Accelerated aging with HIV begins at the time of initial HIV infection.
Level 3 - non-randomized controlled study
Longitudinal non-randomized controlled cohort study comparing pre- and post-infection measurements with matched uninfected controls
PubMed 35880029 · doi:10.1016/j.isci.2022.104488
What was done
Five epigenetic DNA methylation measures of aging and estimated telomere length were evaluated longitudinally in 102 individuals before and approximately 3 years after HIV infection. Changes within individuals were compared against age- and time interval-matched HIV-uninfected controls, with statistical adjustments for T cell subset changes.
What was found
From pre- to post-HIV infection, significant epigenetic age acceleration (median 1.9 to 4.8 years) and estimated telomere shortening occurred (all p ≤ 0.001). Epigenetic acceleration remained statistically significant across three measures after controlling for T cell changes. No acceleration occurred in matched HIV-uninfected controls, and genome-wide co-methylation clusters were significantly associated with initial infection (p ≤ 2.0 × 10⁻⁴).
Why it matters
These findings show that biological age acceleration starts early at the time of initial HIV infection rather than solely resulting from decades of chronic infection or antiretroviral therapy. It directly links the onset of HIV infection to epigenetic aging markers.
Limits
The abstract does not state the sample size of the matched uninfected control group, participant demographics such as age and biological sex, or antiretroviral therapy status during the 3-year follow-up. Measurements are molecular surrogates rather than direct clinical outcomes.
Cited by
- supports HIV infection is associated with accelerated epigenetic aging in humans.