Accelerated T-Cell Immunosenescence in Cytomegalovirus-Seropositive Individuals After Severe Acute Respiratory Syndrome Coronavirus 2 Infection

Cytomegalovirus (CMV) infection is a major driver of accelerated immunosenescence related to CD28(null) T cell expansion. CMV infection and these proatherogenic T cells have been independently associated with cardiovascular disease and coronavirus disease 2019 (COVID-19) severity. We investigated the potential contribution of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to immunosenescence and its relationship with CMV. Innate and adaptive immune subpopulations from individuals with mild or asymptomatic SARS-CoV-2 infection (mCOVID-19) and healthy donors were immunophenotyped. A significant increase in CD28(null)CD57(+)CX3CR1(+) T cell percentages (CD4(+) [P <= .01], CD8(+) [P <= .01], and TcR gamma delta (CD4(-)CD8(-)) [P <= .001]) was found in unnvaccinated CMV-seropositive mCOVID-19 individuals stable up to 12 months after infection. This expansion did not occur in CMV-seronegative mCOVID-19 individuals or in CMV-seropositive individuals infected after SARS-CoV-2 vaccination. There were no significant differences between mCOVID-19 and aortic stenosis groups. Thus, individuals coinfected with SARS-CoV-2 and CMV have accelerated T cell senescence, which might lead to an increased risk of cardiovascular disease. In individuals infected with cytomegalovirus, proatherogenic T cells expand following mild or asymptomatic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which may lead to the development of cardiovascular disease. SARS-CoV-2 vaccination seems to prevent this phenomenon to some extent.