Dysregulation of homeostatic cytokine receptors drives prolonged T cell activation following acute SARS-CoV-2 infection in humans.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 41310351.
- Also identified by DOI 10.1038/s41467-025-66753-1 and PMC identifier 12748759.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Acute viral infections are usually cleared by an efficient anti-pathogen immune response, following which immune homeostasis is restored. Occasionally, such pathogen-induced immune response fails to abate despite clinical recovery, but how this occurs in humans has not been thoroughly investigated. Here, we perform a detailed analysis of T cell homeostasis following severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, which reveals persistent activation and dyshomeostasis of CD4<sup>+</sup> and CD8<sup>+</sup> T cells for 6-12 months after acute infection. Compared to steady-state and unlike T cell responses following vaccination, interleukin (IL)-2 receptor and IL-7 receptor expression remains altered on both SARS-CoV-2-specific and bystander T cells for 6-12 months after acute infection. These alterations correlate with increased IL-7 and IL-15 serum levels and are reproduced by in vitro stimulation by IL-7 and IL-15, but surprisingly not by IL-2. Collectively, our study demonstrates prolonged T cell dyshomeostasis driven by dysregulated homeostatic cytokine signals following acute viral infection.
Medical subject headings
- COVID-19
- SARS-CoV-2
- Lymphocyte Activation
- CD8-Positive T-Lymphocytes
- CD4-Positive T-Lymphocytes
- Receptors, Cytokine