Abstract

Immunosenescence is a progressive remodeling of immune functions with a multifactorial etiology (aging, chronic inflammation, persistent infections, cancer). CMV has been shown to act as chronic antigenic stressor and to accelerate immune ageing by affecting peripheral blood T cell phenotypes, including loss of CD28 or overexpression of CD57. Latent viral infections were shown to be associated with chronic type I IFN signature that might promote lymphocyte senescence. We defined SIP as the proportion of CD28–CD57+KLRG1+CD8+ circulating T cells.

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