COVID-19: Not a thrombotic disease but a thromboinflammatory disease

Area of Science:

• * Hematology and Immunology
• * Infectious Diseases
• * Pathophysiology

Background:

• * Coronavirus Disease 2019 (COVID-19), though no longer a global emergency, remains a significant health risk due to thrombotic complications.
• * Previous research suggested COVID-19 is fundamentally a thrombotic disease.
• * Understanding the full impact on the hemostatic system is crucial for managing long-term risks.

Purpose of the Study:

• * To reaffirm the hypothesis that COVID-19 is a thrombotic disease.
• * To comprehensively assess the impact of SARS-CoV-2 on the entire hemostatic system.
• * To elucidate the thromboinflammatory pathogenesis of COVID-19.

Main Methods:

• * Extensive literature review of studies on COVID-19 and the hemostatic system.
• * Analysis of data tracing the reaction process of proteins and cells involved in COVID-19 pathogenesis.
• * Assessment of viral invasion, inflammation, endothelial injury, immune responses, and thrombotic events.

Main Results:

• * SARS-CoV-2 infection enhances thrombin generation, modulated by plasma anticoagulants.
• * Elevated fibrinogen levels, platelet activation, VWF/ADAMTS-13 imbalance, and increased D-dimer contribute to "fibrinolysis shutdown."
• * COVID-19 involves ACE2-dependent viral invasion, inflammation, endothelial injury, and immune responses leading to thrombosis.

Conclusions:

• * COVID-19 is characterized by significant hemostatic system abnormalities, including enhanced coagulation and platelet activation.
• * The condition exhibits a 'fibrinolysis shutdown' phenotype, increasing thrombotic risk.
• * COVID-19 should be classified as a thromboinflammatory disorder due to the interplay between inflammation and coagulopathy.