Viral persistence and immune dysfunction in chronic hepatitis B: Mechanisms of post-treatment antigen asynchrony

Summary: Chronic hepatitis B (CHB) remains a major global health burden. Following antiviral therapy, the dynamics of hepatitis B virus (HBV) DNA and hepatitis B surface antigen (HBsAg) may become discordant, a phenomenon referred to as post-treatment asynchrony. This review summarizes the three principal forms of post-treatment asynchrony and examines their underlying mechanisms. We integrate the limitations of current antiviral targets, host immune dysfunction, virological characteristics, and host genetic factors into a unified framework to explain the discordant dynamics between HBsAg and HBV DNA. A better understanding of post-treatment asynchrony may help refine the interpretation of serological markers and inform patient stratification and individualized therapeutic strategies. Overall, this review provides an integrated perspective on the mechanisms and clinical significance of post-treatment asynchrony in CHB.