aDepartment of Biostatistics and Epidemiology, Rutgers School of Public Health, Piscataway, NJ;

bDepartment of Medicine, College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY;

cGertrude H. Sergievsky Center, College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY;

dDepartment of Environmental Health Sciences, Mailman School of Public Health, Columbia University Irving Medical Center, New York, NY;

eDepartment of Pediatrics, College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY; and

fICAP at Columbia, Mailman School of Public Health, Columbia University Irving Medical Center, New York, NY.

Correspondence to: Stephanie Shiau, PhD, MPH, Department of Biostatistics and Epidemiology, Rutgers School of Public Health, Piscataway, NJ 08854 (e-mail: [email protected]).

Supported by the funding from the National Institutes of Health, through Grant Number UL1 TR001873 (National Center for Advancing Translational Sciences) and Grant Number R21 AG056175. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. S.S. was supported by R25 MH108389.

The authors have no conflicts of interest to disclose.

Prior studies have measured accelerated aging in people with HIV using a DNA methylation (DNAm)-based biomarker of aging, “epigenetic age,” but data are limited in African American (AA) young adults with perinatally acquired HIV infection (PHIV).

We performed a cross-sectional study of AA young adults aged 20–35 years with PHIV (N = 31) and seronegative controls (N = 30) using DNAm measured in whole blood and cognitive function measured by the NIH Toolbox. Illumina EPIC array was used to measure DNAm age and accelerated aging markers including epigenetic age acceleration (EAA), as well as extrinsic (EEAA) and intrinsic (IEAA) EAA.

PHIV and controls did not differ by sex (45 vs. 43% male), chronological age (26.2 vs. 28.0 years), or ethnicity. Chronological age and DNAm age were correlated (r = 0.56, P < 0.01). PHIV had a higher mean EAA (2.86 ± 6.5 vs. −2.96 ± 3.9, P < 0.01) and EEAA (4.57 ± 13.0 vs. −4.72 ± 6.0, P < 0.01) than controls; however, IEAA was not different between groups. Among PHIV, EAA and EEAA were higher in those with HIV viral load ≥50 copies/mL than <50 copies/mL (EEA: 8.1 ± 5.2 vs. 0.11 ± 5.5, P = 0 < 0.01 and EEAA: 16.1 ± 10.6 vs. −1.83 ± 9.7, P < 0.01). We observed negative correlations (r = −0.36 to −0.31) between EEAA and executive function, attention, and language scores.

This content was originally published here.

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