Abstract Body

People with HIV (PWH) suffer higher age-related comorbidities including frailty, neurocognitive impairment (NCI), and cardiometabolic diseases than people without HIV. Aging among PWH occurs heterogeneously, however some prior studies suggest that the aging process among PWH is faster than people without HIV.

A cross-sectional study was conducted among older PWH and age- and sex-matched HIV-negative controls to compare phenotypic age and phenotypic age acceleration (PAA) in older PWH and HIV-negative controls. Phenotypic age was calculated using chronological age and 9 biomarkers from complete blood counts, inflammatory, metabolic-, liver- and kidney-related parameters. PAA was calculated as the difference between chronological age and phenotypic age. Multivariate logistic regression models were used to identify the factors associated with higher PAA, defined as having higher than the median value. We assessed aging-related comorbidities including the Veterans Aging Cohort Study (VACS) index, frailty, NCI and inflammation (hsCRP and IL-6). Area under the receiver operating characteristics curve (AROC) was used to assess model discrimination for frailty.

Between 2017 and 2018, 333 PWH and 102 HIV-negative controls (38% female) with median chronological age of 54 (IQR 52-59) and 55 (IQR 53-58) years, respectively, were enrolled. Median phenotypic age (49.4 vs. 48.5 years, p=0.54) and PAA (-6.7 vs. -7.5, p=0.24) were higher in PWH than the controls, although not statistically significant. PWH with higher PAA had lower CD4/CD8 ratio (0.88 [IQR 0.63-1.22] vs. 1.00 [IQR 0.74-1.33], p=0.03) and higher VACS index (22.2 [IQR 12-28] vs. 22.6 [IQR 18-34], p=0.01). In multivariate analysis including both PWH and uninfected controls, male sex (adjusted odds ratio=1.68 [95%CI=1.03-2.73]), current smoking (2.74 [1.30-5.79]), diabetes mellitus (2.97 [1.48-5.99]), hypertension (1.67 [1.02-2.72]), frailty (3.82 [1.33-10.93]), and higher IL-6 levels (1.09 [1.04-1.15]), but not HIV status and NCI, were independently associated with higher PAA. Phenotypic age discriminated frailty better than chronological age alone (AROC 0.76 [0.66-0.85] vs. 0.66 [0.55-0.77], p=0.04).

While PWH did not appear to have accelerated aging in our cohort, the phenotypic aging marker was significantly associated with systemic inflammation, frailty, and cardiovascular disease risk factors. This simple aging marker could be useful to identify high-risk PWH within the similar chronological age group.