Mouse Anti HBsAg Hybridoma [I36C21]

Background and aims The effect of hepatitis B virus (HBV) infection on diabetes has remained unclear. We thus conducted a prospective cohort study to investigate the association between different HBV infection status and new-onset diabetes in a Chinese population. Methods We enrolled 55,520 participants with HBV serological markers and diabetes free in 2010 in Kailuan cohort. Cox regression models were used to analyze the relationship between different HBV infection status and incidence of diabetes after adjusting different confounders. Results During an average follow-up of 5.6 years, we identified 6008 incident patients with diabetes. Compared to the participants with hepatitis B surface antigen (HBsAg) negative/hepatitis B surface antibody (anti-HBs) negative/hepatitis B core antibody (anti-HBc) negative, those with chronic HBV infection or with HBsAg negative/anti-HBc positive had a higher risk to occur diabetes. The hazard ratios were 1.18 (95% CI 0.99-1.40,p = 0.0588) and 1.22 (95% CI 1.08-1.36,p = 0.0009), respectively. The association between chronic HBV infection, anti-HBc positive and diabetes was different between those with different levels of high density lipoprotein cholesterol, blood pressure, body mass index, and age. Conclusion The individuals with chronic HBV infection or anti-HBc positive may have an increased risk of diabetes, and the association may be modified by the different status of metabolism related variables and age. Effective management of HBV infection may contribute to the reduction of the burden of both hepatitis B and diabetes.

Background and Aims A dichotomous separation of hepatitis B viral DNA and hepatitis B surface antigen (HBsAg) concentrations occurs during the natural history and treatment of chronic hepatitis B. We have evaluated the ability of hepatitis B virus (HBV) RNA and hepatitis B core-related antigen (HBcrAg) as surrogates of silencing of covalently closed circular DNA (cccDNA), to characterize this dissociation, and virological outcomes. Approach and Results Three cohorts of hepatitis B e antigen (HBeAg)-negative patients were studied: cohort A: 66 HBeAg-negative patients on long-term nucleos(t)ide analogue (NA) therapy; cohort B: 23 antibodies against hepatitis B e antigen (anti-HBe)-positive patients who stopped treatment; and Cohort C: 19 anti-HBe-positive patients on long-term NA treatment who achieved HBsAg loss and in whom treatment was withdrawn. Concentrations of HBV serological/virological biomarkers (HBV DNA, HBsAg, HBcrAg, and HBV RNA) were measured in sequential samples at different time points on/off therapy. Cohort A: After 3 years of antiviral therapy, 33% and 30% had detectable HBcrAg and HBV RNA, respectively, despite all being HBV-DNA negative. After 5 years' therapy with NA, 27% and 14% had detectable HBcrAg and HBV RNA. Detectable HBcrAg and HBV RNA at the time of treatment withdrawal was only observed in those patients who developed a severe aminotransferase flare. Only those patients with HBV reactivation in cohort C had detectable HBV RNA at treatment withdrawal, but HBcrAg and HBV DNA were not detected. Conclusions HBcrAg and HBV RNA are sensitive biomarkers of continued transcription of cccDNA in HBeAg-negative patients despite marked HBV-DNA suppression by NA. These markers were predictors of severe alanine transaminase flares, after treatment withdrawal, and HBV-DNA reactivation. Their measurement during the natural history of hepatitis B, and on treatment with current and new agents, could characterize residual HBV-RNA transcription from cccDNA and assist drug development and disease management.