Does HIV accelerate biological aging?
A recent perspective from members of the Swiss HIV Cohort Study reviews what we currently know about biological aging in people with HIV (PWH). With modern antiretroviral therapy (ART), life expectancy for PWH has approached that of the general population. Nevertheless, chronic low-level inflammation persists in some individuals, and age-related conditions remain more common, raising the question of whether HIV influences the biological aging process.
Studies using telomere length and DNA methylation-based “epigenetic clocks” suggest that biological aging may accelerate particularly around HIV acquisition and during untreated infection. Importantly, effective ART appears to substantially modify this process: telomere shortening stabilizes following viral suppression, and several longitudinal studies have demonstrated that epigenetic age acceleration can partially reverse after ART initiation.
Whether these molecular measures of aging translate into clinically meaningful outcomes remains less clear. Some studies have linked shorter telomeres or greater epigenetic age acceleration to cardiovascular disease, frailty, cancer and mortality, but larger longitudinal studies are needed. The authors highlight the importance of determining whether epigenetic aging can ultimately help predict age-related outcomes and serve as a biomarker for interventions aimed at promoting healthy aging in PWH.
Key message: HIV may leave a measurable imprint on biological aging, particularly before effective treatment, but suppressive ART appears capable of slowing and potentially partially reversing this process. This perspective provides an excellent overview of the evolving evidence on biological aging in HIV—a particularly relevant topic as the focus of HIV care increasingly extends beyond survival towards healthy aging and longevity.