Persistent complement dysregulation with signs of thromboinflammation in active Long Covid.

Persistent complement dysregulation with signs of thromboinflammation in active Long Covid.

Publication date: Jan 19, 2024

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.

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Concepts Keywords
Classical Activation
Debilitating Active
Hemolysis Complement
Herpesviruses Condition
Months Confirmed
Covid
Debilitating
Dysregulation
Increased
Long
Persistent
Platelet
Signs
System
Thromboinflammation

Semantics

Type Source Name
disease MESH thromboinflammation
disease MESH Long Covid
disease MESH etiology
disease MESH COVID-19
disease MESH hemolysis
pathway KEGG Platelet activation

Original Article

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