CMV and Immunosenescence: from basics to clinics

Abstract

Alone among herpesviruses, persistent Cytomegalovirus (CMV) markedly alters the numbers and proportions of peripheral immune cells in infected-vs-uninfected people. Because the rate of CMV infection increases with age in most countries, it has been suggested that it drives or at least exacerbates "immunosenescence". This contention remains controversial and was the primary subject of the Third International Workshop on CMV & Immunosenescence which was held in Cordoba, Spain, 15-16th March, 2012. Discussions focused on several main themes including the effects of CMV on adaptive immunity and immunosenescence, characterization of CMV-specific T cells, impact of CMV infection and ageing on innate immunity, and finally, most important, the clinical implications of immunosenescence and CMV infection. Here we summarize the major findings of this workshop.

Figure 1

CMV and immunosenescence: Open questions. The relevance of the following questions on the role of CMV infection on immunosenescence and inflamm-aging were highlighted: 1) the need to standardize the panel of mAbs used to asses lymphocyte subsets alterations, 2) the role of each lymphoid subset in anti-CMV response, 3) the significance of CMV-induced inflammation and 4) the complexity of CMV infection in humans.

Figure 2

Age and CMV infection are major driving forces contributing to the deterioration of innate and adaptive immunity. Age-associated decrease of adaptive immunity is termed immunosenescence. The deregulation of innate immunity is associated with inflammageing. Immunosenescence and inflammageing play a significant role in the pathogenesis of different clinical situations that can lead to increased risk of frailty and death in the elderly.