Aging represents a paradox of immunodeficiency and inflammation (inflamm-aging) and autoimmunity. Over the lifespan there are changes in the architecture and functioning of the immune system often termed “Immunosenescence”. Recently, there have been major developments in understanding the cellular and molecular bases, and genetic and epigenetic changes, in innate and the adaptive immune system during aging.
Limited longitudinal studies have begun to reveal biomarkers of immune aging, which are recognized as an “immune risk profile” (IRP) predicting mortality in the very elderly. Hallmark parameters of the IRP may also be associated with poorer responses to vaccination. The usually asymptomatic infection with the widespread persistent beta-herpesvirus HHV5 (Cytomegalovirus, CMV) has an enormous impact on these immune biomarkers. The prevalence of CMV infection in populations in industrialized countries increases with age, and within individuals, the degree of immune commitment also increases with age. This may cause pathology by maintaining higher systemic levels of inflammatory mediators and decreasing the “immunological space” available for immune cells with other specificities. Modalities to prevent or reverse immunosenescence may therefore need to include targeting infectious agents such as CMV
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