Semin Liver Dis 2009; 29(2): 188-199
DOI: 10.1055/s-0029-1214374
© Thieme Medical Publishers

Hepatitis C Virus and Alcohol

Larry Siu1 , Julie Foont1 , Jack R. Wands1
  • 1Warren Alpert Medical School of Brown University, Providence, Rhode Island
Further Information

Publication History

Publication Date:
22 April 2009 (online)

ABSTRACT

This review will focus on the prevalence of hepatitis c virus (HCV) infection in alcoholics with and without liver disease. Evidence will be presented to demonstrate that ethanol and chronic HCV infection synergistically accelerate liver injury. Some of the major postulated mechanisms responsible for disease progression include high rates of apoptosis, lipid peroxidation, and generation of free radicals and reactive oxygen species with reduced antioxidant capacity of the liver. Acquisition and persistence of HCV infection may be due to the adverse effects of ethanol on humoral and cellular immune responses to HCV. Dendritic cells (DC) appear to be one of the major targets for ethanol's action and DC dysfunction impairs the ability of the host to generate viral specific cluster of differentiation 4 (CD4+) and cluster of differentiation 8 (CD8+) immune responses. There is a relationship between increased alcohol intake and decreased response to interferon (IFN) therapy, which may be reversed by abstinence. Clinical studies are needed to optimize treatment responses in alcoholic patients with chronic HCV infection.

REFERENCES

Jack R Wands, M.D. 

Director, Division of Gastroenterology and The Liver Research Center, Warren Alpert Medical School of Brown University

55 Claverick Street, 4th Floor, Providence, RI 02903

Email: jack_wands_md@brown.edu