Cytomegalovirus (CMV) infection is a major driver of accelerated immunosenescence related to CD28null T cells expansion. CMV infection and these proatherogenic T cells have been independently associated with cardiovascular disease and COVID-19 severity. We have investigated the potential contribution of SARS-CoV-2 to immunosenescence and its relationship with CMV.Innate and adaptive immune subpopulations from mild/asymptomatic SARS-CoV-2 infected (mCOVID-19) individuals, and healthy donors (HD) were immunophenotyped. A significant increase of CD28nullCD57 + CX3CR1+ T cell percentages (CD4+ (P ≤ 0.01), CD8+ (P ≤ 0.01) and TcRγδ (CD4−CD8-) (P ≤ 0.001)) was found in mCOVID-19 CMV + individuals stable up to 12 months post-infection. This expansion did not occur in mCOVID-19 CMV- individuals or in CMV + individuals that were infected post SARS-CoV-2 vaccination (vmCOVID-19). Moreover, mCOVID-19 individuals showed no significant differences with aortic stenosis patients. Thus, individuals coinfected with SARS-CoV-2 and CMV suffer accelerated T cell senescence, which might ultimately lead to an increased risk of cardiovascular disease.