A multi-trait epigenome-wide association study identified DNA methylation signature of inflammation among men with HIV

Clin Epigenetics. 2024 Nov 2;16(1):152. doi: 10.1186/s13148-024-01763-2.

Abstract

Inflammation underlies many conditions causing excess morbidity and mortality among people with HIV (PWH). A handful of single-trait epigenome-wide association studies (EWAS) have suggested that inflammation is associated with DNA methylation (DNAm) among PWH. Multi-trait EWAS may further improve statistical power and reveal pathways in common between different inflammatory markers. We conducted single-trait EWAS of three inflammatory markers (soluble CD14, D-dimers and interleukin-6) in the Veterans Aging Cohort Study (n = 920). The study population was all male PWH with an average age of 51 years, and 82.3% self-reported as Black. We then applied two multi-trait EWAS methods-CPASSOC and OmniTest-to combine single-trait EWAS results. CPASSOC and OmniTest identified 189 and 157 inflammation-associated DNAm sites, respectively, of which 112 overlapped. Among the identified sites, 56% were not significant in any single-trait EWAS. Top sites were mapped to inflammation-related genes including IFITM1, PARP9 and STAT1. These genes were significantly enriched in pathways such as "type I interferon signaling" and "immune response to virus." We demonstrate that multi-trait EWAS can improve the discovery of inflammation-associated DNAm sites, genes and pathways. These DNAm sites might hold the key to addressing persistent inflammation in PWH.

Keywords: D-dimer; EWAS; HIV; IL-6; sCD14.

MeSH terms

  • Adult
  • Cohort Studies
  • DNA Methylation* / genetics
  • Epigenesis, Genetic / genetics
  • Epigenome* / genetics
  • Genome-Wide Association Study* / methods
  • HIV Infections* / genetics
  • Humans
  • Inflammation* / genetics
  • Interleukin-6 / genetics
  • Lipopolysaccharide Receptors / genetics
  • Male
  • Middle Aged
  • STAT1 Transcription Factor / genetics
  • Veterans / statistics & numerical data

Substances

  • Lipopolysaccharide Receptors
  • Interleukin-6
  • STAT1 Transcription Factor
  • STAT1 protein, human
  • CD14 protein, human