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Processing of Bronchoalveolar Lavage Fluid and Matched Blood for Alveolar Macrophage and CD4+ T-cell Immunophenotyping and HIV Reservoir Assessment

Processing of Bronchoalveolar Lavage Fluid and Matched Blood for Alveolar Macrophage and CD4⁺ T-cell Immunophenotyping and HIV Reservoir Assessment

Published on: June 23, 2019

The pleural tuberculosis-associated microenvironment promotes HIV-1 persistence by impairing CD8+ T cell-mediated

Samantha Cronin¹, Jennifer Simpson¹, Andrea Pereyra-Casanova¹

¹Centre for Virus Research, The Westmead Institute for Medical Research, Sydney, Australia.

|August 20, 2026

Abstract:

Mycobacteriumtuberculosis (Mtb), the causative agent of tuberculosis (TB), is the most common coinfection in people living with HIV-1 (PLWH). 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 PLWH 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 PLWH and TB.

Insights

Tuberculosis coinfection in people living with HIV-1 (PLWH) accelerates disease. A TB-associated microenvironment in pleural fluid enriches intact HIV-1 and impairs CD8+ T cell antiviral responses, worsening outcomes.

Area of Science:

Immunology
Virology
Infectious Diseases

Background:

Mycobacterium tuberculosis (Mtb) coinfection is common in people living with HIV-1 (PLWH).
This coinfection accelerates HIV-1 disease progression and reduces survival.
The underlying immunological and virological mechanisms are not fully understood.

Purpose of the Study:

To investigate the impact of the TB-associated microenvironment on HIV-1 genetic landscape and anti-HIV-1 immune response in PLWH with TB coinfection.

Main Methods:

Analysis of pleural effusion samples from PLWH with TB coinfection.
Assessment of HIV-1 genetic integrity.
Evaluation of CD8+ T cell-mediated antiviral response and activation.

Main Results:

Enrichment of genetically intact HIV-1 was observed in the pleural effusion.
Impaired CD8+ T cell-mediated antiviral response at the site of HIV-1/Mtb coinfection.
Lipids in pleural effusion inhibited efficient CD8+ T cell activation.

Conclusions:

The TB-induced immune microenvironment promotes persistence of replication-competent HIV-1.
This niche creates reduced antiviral immune pressure, contributing to worsened clinical outcomes in PLWH and TB.

Read full analysis

Keywords:

AIDS/HIV Immunology Infectious disease Tuberculosis

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