研究人员对确诊感染严重急性呼吸系统综合征冠状病毒2后随访长达12个月的COVID-19患者的血清，进行了多模式蛋白质组学分析。对268份纵向样本中超过6500个蛋白质的分析表明，长新冠患者的补体系统激活失调，而补体系统是一种先天性免疫保护和平衡机制。因此，活跃性长新冠的特征是末端补体系统失调以及替代和经典补体途径的持续激活，后者与针对几种疱疹病毒的抗体滴度升高有关，可能刺激了这一途径。
此外，溶血、组织损伤、血小板活化和单核细胞-血小板聚集等指标在长新冠中也有所增加。机器学习证实补体和血栓炎症蛋白是最重要的生物标记物，因此有必要对这些系统进行诊断和治疗检查。
据悉，长新冠是一种病因不明的衰弱病症。
附：英文原文
Title: Persistent complement dysregulation with signs of thromboinflammation in active Long Covid
Author: Carlo Cervia-Hasler, Sarah C. Brüningk, Tobias Hoch, Bowen Fan, Giulia Muzio, Ryan C. Thompson, Laura Ceglarek, Roman Meledin, Patrick Westermann, Marc Emmenegger, Patrick Taeschler, Yves Zurbuchen, Michele Pons, Dominik Menges, Tala Ballouz, Sara Cervia-Hasler, Sarah Adamo, Miriam Merad, Alexander W. Charney, Milo Puhan, Petter Brodin, Jakob Nilsson, Adriano Aguzzi, Miro E. Raeber, Christoph B. Messner, Noam D. Beckmann, Karsten Borgwardt, Onur Boyman
Issue&Volume: 2024-01-19
Abstract: 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.
DOI: adg7942
Source: https://www.science.org/doi/10.1126/science.adg7942