Figure 1.

Multiple epigenetic measures in peripheral blood mononuclear cells (PBMC) demonstrate significant differences in biological aging after initial HIV infection, compared to age-matched HIV-uninfected persons

Longitudinal PBMC samples from men before (Visit A) and after (Visit B) documented HIV infection and seroconversion (SC), and from matched (chronologic age, Hepatitis C status, and time interval) persistently HIV seronegative men (SN), were evaluated for biological aging by five different age-adjusted epigenetic measures: (A) Age Acceleration Residual (AAR), (B) Extrinsic Epigenetic Age Acceleration (EEAA), (C) Phenotypic Epigenetic Age Acceleration (PEAA), (D) Grim Epigenetic Age Acceleration (GEAA), and (E) age-adjusted DNA methylation-based estimate of telomere length (aaDNAmTL) (see also Table S1). The first four are epigenetic “clocks” which increase with aging whereas estimated TL shortens (decreases) with aging. Each panel shows box and whisker plots (heavy line = median, box = 25^th-75^th percentile, whiskers = 5^th-95^th percentile) for SC (yellow) and SN (blue) participants at Visit A and Visit B; p values are for comparison of SN vs. SC at each visit by t-tests. 102 matched SC/SN pairs were evaluated; one SN participant was missing a PBMC sample at Visit A.