ARTICLE: HIV causes global B cell dysregulation and restricts HBV-specific B cell development in an incident HBV cohort
AUTHORS: Katherine E Cascino, Thomas Liechti, Eric C Seaberg, Kathleen Stevens, Steven M Wolinsky, Mallory D Witt, Robbie B Mailliard, Mario Roederer, Justin R Bailey, Chloe L Thio, Andrea L Cox
JOURNAL: J Clin Invest. 2026 Apr 7;136(11):e203138. doi: 10.1172/JCI203138. eCollection 2026 Jun 1.
Abstract
BACKGROUND: Functional B cell responses for both prevention and control of hepatitis B virus (HBV) infection remain poorly understood, including in the context of HBV/HIV coinfection.
METHODS: Here, we employed high-dimensional single-cell analysis to assess global and hepatitis B surface antigen-specific (HBsAg-specific) B cells in a longitudinal cohort of incident HBV from the Multicenter AIDS Cohort Study, with a subset of the cohort living with HIV-1
RESULTS: We observed that prior HIV infection has negative consequences for B cell function in early post-acute HBV infection, including increased frequencies of atypical memory B cells and regulatory B cells, expression of the activation marker CD86 on multiple B cell subsets in chronic HBV (CHB), and restricted expansion of HBsAg-specific B cells. In contrast, in HBV monoinfection, we observed no changes in the global B cell population from prior to infection and robust expansion of HBsAg-specific B cells. These expanded antigen-specific B cells resembled class-switched intermediate and resting memory B cells, with activation phenotypes that may contribute to ongoing HBV control.
CONCLUSION: HIV infection has a significant impact on B cell responses to subsequent HBV infection that may promote development of CHB in HBV/HIV coinfection.
FUNDING: Vaccine Research Center, NIAID, Bill & Melinda Gates Foundation, and NIH.
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