COVID-19 Research Paper Volume 12, Issue 16 pp 15954—15961
COVID-19: a probable role of the anticoagulant Protein S in managing COVID-19-associated coagulopathy
- 1 Department of Biochemistry and Molecular Biology, LSU Health Science Center, New Orleans, LA 70112, USA
- 2 Department of Chemistry, Sri Sivasubramaniya Nadar College of Engineering, Tamilnadu, India
- 3 Department of Genetics, LSU Health Science Center, New Orleans, LA 70112, USA
Received: June 9, 2020 Accepted: July 21, 2020 Published: August 19, 2020https://doi.org/10.18632/aging.103869
How to Cite
Copyright © 2020 Chatterjee et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The COVID-19 pandemic has caused monumental mortality, and there are still no adequate therapies. Most severely ill COVID-19 patients manifest a hyperactivated immune response, instigated by interleukin 6 (IL6) that triggers a so called “cytokine storm” and coagulopathy. Hypoxia is also associated with COVID-19. So far overlooked is the fact that both IL6 and hypoxia depress the abundance of a key anticoagulant, Protein S. We speculate that the IL6-driven cytokine explosion plus hypoxemia causes a severe drop in Protein S level that exacerbates the thrombotic risk in COVID-19 patients. Here we highlight a mechanism by which the IL6-hypoxia curse causes a deadly hypercoagulable state in COVID-19 patients, and we suggest a path to therapy.