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DNA methylation signatures of illicit drug injection and hepatitis C are associated with HIV frailty

Author

Listed:
  • Xinyu Zhang

    (Yale School of Medicine
    VA Connecticut Healthcare System)

  • Ying Hu

    (National Cancer Institute Center for Biomedical Information & Information Technology)

  • Amy C Justice

    (VA Connecticut Healthcare System
    New Haven Veterans Affairs Connecticut Healthcare System)

  • Boyang Li

    (Yale School of Public Health)

  • Zuoheng Wang

    (Yale School of Public Health)

  • Hongyu Zhao

    (Yale School of Public Health)

  • John H Krystal

    (Yale School of Medicine
    VA Connecticut Healthcare System)

  • Ke Xu

    (Yale School of Medicine
    VA Connecticut Healthcare System)

Abstract

Intravenous illicit drug use (IDU) and hepatitis C infection (HCV) commonly co-occur among HIV-infected individuals. These co-occurring conditions may produce interacting epigenetic effects in white blood cells that influence immune function and health outcomes. Here, we report an epigenome-wide association analysis comparing IDU+/ HCV+ and IDU−/HCV− in 386 HIV-infected individuals as a discovery sample and in 412 individuals as a replication sample. We observe 6 significant CpGs in the promoters of 4 genes, NLRC5, TRIM69, CX3CR1, and BCL9, in the discovery sample and in meta-analysis. We identify 19 differentially methylated regions on chromosome 6 harboring MHC gene clusters. Importantly, a panel of IDU+/HCV+-associated CpGs discriminated HIV frailty based upon a validated index with an area under the curve of 79.3% for high frailty and 82.3% for low frailty. These findings suggest that IDU and HCV involve epigenetic programming and that their associated methylation signatures discriminate HIV pathophysiologic frailty.

Suggested Citation

  • Xinyu Zhang & Ying Hu & Amy C Justice & Boyang Li & Zuoheng Wang & Hongyu Zhao & John H Krystal & Ke Xu, 2017. "DNA methylation signatures of illicit drug injection and hepatitis C are associated with HIV frailty," Nature Communications, Nature, vol. 8(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-02326-1
    DOI: 10.1038/s41467-017-02326-1
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