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COVID-19: A collision of complement, coagulation and inflammatory pathways.
Anoop J Chauhan1,2,3, Laura J Wiffen1,3, Thomas P Brown1,3
1Research and Innovation, Queen Alexandra Hospital, Portsmouth, UK.
Journal of Thrombosis and Haemostasis : JTH
|July 2, 2020
Summary
COVID-19 causes inflammation and clotting by activating the complement system, particularly C5a. Blocking C5a may treat severe COVID-19 by reducing harmful inflammatory responses and organ damage.
Area of Science:
- Immunology
- Pathophysiology
- Virology
Background:
- COVID-19 presents with hypercoagulability and inflammation, potentially involving the complement system.
- Similarities to atypical hemolytic uremic syndrome (aHUS) suggest complement pathway involvement in COVID-19 pathogenesis.
Purpose of the Study:
- To review the role of the complement pathway, specifically C5a, in severe viral infections like COVID-19.
- To explore C5a as a potential therapeutic target for COVID-19 treatment.
Main Methods:
- Literature review focusing on the complement system's role in COVID-19 pathophysiology.
- Analysis of C5a's function in inflammation, coagulation, and organ injury.
Main Results:
- C5a drives a cytokine storm, leading to lung injury, immune exhaustion, and a pro-coagulant state.
- Complement activation and microvascular thrombi are evident in fatal COVID-19 cases, particularly in the lungs and kidneys.
Conclusions:
- Aberrations in the complement pathway, especially C5a, are implicated in severe COVID-19.
- C5 blockade shows promise as a therapeutic strategy, supported by animal studies and aHUS treatment data.
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