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 (IFNalpha2b) 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 IFNalpha2b+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: IFNalpha2b+RBV treatment, by bcl-2 protein expression decrease, enables apoptosis of hepatocytes and associated liver lymphocytes, which in turn eliminate hepatitis C viruses.
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 (IFNalpha2b) 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 IFNalpha2b+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: IFNalpha2b+RBV treatment, by bcl-2 protein expression decrease, enables apoptosis of hepatocytes and associated liver lymphocytes, which in turn eliminate hepatitis C viruses.
Authors: P Botarelli; M R Brunetto; M A Minutello; P Calvo; D Unutmaz; A J Weiner; Q L Choo; J R Shuster; G Kuo; F Bonino Journal: Gastroenterology Date: 1993-02 Impact factor: 22.682
Authors: Dale L Barnard; Craig W Day; Kevin Bailey; Matthew Heiner; Robert Montgomery; Larry Lauridsen; Scott Winslow; Justin Hoopes; Joseph K-K Li; Jongdae Lee; Dennis A Carson; Howard B Cottam; Robert W Sidwell Journal: Antiviral Res Date: 2006-03-24 Impact factor: 5.970