Abstract

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.(ABSTRACT TRUNCATED AT 250 WORDS)

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call