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<p>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 &lt; 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<sup>+</sup>HLA-DR<sup>-</sup> expression on both CD4<sup>+</sup> and CD8<sup>+</sup> T cells in people with HIV-HBV co-infection and HIV alone compared with HBV mono-infection. PD-1 expression on CD4<sup>+</sup> T cells was also higher in the HIV-HBV and HIV mono-infection groups than with HBV alone. After stimulation, CD69 expression on both CD4<sup>+</sup> and CD8<sup>+</sup> T cells was higher in the HIV-HBV and HIV-only groups than in HBV alone. CD8<sup>+</sup> T cells from individuals with co-infection showed higher PD-1 expression, while CD4<sup>+</sup> PD-1 expression was similar across groups. CD38⁺HLA-DR⁺ co-expression on CD4⁺ T cells was increased in the HIV–HBV and HIV mono-infection groups but was similar on CD8⁺ T cells across groups. Pro- and anti-inflammatory cytokine levels were highest in the co-infected group. The usRNA reservoir transcriptional activity level was significantly higher in HIV-HBV co-infection (<i>p</i> = 0.022) while cell-associated DNA remained the same for both groups. Among individuals with HIV–HBV co-infection who have achieved virological suppression, while HIV appears to be the main driver of T cell responses, HBV can result in a more active reservoir.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月9日

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  • Helena Lamptey,
  • Abigail Naa Adjorkor Pobee,
  • James Odame Aboagye,
  • Jonathan Klutse,
  • Anthony Twumasi Boateng,
  • Christopher Zab-Yen Abana,
  • Dzidzor Aku Attoh,
  • Ephraim Mawufemor Kofi Kanda,
  • John Atanniba,
  • Prince Adom Nartey,
  • Yeena Abla Tay,
  • Ebenezer Adjei-Gati,
  • Prince Charles O. Lamptey,
  • Kwadwo Asamoah Kusi,
  • Evelyn Yayra Bonney,
  • George Boateng Kyei

摘要

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+HLA-DR- expression on both CD4+ and CD8+ T cells in people with HIV-HBV co-infection and HIV alone compared with HBV mono-infection. PD-1 expression on CD4+ T cells was also higher in the HIV-HBV and HIV mono-infection groups than with HBV alone. After stimulation, CD69 expression on both CD4+ and CD8+ T cells was higher in the HIV-HBV and HIV-only groups than in HBV alone. CD8+ T cells from individuals with co-infection showed higher PD-1 expression, while CD4+ PD-1 expression was similar across groups. CD38⁺HLA-DR⁺ co-expression on CD4⁺ T cells was increased in the HIV–HBV and HIV mono-infection groups but was similar on CD8⁺ T cells across groups. Pro- and anti-inflammatory cytokine levels were highest in the co-infected group. The usRNA reservoir transcriptional activity level was significantly higher in HIV-HBV co-infection (p = 0.022) while cell-associated DNA remained the same for both groups. Among individuals with HIV–HBV co-infection who have achieved virological suppression, while HIV appears to be the main driver of T cell responses, HBV can result in a more active reservoir.