Anti-HBV Surface Antigen Monoclonal antibody, Clone C119M

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.

Purpose of review To examine issues specific to HIV--HBV co-infection that are relevant to the search for and achieving hepatitis B cure in this the setting Recent findings In HIV--HBV co-infection, high rates of hepatitis B surface antigen (HBsAg) loss early after initiation of HBV-active antiretroviral therapy (ART) have previously been reported. Between 2012 and 2016, HBsAg loss from 2.8 to 23% was reported in numerous studies, including those already on suppressive HBV-active ART. Data published in 2018-2019 show that these rates have remained fairly stable (3.0-13.9%). However, it appears that higher HBsAg loss on starting HBV-active ART in co-infection falls within a few years to levels similar to that observed in long-term treated HBV mono-infection. Immune reconstitution and CD4+ T-cell recovery are likely to play a role in high HBsAg loss rates seen in early treated co-infection, although the mechanisms driving this are yet to be fully elucidated. High rates of HBsAg loss early after HBV-active ART initiation is unique to HIV--HBV co-infection, making it the ideal setting to investigate underlying mechanisms of HBV loss and develop new HBV cure strategies. This phenomenon could be used to enhance HBsAg loss with new therapeutic approaches currently being investigated; however, this is obstructed by excluding co-infection from such studies.