---
title: "Stem-like CD8+ T cells preserve HBV-specific responses in HBV/HIV co-infection"
id: "gut-14-stem-like-cd8-t-cells-preserve-hbv-specific-responses-in-hbv-hiv-co-infection"
canonical_url: "https://medichelpline.com/clinical-feed/gut-14-stem-like-cd8-t-cells-preserve-hbv-specific-responses-in-hbv-hiv-co-infection"
content_type: "clinical_feed_article"
specialty: "Gastroenterology"
source_name: "Gut (BMJ)"
source_url: "http://gut.bmj.com/cgi/content/short/75/7/1397?rss=1"
published_at: "2026-06-09T10:23:36.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Stem-like CD8+ T cells preserve HBV-specific responses in HBV/HIV co-infection
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/gut-14-stem-like-cd8-t-cells-preserve-hbv-specific-responses-in-hbv-hiv-co-infection
- **Specialty:** [Gastroenterology](https://medichelpline.com/clinical-feed/gastroenterology.md)
- **Primary Source:** Gut (BMJ)
- **Source URL:** [Original Journal Publication](http://gut.bmj.com/cgi/content/short/75/7/1397?rss=1)
- **Published At:** 2026-06-09T10:23:36.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
Background Chronic hepatitis B virus (HBV) infection disproportionately affects people living with HIV, who are often excluded from functional cure studies. Objective This study investigates CD8 + T cell profiles in HBV mono-infection versus HBV/HIV co-infection, examining the impact of long-term therapy on virus-specific responses to inform therapeutic strategies for immune restoration. Design We analysed CD8 + T cell responses in 61 participants (HBV n=20, HBV/HIV n=20, HIV n=21), on suppressive antiviral therapy, assessing transcriptomic and proteomic profiles, focusing on exhaustion markers alongside virus-specific functional capabilities. Results Transcriptomic analysis revealed distinct signatures in co-infection, with upregulation of TCR signalling genes, inhibitory pathways and progenitor-exhausted markers ( XCL2, TCF7, PDCD1, IL7R ). This profile scored highly for a precursor exhausted (Tpex) CD8 + T cell signature, reflecting stemness that maintains plasticity despite chronic antigen exposure. Proteomic analysis confirmed higher frequencies of Tpex (TCF-1 + CD127 + PD-1 + ) CD8 + T cells in co-infection, while HBV mono-infection showed predominance of terminally exhausted Tox high TCF-1 - CD127 - cells. Tpex enrichment extended to HBV-specific populations corresponding with more robust, polyfunctional HBV-specific responses in co-infection against surface and core antigens. HBV-specific CD8 T cells maintained enhanced proliferative capacity and checkpoint responsiveness to anti-PDL1 blockade compared with HBV mono-infection. While co-infection was characterised by lower HBsAg levels and longer treatment duration, these factors alone did not account for the distinct immunological profiles. Conclusions People with well-controlled HBV/HIV co-infection maintain robust CD8 + T cell responses with preserved stem-like properties supporting antiviral function. These results challenge assumptions about additive immune dysfunction in dual chronic infections and highlight the need for tailored immune-modulatory therapies.
## Clinical Analysis & Structured Key Points
Background Chronic hepatitis B virus (HBV) infection disproportionately affects people living with HIV, who are often excluded from functional cure studies. Objective This study investigates CD8 + T cell profiles in HBV mono-infection versus HBV/HIV co-infection, examining the impact of long-term therapy on virus-specific responses to inform therapeutic strategies for immune restoration. Design We analysed CD8 + T cell responses in 61 participants (HBV n=20, HBV/HIV n=20, HIV n=21), on suppressive antiviral therapy, assessing transcriptomic and proteomic profiles, focusing on exhaustion markers alongside virus-specific functional capabilities. Results Transcriptomic analysis revealed distinct signatures in co-infection, with upregulation of TCR signalling genes, inhibitory pathways and progenitor-exhausted markers ( XCL2, TCF7, PDCD1, IL7R ). This profile scored highly for a precursor exhausted (Tpex) CD8 + T cell signature, reflecting stemness that maintains plasticity despite chronic antigen exposure. Proteomic analysis confirmed higher frequencies of Tpex (TCF-1 + CD127 + PD-1 + ) CD8 + T cells in co-infection, while HBV mono-infection showed predominance of terminally exhausted Tox high TCF-1 - CD127 - cells. Tpex enrichment extended to HBV-specific populations corresponding with more robust, polyfunctional HBV-specific responses in co-infection against surface and core antigens. HBV-specific CD8 T cells maintained enhanced proliferative capacity and checkpoint responsiveness to anti-PDL1 blockade compared with HBV mono-infection. While co-infection was characterised by lower HBsAg levels and longer treatment duration, these factors alone did not account for the distinct immunological profiles. Conclusions People with well-controlled HBV/HIV co-infection maintain robust CD8 + T cell responses with preserved stem-like properties supporting antiviral function. These results challenge assumptions about additive immune dysfunction in dual chronic infections and highlight the need for tailored immune-modulatory therapies.
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