The tuberculosis-associated microenvironment promotes HIV-1 persistence by impairing CD8+ T cell-mediated viral
Samantha Cronin1,2, Jennifer Simpson1,2, Andrea Pereyra Casanova1,2
1The University of Sydney, Faculty of Medicine and Health, Sydney, Australia.
Biorxiv : the Preprint Server for Biology
|November 24, 2025
Summary
Tuberculosis coinfection with HIV-1 accelerates disease by promoting intact HIV-1 persistence. The TB microenvironment impairs immune responses, leading to worse outcomes in coinfected individuals.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Tuberculosis (TB) is the most common coinfection in people living with HIV-1 (PLWH).
- HIV-1/TB 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 HIV-1 genetic landscape.
- To examine the anti-HIV-1 immune response.
- To understand the impact of the TB-associated microenvironment in PLWH with TB.
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 responses.
Main Results:
- Enrichment of genetically intact HIV-1 was observed at the site of coinfection.
- Impaired CD8+ T cell-mediated antiviral response was detected.
- The TB microenvironment creates a niche of reduced antiviral immune pressure.
Conclusions:
- The TB-associated microenvironment promotes the persistence of replication-competent HIV-1.
- This persistence may contribute to worsened clinical outcomes in PLWH and TB.
- Understanding these mechanisms is crucial for managing HIV-1/TB coinfection.
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