However, we cannot exclude an unintended selection bias in our present study because it appears likely that patients who suffered from an aggressive course of HCV infection were more readily considered for antiviral treatment during their scheduled follow-up visits, compared with patients with a mild disease course. Second, our study lacks the comparison of paired biopsy samples obtained at 20, 25, and 35 years after infection to evaluate the histological rate of fibrosis progression. However, our present findings are in agreement with a recent report showing slow histological
fibrosis progression rates in Fulvestrant supplier paired biopsy samples obtained from treatment-naïve patients of the Irish anti-D cohort over a period of 5 years. Our findings are also consistent with another extensive histological follow-up study by Poynard et al., who reported similar slow fibrosis progression patterns in young women with chronic hepatitis C (CHC). In the Irish anti-D cohort, a 22-year follow-up study also showed mild fibrosis progression in affected women. Third, we could not reliably evaluate alcohol consumption in our patients over this long observation period. However, we observed only a minority of patients with excessive alcohol consumption in our 25-year follow-up study. In summary, we provide evidence for a mild, but
significant, Alvelestat in vivo disease progression at 35 years after infection in the German HCV (1b)-contaminated anti-D cohort, which largely depended on the HCV infection status of the participating patients. Patients with self-limited HCV infection or SVRs to antiviral treatment were protected from progressive liver fibrosis and showed the best clinical long-term outcome. The results of the present study will help attending physicians to counsel patients on the long-term outcome Bcl-w of CHC. Additional Supporting Information may be found in the online version of this article. “
“Non-alcoholic fatty liver disease (NAFLD) overlapping with chronic hepatitis B virus (HBV) infection is undergoing a rapid increase in China. Therefore,
the establishment and character of an animal model with both NAFLD and chronic HBV infection has become an urgent task. Mice with chronic HBV genotype B infection were established with a microinjection of oocytes. Transgenic and nontransgenic mice were then randomized into groups of NAFLD + HBV, HBV, NAFLD, and control and were treated with high-fat diets or common forage. At 8, 16, and 24 weeks, characteristics of NAFLD were evaluated by physical indices, liver function tests, glycolipid metabolism, and histopathological scoring. Viral dynamics were also analyzed by HBV-DNA and HBV-related antigens. Hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were expressed, and HBV-DNA was replicated in HBV transgenic mice at different stages in the serum and liver.