Platelet Dysregulation in the Pathobiology of COVID-19

Rebecca A Mellema1, Jacob Crandell2, Aaron C Petrey1,2

  • 1Division of Microbiology and Immunology, Department of Pathology, University of Utah, Salt Lake City, Utah, United States.

Hamostaseologie
|December 8, 2021
PubMed

Insights

Severe COVID-19 involves thromboinflammation, with platelet alterations significantly impacting disease severity and outcomes. This review details these platelet changes and their role in COVID-19 pathobiology.

Area of Science:

  • Immunology
  • Hematology
  • Infectious Diseases

Background:

  • Coronavirus disease 2019 (COVID-19) presents with diverse clinical manifestations, often including hyperinflammation and thrombotic events in severe cases.
  • COVID-19 is recognized as a thromboinflammatory disease, with coagulation and platelet abnormalities linked to mortality.
  • Platelets, beyond hemostasis, play crucial roles in immune response regulation through various secreted and cell-surface molecules.

Purpose of the Study:

  • To review current knowledge on platelet alterations in COVID-19.
  • To elucidate the impact of these platelet changes on COVID-19 pathobiology.

Main Methods:

  • Literature review of studies investigating platelet function and characteristics in COVID-19 patients.
  • Synthesis of findings on platelet count, activation, aggregation, and their molecular mediators.

Main Results:

  • Significant alterations in platelet count and function are observed in COVID-19 patients.
  • Platelet activation and prothrombotic potential are heightened, contributing to microvascular and macrovascular thrombi.
  • Platelet-derived inflammatory mediators exacerbate hyperinflammation and multi-organ dysfunction.

Conclusions:

  • Platelet alterations are central to the thromboinflammatory state in severe COVID-19.
  • Understanding these platelet changes is critical for developing targeted therapies to improve clinical outcomes.

Related Concept Videos

Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
2.1K
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
7.7K
Disorders of Hemostasis01:24

Disorders of Hemostasis

Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
1.3K
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
1.0K
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
734