Since Looney at al. published their seminal paper a decade ago [1] it has become clear that many of the differences in T cell immunological parameters observed between young and old people are related to the ageassociated increasing prevalence of infection with the persistent b-herpesvirus HHV-5 (Cytomegalovirus). Ten years later, studies suggest that hallmark age-associated changes in peripheral blood T cell subset distribution may not occur at all in people who are not infected with this virus [[2]; Derhovanessian et al., in press]. Whether the observed changes are actually caused by CMV is an open question, but very similar, rapid changes observed in uninfected patients receiving CMV-infected kidney grafts are consistent with a causative role [3]. This meeting intensively discussed these and other questions related to the impact of CMV on human immune status and its relevance for immune function in later life.

A more difficult question to answer is whether ageassociated immune changes believed to contribute to the immunodeficiency of ageing are likewise caused by CMV. This seems a priori unlikely because CMV infection is very widespread, yet very elderly CMV-seropositive individuals are easily identified (although formally it is impossible to exclude that they were only recently infected). Thus, an important question becomes whether the CMV-sensitive altered immune cell subset distributions in the elderly, particularly the decreased numbers and percentages of naïve T cells and increased late-stage differentiated memory T cells (commonly used as biomarkers to assess “immunosenescence”), are in reality