The pleural tuberculosis–associated microenvironment promotes HIV-1 persistence by impairing CD8+ T cell–mediated viral control
7 affiliations
- 1The University of Sydney, Faculty of Medicine and Health, Sydney, New South Wales, Australia.
- 2The Westmead Institute for Medical Rese arch, Centre for Virus Research, Sydney, New South Wales, Australia.
- 3Université de Toulouse, CNRS, Institut de Pharmacologie et de Biologie Structurale (IPBS), Toulouse, France.
- 4Universidad de Buenos Aires, Facultad de Medicina, Departamento de Microbiología, Parasitología e Inmunología, Buenos Aires, Argentina.
- 5Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) – Universidad de Buenos Aires. Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS). Buenos Aires. Argentina.
- 6Kirby Institute, University of New South Wales, Sydney, New South Wales, Australia.
- 7International Research Project CNRS “MAC-TB/HIV,” Toulouse, France, and Buenos Aires, Argentina.
Abstract
Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), is the most common coinfection in people living with HIV-1. This coinfection is associated with accelerated HIV-1 disease progression and reduced survival. However, the immunological and virological mechanisms driving this progression are not completely understood. To address this knowledge gap, using pleural effusion samples from people living with HIV-1 and TB, we investigated how the HIV-1 genetic landscape and the anti–HIV-1 immune response are impacted by a TB-associated microenvironment. Our results revealed an enrichment of genetically intact HIV-1 and impaired CD8+ T cell–mediated antiviral response at this site of HIV-1/Mtb coinfection. Moreover, efficient CD8+ T cell activation was inhibited by lipids present in the TB-associated pleural effusion. These findings indicate that this immune microenvironment induced by TB promotes the persistence of cells infected with replication-competent HIV-1 by creating a niche of reduced antiviral immune pressure, potentially contributing to the worsened clinical outcomes observed in people living with HIV-1 and TB.
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BibTeX
@article{cronin2026pleural,
title = {{The pleural tuberculosis–associated microenvironment promotes HIV-1 persistence by impairing CD8+ T cell–mediated viral control}},
author = {Samantha Cronin and Jennifer Simpson and Andrea Pereyra-Casanova and Yuchen Li and Josefina Marín-Rojas and Freja A. Warner van Dijk and Katie Fisher and Daniel J. Buffa and Hafsa Rana and Zoï Vahlas and Joaquina Barros and Mariano Maio and Thomas R. O’Neil and Kirstie M. Bertram and Eunok Lee and Najla Nasr and Andrew N. Harman and Gabriela Turk and Maria Florencia Quiroga and Anthony D. Kelleher and Christel Vérollet and Luciana Balboa and Sarah Palmer and Gabriel Duette},
journal = {JCI Insight},
year = {2026},
month = aug,
doi = {10.1172/jci.insight.201268},
url = {https://doi.org/10.1172/jci.insight.201268},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The pleural tuberculosis–associated microenvironment promotes HIV-1 persistence by impairing CD8+ T cell–mediated viral control
AU - Samantha Cronin
AU - Jennifer Simpson
AU - Andrea Pereyra-Casanova
AU - Yuchen Li
AU - Josefina Marín-Rojas
AU - Freja A. Warner van Dijk
AU - Katie Fisher
AU - Daniel J. Buffa
AU - Hafsa Rana
AU - Zoï Vahlas
AU - Joaquina Barros
AU - Mariano Maio
AU - Thomas R. O’Neil
AU - Kirstie M. Bertram
AU - Eunok Lee
AU - Najla Nasr
AU - Andrew N. Harman
AU - Gabriela Turk
AU - Maria Florencia Quiroga
AU - Anthony D. Kelleher
AU - Christel Vérollet
AU - Luciana Balboa
AU - Sarah Palmer
AU - Gabriel Duette
PY - 2026
DA - 2026/08/20
JO - JCI Insight
DO - 10.1172/jci.insight.201268
UR - https://doi.org/10.1172/jci.insight.201268
AB - Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), is the most common coinfection in people living with HIV-1. This coinfection is associated with accelerated HIV-1 disease progression and reduced survival. However, the immunological and virological mechanisms driving this progression are not completely understood. To address this knowledge gap, using pleural effusion samples from people living with HIV-1 and TB, we investigated how the HIV-1 genetic landscape and the anti–HIV-1 immune response are impacted by a TB-associated microenvironment. Our results revealed an enrichment of genetically intact HIV-1 and impaired CD8+ T cell–mediated antiviral response at this site of HIV-1/Mtb coinfection. Moreover, efficient CD8+ T cell activation was inhibited by lipids present in the TB-associated pleural effusion. These findings indicate that this immune microenvironment induced by TB promotes the persistence of cells infected with replication-competent HIV-1 by creating a niche of reduced antiviral immune pressure, potentially contributing to the worsened clinical outcomes observed in people living with HIV-1 and TB.
SN - 2379-3708
ER -