Publication date: May 19, 2025
In this study, we tested the hypothesis that the immunosenescence profile could account for the disproportional susceptibility of the elderly to severe forms of COVID-19. The immunological profiles of volunteers residing in endemic and non-endemic areas for chronic infectious diseases were analyzed at the early stage of SARS-CoV-2 infection. A unique signature of inflammatory plasma mediators was identified in COVID-19 volunteers when compared to individuals with other flu-like syndromes. COVID-19 severity correlated with high levels of inflammatory mediators; among them, CXCL9, a serum marker of aging. Patients who progressed to hospitalization displayed high frequencies of CD8 and CD4 T cells expressing exhaustion and senescence markers and showed reduced and more mature B cell repertoires, which are typical of senescence. They also had an acceleration of epigenetic age measured by DNA methylation. Therefore, severe COVID-19 correlated with phenotypic, functional, and epigenetic features of accelerated immunosenescence at the onset of infection.
| Concepts | Keywords |
|---|---|
| Cd4 | COVID‐19 |
| Hospitalization | epigenetic clock |
| Inflammatory | immunoglobulin repertoire |
| Serum | immunosenescence |
| Volunteers | inflammaging |
| T cell exhaustion | |
| T cell senescence |
Semantics
| Type | Source | Name |
|---|---|---|
| disease | IDO | susceptibility |
| disease | MESH | COVID-19 |
| disease | MESH | infectious diseases |
| pathway | REACTOME | SARS-CoV-2 Infection |
| disease | MESH | syndromes |
| disease | IDO | cell |
| pathway | REACTOME | DNA methylation |
| disease | MESH | infection |
| disease | MESH | T cell exhaustion |