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World J Gastroenterol. 2005 May 21;11(19):2949-52.

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

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Department of Infectious Diseases, Medical University of Bialystok, Zurawia Str, 14, 15-540 Bialystok, Poland.



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 (IFNalpha2b) and ribavirin (RBV) were analyzed in patients with chronic hepatitis C.


In 30 patients with chronic hepatitis C (responders--R and non-responders--NR) treated with IFNalpha2b+RBV, protein bcl-2 was determined in hepatocytes and in liver associated lymphocytes before and after the treatment.


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.


IFNalpha2b+RBV treatment, by bcl-2 protein expression decrease, enables apoptosis of hepatocytes and associated liver lymphocytes, which in turn eliminate hepatitis C viruses.

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