INVITRO CYTOPATHOGENICITY AND INVIVO VIRULENCE OF 2 STRAINS OF CANINE PARAINFLUENZA VIRUS
INVITRO CYTOPATHOGENICITY AND INVIVO VIRULENCE OF 2 STRAINS OF CANINE PARAINFLUENZA VIRUS
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DOI：
10.1177/030098589102800409
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发表时间：
1991-07-01
影响因子：
2.4
通讯作者：
DURCHFELD, B
中科院分区：
文献类型：
--
作者：
BAUMGARTNER, W;KRAKOWKA, S;DURCHFELD, B
研究了两种犬副流感病毒（CPIV）毒株的体内和体外特性。 一种菌株，命名为 CPIV(+)，在体外诱导合胞体巨细胞形成和细胞溶解，而第二种菌株，CPIV(-)，仅引起轻微的链形成细胞病变效应，具有少量的小合胞体巨细胞。 免疫荧光染色测定感染CPIV(+)或CPIV(-)的Vero细胞CPIV抗原100%阳性；然而，100% 的 CPIV(+) 和不到 10% 的 CPIV(-) 感染细胞呈血吸附阳性。 十二烷基硫酸钠-聚丙烯酰胺凝胶电泳分析显示，两种毒株之间病毒多肽的电泳迁移率没有差异；然而，在 CPIV(-) 中，观察到假定的 HN 和 F1 蛋白的合成减少或缺失。 CPIV(+) 子代病毒颗粒的等密度分离显示出高比例的病毒颗粒，浮力密度为 1.18 g/cm3。 相比之下，CPIV(-) 子代病毒体的密度分布不均匀，范围为 1.08 至 1.18 g/cm3。 六只雪貂脑内感染 CPIV(+) 导致中度淋巴细胞性和组织细胞性脉络膜炎、脑膜炎和室管膜炎，而 CPIV(-) 感染仅引起轻度至中度炎症。 免疫组织学上，CPIV 抗原在 CPIV(+) 感染的雪貂心室室管膜衬里细胞中突出，而在 CPIV(-) 感染的雪貂中减少或缺乏 (n = 6)。 假注射的雪貂（n = 6）没有组织学病变，也没有鉴定出病毒抗原。 目前的研究结果表明，CPIV 糖蛋白活性的某些变化可能导致 CPIV 体内毒力的改变。
In vivo and in vitro properties of two strains of canine parainfluenza virus (CPIV) were investigated. One strain, designated CPIV(+), induced syncytial giant cell formation and cytolysis in vitro, whereas the second strain, CPIV(-), caused only a mild strand-forming cytopathic effect with few, small syncytial giant cells. Vero cells infected with CPIV(+) or CPIV(-) were 100% positive for CPIV antigen as determined by immunofluorescent staining; however, 100% of CPIV(+) and less than 10% of CPIV(-) infected cells were hemadsorption positive. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis analysis revealed no differences in electrophoretic mobility of viral polypeptides between both strains; however, in CPIV(-), reduced or absent synthesis of the putative HN and F1 proteins was observed. Isopycnic separation of CPIV(+) progeny virions showed a high proportion of viral particles with a buoyant density of 1.18 g/cm3. In contrast, CPIV(-) progeny virions had a heterogeneous density profile ranging from 1.08 to 1.18 g/cm3. Intracerebral infection of six ferrets with CPIV(+) resulted in moderate lymphocytic and histiocytic choroiditis, meningitis, and ependymitis, whereas CPIV(-) infection caused only mild to moderate inflammation. Immunohistologically, CPIV antigen was prominent in ependymal lining cells of the ventricles in CPIV(+)-infected ferrets and was reduced or lacking in CPIV(-)-infected ferrets (n = 6). Sham-injected ferrets (n = 6) did not have histologic lesions and no viral antigen was identified. The present findings suggest that certain changes in the activities of CPIV glycoproteins may lead to alterations of CPIV virulence in vivo.