Background: Following myocardial infarction (MI), T cells play a central role in regulating local inflammation and repair. Common viral infections critically impact tissue immunity and can therefore indirectly impact myocardial inflammation. Emerging evidence has shown that previous exposure to cytomegalovirus (CMV) can impact cardiovascular risk and post-MI outcomes, but the mechanism underlying this association remains poorly understood. The aim of this study was to gain further insights how chronic CMV infection influences T cell dynamics in patients with MI.
Methods: To investigate this possible connection, we monitored the CMV serostatus of MI patients previously recruited in the frame of the Cardiac Antigens in Myocardial Infarction (CAMI) study using specific ELISA. After stratifying the MI patients according to their CMV serostatus, T cells present in peripheral blood samples obtained from CMV-seropositive MI and control patients were immunophenotyped using a spectral flow cytometer and CMV-specific HLA multimers.
Results: Comparison of CMV-seropositive MI with control patients revealed an altered global CD8+ T cell immune profile, marked by downregulation of the activation markers CD69 and fraktalkine receptor (CX3CR1). Furthermore, the frequencies of effector memory and central memory CD8+ T cells were reduced in MI patients compared with controls, suggesting rapid redistribution of these cells. Most importantly, the frequency of circulating CMV-specific CD8+ T cells were decreased in MI seropositive patients, compared to age-matched CMV+ control patients with no MI
Conclusion: Taken together, these observations indicate a possible crosstalk between virus-specific and post-MI CD8+ T cell responses in CMV-seropositive MI patients, marked by reduced frequencies of circulating virus-specific and effector cells in MI patients. This supports the need for future studies designed to assess whether CMV‑specific CD8+ T cells readily infiltrate the infarcted myocardium and whether they could impact in situ inflammatory mechanisms.
