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

Sabyasachi Chatterjee¹, Tanusree Sengupta², Samarpan Majumder³, Rinku Majumder¹

¹Department of Biochemistry and Molecular Biology, LSU Health Science Center, New Orleans, LA 70112, USA
²Department of Chemistry, Sri Sivasubramaniya Nadar College of Engineering, Tamilnadu, India
³Department of Genetics, LSU Health Science Center, New Orleans, LA 70112, USA

* Equal contribution

Received: June 9, 2020Accepted: July 21, 2020Published: August 19, 2020

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.

Abstract

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.