which support consistent levels of virus replication, were fed with a standard Lieber-DiCarli or isocaloric diet for 5 weeks. In ethanol-fed mice, the levels of hepatitis B surface antigen (HBsAg) and viral DNA in serum increased by up to 7-fold compared with mice fed the control diet. Ethanol-treated mice also had elevated HBV-RNA levels, and increased expression of surface, core, and X antigens in the liver, especially in the pericentral regions. None of these changes were observed in transgenic mice fed isocaloric diets. Thus, chronic alcohol consumption alters the patterns of HBV gene expression and replication in the serum and liver of HBV transgenic SCID mice, and may provide a partial explanation for the increased frequency of HBV markers among alcoholics.