Science (New York, N.Y.) · 2024
Persistent complement dysregulation with signs of thromboinflammation in active Long Covid.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
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Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Cervia-Hasler Carlo, Brüningk Sarah C, Hoch Tobias, Fan Bowen, Muzio Giulia, Thompson Ryan C, Ceglarek Laura, Meledin Roman, Westermann Patrick, Emmenegger Marc, Taeschler Patrick, Zurbuchen Yves, Pons Michele, Menges Dominik, Ballouz Tala, Cervia-Hasler Sara, Adamo Sarah, Merad Miriam, Charney Alexander W, Puhan Milo, Brodin Petter, Nilsson Jakob, Aguzzi Adriano, Raeber Miro E, Messner Christoph B, Beckmann Noam D, Borgwardt Karsten, Boyman Onur
Аннотация
Long Covid is a debilitating condition of unknown etiology. We performed multimodal proteomics analyses of blood serum from COVID-19 patients followed up to 12 months after confirmed severe acute respiratory syndrome coronavirus 2 infection. Analysis of >6500 proteins in 268 longitudinal samples revealed dysregulated activation of the complement system, an innate immune protection and homeostasis mechanism, in individuals experiencing Long Covid. Thus, active Long Covid was characterized by terminal complement system dysregulation and ongoing activation of the alternative and classical complement pathways, the latter associated with increased antibody titers against several herpesviruses possibly stimulating this pathway. Moreover, markers of hemolysis, tissue injury, platelet activation, and monocyte-platelet aggregates were increased in Long Covid. Machine learning confirmed complement and thromboinflammatory proteins as top biomarkers, warranting diagnostic and therapeutic interrogation of these systems.