Baumgärtner W, Krakowka S, Durchfeld B
Department of Veterinary Pathobiology, College of Veterinary Medicine, Ohio State University, Columbus.
Vet Pathol. 1991 Jul;28(4):324-31. doi: 10.1177/030098589102800409.
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.
对两株犬副流感病毒(CPIV)的体内和体外特性进行了研究。其中一株命名为CPIV(+),在体外可诱导多核巨细胞形成和细胞溶解,而另一株CPIV(-)仅引起轻微的条索状细胞病变效应,伴有少量小多核巨细胞。通过免疫荧光染色测定,感染CPIV(+)或CPIV(-)的Vero细胞CPIV抗原均呈100%阳性;然而,100%的CPIV(+)感染细胞和不到10%的CPIV(-)感染细胞血吸附呈阳性。十二烷基硫酸钠-聚丙烯酰胺凝胶电泳分析显示,两株病毒的病毒多肽电泳迁移率无差异;然而,在CPIV(-)中,观察到假定的HN和F1蛋白合成减少或缺失。CPIV(+)子代病毒粒子的等密度分离显示,大量病毒粒子的浮力密度为1.18 g/cm3。相比之下,CPIV(-)子代病毒粒子的密度分布不均一,范围为1.08至1.18 g/cm3。用CPIV(+)对6只雪貂进行脑内感染,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。免疫组织化学检查显示,CPIV(+)感染的雪貂脑室室管膜衬里细胞中CPIV抗原显著,而CPIV(-)感染的雪貂中CPIV抗原减少或缺乏(n = 6)。假注射的雪貂(n = 6)没有组织学病变,也未鉴定出病毒抗原。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在体内毒力的改变。