Does HIV accelerate the aging process? An assessment of clinical, ophthalmic and serum parameters in HIV-infected individuals in South Africa

Abstract

HIV-infected individuals are at increased risk of age-related non-AIDS morbidity and mortality compared with HIV-uninfected persons. It is speculated that HIV-infected individuals may not only be aging chronologically, but also undergoing accelerated biological aging. This is supported by clinical reports of conditions classically associated with the normal aging process appearing at an earlier age in HIV-infected persons compared to age-matched controls. Chronological age is an imprecise measure of biological aging due to inter-individual differences in rates of aging and therefore ‘biomarkers of aging’ may be used to assess biological age. The eye may be a uniquely useful site as a model of aging. It is easily accessible for examination and several components can be measured and assessed objectively e.g. lens density, retinal vascular calibre, corneal endothelial cell counts and the retinal nerve fibre layer thickness. This case-control study of 504 adults recruited from one district in Cape Town, South Africa assessed whether HIV-infected individuals have more advanced ocular aging, systemic frailty and cellular senescence than an HIV-uninfected group of similar age. Accelerated biological aging was demonstrated in HIV-infected individuals compared to their uninfected counterparts. HIV infection was also associated with frailty. Ocular parameters provided evidence of greater aging within the HIV-infected group, particularly objective measurement of retinal vascular calibre and lens density. These data suggest that as well as increased biological aging at a cellular and systemic level, ocular aging occurs as part of the accelerated aging phenotype in HIV infection. This study provides novel data about accelerated biological aging in sub- Saharan Africa and a platform for addressing future research questions relating to accelerated aging trajectories in HIV infection, the relative contributions of the infection and antiretroviral therapy, and whether biological age is dependent upon the duration of untreated disease or nadir CD4 count. As the HIV-infected population continues to age and expand, accelerated biological aging may have wideranging implications for the burden and management of HIV-related morbidity.