Immune dysregulation in prolonged Long-COVID: lymphocytes emerge as key mediators of persistent inflammation, exhaustion and cytotoxicity,2026,Springe

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Immune dysregulation in prolonged Long-COVID: lymphocytes emerge as key mediators of persistent inflammation, exhaustion and cytotoxicity

Springe, Marta Liva; Vaivode, Kristīne; Saksis, Rihards; Vainšeļbauma, Nineļa Miriama; Ansone, Laura; Brīvība, Monta; Niedra, Helvijs; Rovite, Vita

Abstract​

Background​

Long-COVID affects at least 10% of COVID-19 survivors, displaying debilitating symptoms across multiple organ systems.
Despite the widespread prevalence, Long-COVID aetiology remains poorly understood, but emerging evidence points to immune dysregulation as a potential mechanism involved in its development or persistence.

Methods​

This study presents a unique analysis of the peripheral blood mononuclear cell transcriptomic profile of COVID-19 and Long-COVID patients at single-cell resolution.
We reconstructed the cell state and intercellular communication using differentially expressed gene profiling and ligand–receptor interaction analyses.

Results​

Our results reveal altered T and natural killer cell subset proportions, diminished proliferating lymphocyte and B cell signalling capacity, and the expression of exhaustion and cytotoxicity associated genes 1.5–2 years post-infection, suggesting incomplete immune recovery.
Distinct interferon responses in these cell populations at the acute phase for patients who go on to develop Long-COVID indicate early disease mediator potential.

Conclusions​

Collectively, these findings provide insight into the immune processes underlying the progression of COVID-19 into a chronic Long-COVID state.
The observed changes in immune cell subsets at the acute phase of the infection may be predictive of Long-COVID progression and could be useful in understanding disease aetiology while the observed long-term effects are crucial to developing therapeutic and diagnostic tools.

Web | DOI | PDF | Journal of Translational Medicine
 
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