Background: Despite effective antiretroviral therapy (ART), HIV-infected patients exhibit systemic inflammation, early\nonset of age-related diseases, and features of immunosenescence. The role of inflammation in the development of\nage-related diseases is widely recognized. However, the role of immunosenescence is not well established. Studying\nimmunosenescence in HIV-infection could give insight into its role in ageing processes. In this cross-sectional study,\nwe aimed to investigate whether ART-treated HIV-infected patients exhibit immunosenescence; and whether\nimmunosenescence is associated with age-related processes of inflammation, metabolism, adipose tissue, and\nmuscle. T cell immunosenescence and exhaustion were assessed by flow cytometry analysis of CD8+ cells from 43\nART-treated HIV-infected patients (HIV+) and ten Controls using markers of differentiation: CD27/CD28; maturation:\nCD27/CD45RA; senescence: killer cell lectin-like receptor G1 (KLRG1); and exhaustion: programmed death-1 (PD-1).\nRelationships between CD8+ T cell immunosenescence, exhaustion, and age-related processes were assessed using\nlinear regressions.\nResults: HIV-infection was strongly associated with more highly differentiated and mature CD8+ T cell\nphenotypes. PD-1 and KLRG1 expression did not differ between HIV+ and Controls, but depended on\ndifferentiation and maturation stages of the cells. CD8+ T cell maturation was associated with age. KLRG1\nexpression was associated with age, metabolic syndrome, visceral adipose tissue, and high muscle mass.\nPD-1 expression was not associated with age-related parameters.\nConclusions: HIV-infection strongly affected CD8+ T cell differentiation and maturation, whereas age-related\nprocesses were only weakly associated with immune parameters. Our findings suggest that, in contrast to\ninflammation, immunosenescence appears to be highly dependent on HIV-infection and is only to a small\nextent associated with age-related parameters in well-treated HIV-infection.
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