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Increased histone-DNA complexes and endothelial-dependent thrombin generation in severe COVID-19
Beth A Bouchard1, Christos Colovos2, Michael A Lawson2
1Department of Biochemistry, University of Vermont, Burlington, VT, USA.
Vascular Pharmacology
|December 6, 2021
Summary
Severe COVID-19 coagulopathy involves elevated histones and altered thrombin generation, particularly with endothelial cells. This impacts fibrin structure, contributing to clotting issues in patients.
Area of Science:
- Hematology
- Infectious Diseases
- Critical Care Medicine
Background:
- Coagulopathy is a frequent complication of severe COVID-19, but its underlying mechanisms remain unclear.
- Understanding the role of SARS-CoV-2 in hemostatic alterations is crucial for patient management.
Purpose of the Study:
- To investigate the impact of SARS-CoV-2 infection on histone levels, fibrin structure, and endogenous thrombin potential.
- To compare thrombin generation in COVID-19 patients versus healthy controls, with and without endothelial cells.
Main Methods:
- Analysis of plasma from COVID-19 patients with ARDS and healthy controls.
- Measurement of histone-DNA complexes and assessment of thrombin generation using calibrated automated thrombography.
- Evaluation of fibrin clot structure and resolvability.
Main Results:
- COVID-19 patients exhibited elevated circulating histone-DNA complexes compared to controls.
- Thrombin generation was altered, with increased endogenous thrombin potential but prolonged lag times in the presence of tissue factor.
- Plasma from COVID-19 patients generated significant thrombin on endothelial cells, unlike controls, and formed denser fibrin clots.
Conclusions:
- Elevated histones, abnormal fibrin formation, and enhanced endothelial-dependent thrombin generation are implicated in COVID-19 coagulopathy.
- These findings highlight the critical role of endothelial cells in SARS-CoV-2-associated hemostatic dysregulation.
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