Journal of translational medicine · 2026
Immune dysregulation in prolonged Long-COVID: lymphocytes emerge as key mediators of persistent inflammation, exhaustion and cytotoxicity.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Springe Marta Liva, Vaivode Kristīne, Saksis Rihards, Vainšeļbauma Nineļa Miriama, Ansone Laura, Brīvība Monta, Niedra Helvijs, Rovite Vita
Аннотация
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.
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.