Clot-forming abilities of EHV-1 probed by researcher

Dr Tracy Stokol has been investigating the role of EHV-1 in triggering potentially damaging clots.
Dr Tracy Stokol has been investigating the role of EHV-1 in triggering potentially damaging clots.

An American researcher has shown the ability of equine herpes virus-1 (EHV-1) to activate blood platelets, triggering clots that can cause abortions and neurological disease.

Clinical pathologist Dr Tracy Stokol has been investigating how the virus triggers these clots.

Her work investigating the role of platelets in the mechanism of EHV-1 infection, funded by the Harry M. Zweig Memorial Fund for Equine Research, has shown that EHV-1 virus particles seem to be binding to platelets, the small cells in blood involved in clotting.

When incubated together with platelets at a ratio of one virus particle per platelet, particles of the neuropathogenic strain Ab4 and abortion-inducing strain RacL11 sparked platelet activation within 10 minutes.

Activation causes the release of P selectin, a protein that platelets use to bind to other cells, such as the cells lining blood vessels.

The viral gene product glycoprotein B was also amplified from platelets, suggesting that the virus is binding to them directly.

“We are excited to discover that EHV-1 activates platelets,” Stokol said.

“Platelets play a crucial role in thrombosis, a major cause of abortion and neurological symptoms due to EHV-1.

She said if platelets were involved in the mechanisim through which EHV-1 caused disease, the use of platelet-inhibiting medications such as Plavix or aspirin may prove useful in the treatment of infected horses.

Stokol is planning several experiments to address the many remaining questions regarding how EHV-1 activates platelets. These include projects that will determine if virus-mediated platelet activation requires other clotting proteins in blood, if the virus uses known cell receptors, such as MHCI, to bind to and then activate platelets, and if inhibitors, such as Plavix and aspirin, can prevent the virus-induced platelet activation.

She is continuing an innovative technique involving growing equine endothelial cells, which line blood vessels, in a microfluidic device to determine whether virus-activated platelets show increased binding to these cells, which could spur clotting and potentially inflammation.

Stokol is an associate professor in the Department of Population Medicine and Diagnostic Sciences within the College of Veterinary Medicine at Cornell University, New York.

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