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Potentiation of Platelet Responses In Vitro by Feline Infectious Peritonitis Virus

Boudreaux, M. K., Weiss, R. C., Toivio-Kinnucan, M., Spano, J. S.
serotonin, blood coagulation, blood platelets, platelet aggregation
The effect of feline infectious peritonitis virus (FIPV) on platelet aggregation and ¹⁴C-serotonin release induced by threshold levels of four agonists (adenosine diphosphate [ADP], collagen, arachidonic acid, and epinephrine) was examined in vitro in ten specific-pathogen-free cats. Purified suspensions of FIPV added to stirred platelet suspensions (virus to platelet ratio equal to 1:320) 1 minute prior to the addition of agonist potentiated the ADP-induced aggregation response by greater than 100% in seven cats. Platelet ¹⁴C-serotonin release was increased by greater than 100% in four cats. Collagen-induced platelet aggregation was enhanced in ten cats while collagen-induced ¹⁴C-serotonin release was enhanced in eight cats. Potentiation of arachidonic acid-induced platelet aggregation was observed in three cats, two of which demonstrated enhanced platelet ¹⁴C-serotonin release. Although epinephrine-induced platelet aggregation was enhanced in five cats, the samples displayed only fine microaggregates. Enhanced ¹⁴C-serotonin release from platelets in response to epinephrine was not demonstrated. Interaction with the outer platelet membrane and internalization of viral particles within the surface-connected open canalicular system were demonstrated by electron microscopy within 5 minutes of the addition of virus to platelet suspensions with or without added agonists. Decreasing the virus concentration by ten- or one hundred-fold abolished the potentiating effect observed previously, while increasing the concentration tenfold resulted in direct platelet activation in the absence of agonist. Although the specific mechanism of FIPV-induced platelet responses in vitro was not established, the ability of virus to directly activate platelets and the rapid potentiation of responses observed at lower virus concentrations suggested that virus-mediated ion fluxes across platelet membranes were involved.