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Single-Nucleus Multiomic Analysis Reveals Immune-Metabolic Reprogramming Consistent With Maladaptive Trained Immunity

Siera Martinez1, Anelia Horvath1, Luke Johnson1

  • 1The George Washington University School of Medicine and Health Sciences, Washington, Washington, DC, USA.

Glia
|June 26, 2026
PubMed
Summary
This summary is machine-generated.

Maladaptive trained immunity may drive neuroinflammation in people with HIV, causing persistent cognitive issues despite treatment. This involves immune cell reprogramming, metabolic changes, and epigenetic alterations in the brain.

Keywords:
HIVHIV‐associated neurocognitive disorders (HAND)epigenetic reprogrammingmaladaptive trained immunitymicroglianeuroinflammationneuronssingle‐nucleus multiomics

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Area of Science:

  • Neuroimmunology
  • Neurovirology
  • Epigenetics

Background:

  • HIV-associated neurocognitive disorders (HAND) persist in people with HIV (PWH) even with effective antiretroviral therapy.
  • Persistent immune activation is suspected to cause ongoing neurological dysfunction in PWH.
  • Maladaptive trained immunity (TRIM), a form of innate immune reprogramming, is a proposed mechanism for sustained inflammation in HAND.

Purpose of the Study:

  • To investigate the role of maladaptive trained immunity in the pathogenesis of HAND.
  • To compare multiomic profiles of brain tissue from PWH with different HAND severities and HIV-uninfected individuals.

Main Methods:

  • Single-nucleus RNA sequencing (snRNA-seq) and ATAC sequencing (snATAC-seq) on post-mortem brain tissue.
  • Comparison of PWH (with HIV-associated dementia or asymptomatic neurocognitive impairment) and HIV-uninfected (PWoH) datasets.
  • Analysis focused on glial and neuronal cell types, examining immune signaling, metabolism, and epigenetic modifications.

Main Results:

  • Glia, particularly microglia, in PWH showed enhanced innate immune signaling (NLRP3, TLR2/4) and inflammatory mediator upregulation.
  • Coordinated cholesterol remodeling and partial glycolytic reprogramming were observed in glia.
  • Epigenetic analysis revealed increased chromatin accessibility at inflammatory, cholesterol regulatory (RXRA, APOE), and glycolytic loci.
  • Distinct patterns were observed between HIV-associated dementia and asymptomatic neurocognitive impairment, suggesting selective reorganization.
  • Neurons showed primarily bystander epigenetic changes.

Conclusions:

  • Multiomic data support the hypothesis of maladaptive trained immunity sustaining neuroinflammation in HAND.
  • Key features align with trained immunity hallmarks: concordant transcriptional/epigenetic priming, metabolic rewiring, and persistence despite viral suppression.
  • Further functional studies are needed to validate these findings.