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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.
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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.
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Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
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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...
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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
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A Simple Double Centrifugation Tube Method to Obtain Platelet-rich Plasma from Equine Blood
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Equid herpesvirus type 1 activates platelets.

Tracy Stokol1, Wee Ming Yeo1, Deborah Burnett1

  • 1Department of Population Medicine and Diagnostic Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, United States of America.

Plos One
|April 24, 2015
PubMed
Summary

Equid herpesvirus type 1 (EHV-1) activates equine platelets, contributing to thrombosis in horses. This virus-induced platelet activation involves tissue factor and thrombin generation, impacting hemostasis.

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Area of Science:

  • Veterinary Virology
  • Hemostasis and Thrombosis
  • Equine Infectious Diseases

Background:

  • Equid herpesvirus type 1 (EHV-1) causes significant abortion and neurological disease in horses.
  • Thrombosis in placental and spinal cord vessels is a key factor in EHV-1-associated clinical syndromes.
  • The precise mechanism of thrombus formation in EHV-1 infections remains unclear, despite platelets' role in thrombin generation.

Purpose of the Study:

  • To investigate the hypothesis that EHV-1 directly activates equine platelets.
  • To elucidate the mechanisms by which EHV-1 induces platelet activation and associated hemostatic changes.

Main Methods:

  • Assessing platelet activation markers (P-selectin expression, microvesiculation) upon exposure to EHV-1 strains (RacL11, Ab4).
  • Utilizing factor VII- and X-deficient human plasma to determine the role of the extrinsic coagulation pathway.
  • Investigating the involvement of tissue factor and thrombin in EHV-1-induced platelet responses.
  • Examining the impact of a glycoprotein C-deficient EHV-1 mutant and anti-tissue factor antibodies on platelet activation.

Main Results:

  • EHV-1 strains RacL11 and Ab4 activated platelets within 10 minutes, inducing α-granule secretion and microvesiculation.
  • Virus-induced P-selectin expression and microvesiculation were dependent on plasma, calcium, factor VII, and factor X.
  • Platelet activation was mediated by virus-associated tissue factor triggering factor X activation and thrombin generation.
  • Microvesiculation was only partially dependent on tissue factor and thrombin, suggesting additional virus-induced mechanisms.

Conclusions:

  • EHV-1 activates equine platelets, with α-granule secretion linked to tissue factor-initiated thrombin generation.
  • The findings reveal a novel mechanism of virus-induced hemostasis activation.
  • EHV-1-induced platelet activation likely contributes to thrombosis observed in infected horses.