Expression of bcl-2 protein in chronic hepatitis C: Effect of interferon alpha 2b with ribavirin therapy

AIM: Mechanisms responsible for persistence of HCV infection and liver damage in chronic hepatitis C are not clear. Apoptosis is an important form of host immune response against viral infections. Anti-apoptotic protein bcl-2 expression on liver tissue as well as the influence of interferon alpha 2b (IFN alpha 2b) and ribavirin (RBV) were analyzed in patients with chronic hepatitis C. METHODS: In 30 patients with chronic hepatitis C (responders - R and non-responders - NR) treated with IFN alpha 2b+RBV, protein bcl-2 was determined in hepatocytes and in liver associated lymphocytes before and after the treatment. RESULTS: The treatment diminished bcl-2 protein accumulation in liver cells in(-)patients with hepatitis C (P<0.05). Before and after the therapy, we detected bcl-2 protein in R in 87 +/- 15% and 83 +/- 20% of hepatocytes and in 28 +/- 18% and 26 +/- 10% of liver-associated lymphocytes, respectively. In NR, the values before treatment decreased from 94 +/- 32% to 88 +/- 21% of hepatocytes and 39 +/- 29% to 28 +/- 12% of lymphocytes with bcl-2 expression. There was no statistical correlation between bcl-2 expression on liver tissue with inflammatory activity, fibrosis and biochemical parameters before and after the treatment. CONCLUSION: IFN alpha 2b+RBV treatment, by bcl-2 protein expression decrease, enables apoptosis of hepatocytes and associated liver lymphocytes, which in turn eliminate hepatitis C viruses. (c) 2005 The WJG Press and Elsevier Inc. All rights reserved.