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Updated: May 26, 2026

06:46
Isolation of Exosomes from the Plasma of HIV-1 Positive Individuals
Published on: January 5, 2016
Epigenetic Age Acceleration Is Associated With HIV Infection Independently of Inflammation
James K Gibb1,2,3,4, Joshua M Schrock5,6, Brian Mustanski5,7
1Department of Anthropology, Northwestern University, Evanston, Illinois, USA.
Open Forum Infectious Diseases
|May 25, 2026
Summary
People with HIV (PWH) experience accelerated epigenetic aging, more so than from inflammation. HIV infection, not inflammation, drives this aging in young adults, linked to T-lymphocyte changes.
Area of Science:
- Immunology
- Genetics
- Aging Research
Background:
- People with human immunodeficiency virus (HIV) often show epigenetic age acceleration (EAA) and earlier onset of age-related diseases.
- The relative contributions of systemic inflammation versus HIV-specific factors to EAA require further investigation.
Purpose of the Study:
- To analyze peripheral blood cell DNA methylation (DNAm) in young adults (18-30 years) to assess epigenetic age acceleration (EAA).
- To compare EAA in individuals with HIV on antiretroviral therapy (ART) with detectable viral load against HIV-negative controls matched for risk factors.
- To determine the association of HIV status and systemic inflammation (C-reactive protein levels) with EAA.
Main Methods:
- Analysis of DNA methylation in peripheral blood cells from young adults with and without HIV.
- Matching of HIV-positive individuals (on ART with detectable viral load) with HIV-negative controls based on demographics, substance use, smoking, and inflammation.
- Stratification of systemic inflammation by plasma C-reactive protein (CRP) levels and regression analysis of epigenetic age estimates against chronological age.
Main Results:
- People with HIV (PWH) exhibited significantly greater EAA across multiple measures compared to controls, irrespective of CRP levels.
- HIV status strongly correlated with higher EAA and shorter DNA methylation-derived telomere length.
- Associations between EAA and HIV were not explained by CRP, IL-6, or LBP, but were substantially attenuated after adjusting for T-lymphocyte proportions.
Conclusions:
- In young adults with HIV and detectable viremia despite ART, EAA is more strongly linked to HIV infection than systemic inflammation.
- HIV-induced shifts in blood T-lymphocyte composition contribute to the observed epigenetic aging in PWH within typical clinical settings.
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