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BACH2-driven tissue resident memory programs promote HIV-1 persistence.

Yulong Wei1, Haocong Katherine Ma1, Michelle E Wong1

  • 1Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06519, USA.

Biorxiv : the Preprint Server for Biology
|January 7, 2025
PubMed
Summary
This summary is machine-generated.

Transcription repressor BACH2 promotes HIV-1 persistence by creating long-lived memory T cells in the gut. Targeting BACH2 may offer a new therapeutic strategy for HIV-1 infection.

Keywords:
BACH2HIV-1 persistenceHIV-1 reservoirT cell clonal expansiontissue resident memory T cell

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Transcription repressor BACH2 influences T cell differentiation and memory formation.
  • HIV-1 establishes persistence in specific T cell subsets within the gut.

Purpose of the Study:

  • To investigate the role of BACH2 in HIV-1 persistence within gut CD4+ T cells.
  • To identify BACH2 as a potential therapeutic target for HIV-1 persistence.

Main Methods:

  • Coupled single-cell DOGMA-seq and TREK-seq to analyze chromatin accessibility, transcriptome, surface proteins, T cell receptor, HIV-1 DNA, and RNA in 100,744 gut T cells.
  • Compared cells from aviremic HIV-1+ individuals and HIV-1- donors.
  • Performed in vitro infection of gut CD4+ T cells.

Main Results:

  • BACH2 shapes gut tissue resident memory T cells (TRMs) into long-lived memory cells with reduced effector function.
  • HIV-1-infected cells were enriched in TRMs (80.8%) and showed increased BACH2 accessibility, TRM/survival gene expression, and Th17 polarization.
  • In vitro studies demonstrated preferential HIV-1 infection and persistence in CCR6+ TRMs.

Conclusions:

  • The BACH2-driven TRM program promotes HIV-1 persistence in the gut.
  • BACH2 represents a novel therapeutic target for controlling HIV-1 persistence.