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Galectin 9 Levels as a Potential Predictor of Intact HIV Reservoir Decay.

Sergio Serrano-Villar^1,2,3, Akshay Gala⁴, Peter Bacchetti⁵

¹Division of HIV, Infectious Diseases, and Global Medicine, Department of Medicine, Zuckerberg San Francisco General Hospital, and University of California San Francisco.

The Journal of Infectious Diseases

|August 29, 2024

Summary

Lower levels of Gal-9 predict faster decay of intact HIV genomes during antiretroviral therapy (ART). Targeting Gal-9 and other inflammatory cytokines may help reduce the HIV reservoir.

Keywords:

HIV persistence HIV reservoir cytokines galectin 9 inflammation

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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

Area of Science:

Immunology
Virology
HIV/AIDS Research

Background:

The HIV reservoir's decay rate during antiretroviral therapy (ART) varies.
Cells with intact HIV genomes decay faster than those with defective genomes, especially early in ART.
Host factors influencing this decay are not well understood.

Purpose of the Study:

To investigate host factors, specifically inflammatory cytokines, that influence the decay kinetics of intact HIV genomes during ART.
To identify potential therapeutic targets for HIV reservoir reduction.

Main Methods:

An observational study involving 74 people with HIV (PWH) on ART.
Measurement of intact proviruses using the intact proviral DNA assay.
Quantification of 32 inflammatory cytokines and analysis using linear spline models over seven years.

Main Results:

Lower baseline Gal-9 levels were the strongest predictor of faster intact HIV genome decay.
Higher baseline levels of interferon-inducible T-cell α chemoattractant (ITAC), interleukin 17 (IL-17), and macrophage inflammatory protein 1α (MIP-1α) also predicted faster decay.
Longitudinal increases in MIP-3α and decreases in IL-6 were associated with accelerated decay.

Conclusions:

Lower baseline Gal-9 is linked to faster decay of intact HIV, suggesting Gal-9 as a potential target for reservoir reduction.
The involvement of MIP-3α and IL-6 indicates a broader cytokine network influencing HIV decay, supporting multi-targeted interventions.