HIV dominates T-cell immune responses in HIV-HBV co-infection and is associated with increased HIV reservoir transcription.

Due to the effectiveness of antiretroviral therapy (ART), Human Immunodeficiency Virus (HIV) infection is now managed as a chronic condition. However, people with HIV (PWH) remain susceptible to co-infections, including Hepatitis B virus (HBV), with 15% of PWH in Africa being co-infected. While co-infections may accelerate disease progression and increase AIDS-related mortality, their effects on T-cell responses and HIV reservoir size are unclear. This study compared T-cell responses in people with HIV-HBV co-infection, HIV or HBV alone, and assessed the effects of HBV on the HIV reservoir size. We screened 390 archived samples from virologically suppressed (viral load < 50 copies/mL) PWH and identified 31 individuals with HIV-HBV co-infection. Peripheral blood mononuclear cells (PBMCs) were analyzed at baseline and following stimulation to assess activation and exhaustion markers (CD25, CD38, CD69, HLA-DR, and PD-1) by flow cytometry. Inflammatory cytokines were quantified using a 12-plex Luminex panel. HIV reservoir size was determined by RT-PCR measurements of proviral DNA and unspliced RNA. The prevalence of HIV-HBV co-infection was 7.9% (31/390). At baseline, unstimulated T cells showed increased CD38