There's a fair amount of evidence implicating cytomegalovirus (CMV) in immune system decline, rhe theory here being that the immune system devotes ever more of its fixed resources to dealing with the largely harmless variants of this virus that it cannot clear. Here researchers argue against that view: "Aging is accompanied by the development of low grade systemic inflammation, termed 'inflammaging', characterised by raised serum C-reactive protein (CRP) and pro-inflammatory cytokines. Importantly, inflammaging is implicated in the pathogenesis of several of the major age-related diseases including cardiovascular disease, type 2 diabetes and dementia and is associated with increased mortality. The incidence of infection with the persistent herpes virus cytomegalovirus (CMV) also increases with age. Cross-sectional studies have proposed CMV infection as a significant driver of inflammaging, but a definitive case for CMV as a causative agent in inflammaging has not yet been made. We studied longitudinally 249 subjects (153 men, 96 women) who participated in the Hertfordshire Ageing Study at baseline (1993/5, mean age 67ยท5 years) and at 10 year follow up. At both times [subjects] provided blood samples for analysis of inflammatory status and CMV seropositivity. In the cohort as a whole, serum CRP and pro-inflammatory cytokines [were] increased between baseline and follow up ... These changes to cytokine status over time occurred equally in the 60% of subjects who were seropositive for CMV at baseline and follow up, the 8% who were CMV negative at baseline but who became CMV positive by the 10 year follow up, and also in the 32% who were CMV seronegative throughout. We conclude that CMV infection is not a primary causative factor in the age-related increase in systemic inflammation."
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This study doesn't really tell us anything about the role of CMV in immunosenescence -- or, at least, the aspect of immunosenescence in which it's most specifically implicated (decline in adaptive immunity): they're just presenting evidence that it may not be involved in (some aspects of ) the age-related rise in chronic, systemic inflammation, which clearly has many causes.
This is an important study with useful information. The strongest associations between CMV, inflammation and immunosenescence are not based on whether or not someone was once infected with CMV, but on how the immune system responds to CMV. It may only be the subgroup who make a strong T cell response against CMV who are at greater risk for inflammaging.