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Sophia Pathai, Stephen Lawn, Paul Shiels, Helen Weiss, Colin Cook, Robin Wood, Clare Gilbert; Corneal endothelial cells provide evidence of accelerated cellular senescence associated with HIV infection: a case-control study. Invest. Ophthalmol. Vis. Sci. 2013;54(15):2200.
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Cellular senescence may be a key factor in HIV-related premature biological aging. We assessed features of the corneal endothelium that are known to be associated with biological aging, and cellular senescence markers in HIV-infected adults.
Case-control study of 242 HIV-infected adults and 249 matched controls. Using specular microscopy, the corneal endothelium was assessed for features of aging (low endothelial cell density [ECD], high variation in cell size, and low hexagonality index). Data were analysed by multivariable regression. CDKN2A (a cell senescence mediator) and 8-hydroxy-2′-deoxyguanosine (an oxidative DNA damage marker) were measured in peripheral blood leukocytes.
The median age of both groups was 40 years. Among HIV-infected adults, 88% were receiving antiretroviral therapy (ART); their median CD4 count was 468 cells/μL. HIV infection was associated with increased odds of variation in cell size (OR=1.67; 95%CI: 1.00-2.78, p=0.04). Among HIV-infected participants, low ECD was independently associated with current CD4 count <200 cells/μL (OR=2.77; 95%CI: 1.12-6.81, p=0.03). In participants on ART with undetectable viral load, CDKN2A expression and 8-OHDG levels were higher in those with accelerated aging, as reflected by lower ECD.
The corneal endothelium shows features consistent with HIV-related accelerated senescence, especially among those with poor immune recovery.
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