Investigating the Role of Viral Proteins in COVID-19 Blood Clotting

Abstract

There have been approximately 7 million deaths and 775,522,404 infections worldwide due to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Many of the severe symptoms of COVID infection are associated with blood clot formation during infection. Post-Acute Sequel of COVID is also associated with symptoms that are hypothesized to be the result of clotting as well. Clot formation is a natural response to cellular damage within the vascular system and is facilitated by the release of a series of fiber-like structures known as Von Willebrand Factor (VWF). To prevent unnecessary clots from forming during vascular inflammation, an enzyme called ADAMTS-13 prevents the accumulation of VWF, in the absence of serious cell damage. This paper demonstrates that a viral protein capable of cleaving ADAMTS-13 may be responsible for the reduced levels of ADAMTS-13 noted in COVID-19 patients that is linked to increased clot formation during infection. Additionally, this interaction may provide insights into the rebound symptoms observed with the anti-COVID drug Paxlovid, a 3CL protease inhibitor, and provide clues to the nature of symptoms associated with, and potential diagnostic tools for long COVID.