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Review
. 2021 Jul 5:12:708665.
doi: 10.3389/fphar.2021.708665. eCollection 2021.

Targeting SARS-CoV-2-Platelet Interactions in COVID-19 and Vaccine-Related Thrombosis

Dermot Cox  1
Affiliations
Review

Targeting SARS-CoV-2-Platelet Interactions in COVID-19 and Vaccine-Related Thrombosis

Dermot Cox. Front Pharmacol. .

Abstract

It is clear that COVID-19 is more than a pneumonia and is associated with a coagulopathy and multi-organ failure. While the use of anti-coagulants does reduce the incidence of pulmonary emboli, it does not help with survival. This suggests that the coagulopathy is more likely to be platelet-driven rather than thrombin-driven. There is significant evidence to suggest that SARS-CoV-2 virions directly interact with platelets to trigger activation leading to thrombocytopenia and thrombosis. I propose a model of multiple interactions between SARS-CoV-2 and platelets that has many similarities to that with Staphylococcus aureus and Dengue virus. As platelet activation and thrombosis are major factors in poor prognosis, therapeutics that target the platelet-SARS-CoV-2 interaction have potential in treating COVID-19 and other virus infections.

Keywords: Fcgamma receptor IIA; SARS-CoV-2; bacteria; immunothrombosis; platelets; sepsis; vaccine thrombosis; virus.

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Conflict of interest statement

The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
SARS-CoV-2 spike protein binds to angiotensin converting enzyme (ACE) 2 on any cell that expresses it, which includes platelets. Other platelet receptors can also interact with SARS-CoV-2 virions. Spike protein contains the amino acid sequence RGD, which would allow it to bind to GPIIb/IIIa and it also binds to DC-SIGN. The envelope protein can bind to Toll-like receptor (TLR)-2. Anti-SARS-CoV-2 antibodies can bind to FcγRIIa. Anti-nucleoprotein antibodies can also assemble complement, which in turn binds to a complement receptor on platelets. The combination of activating all of these receptors leads to platelet activation, secretion and ultimately thrombus formation.
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