POTENTIATION OF PLATELET RESPONSES INVITRO BY FELINE INFECTIOUS PERITONITIS VIRUS

被引:13
作者
BOUDREAUX, MK [1 ]
WEISS, RC [1 ]
TOIVIOKINNUCAN, M [1 ]
SPANO, JS [1 ]
机构
[1] SCOTT RITCHEY RES PROGRAM,AUBURN,AL
关键词
Cat; feline infectious peritonitis virus; platelets;
D O I
10.1177/030098589002700407
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
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. © 1990, American College of Veterinary Pathologists. All rights reserved.
引用
收藏
页码:261 / 268
页数:8
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