Zurbriggen A, Vandevelde M, Dumas M
Lab Invest. 1986 Apr;54(4):424-31.
To study the pathogenesis of demyelination in canine distemper virus (CDV) infection, primary canine brain cell cultures were infected with CDV to examine specific virus-induced glial cell changes. Cultures were harvested at regular intervals after inoculation and were immunostained for the specific demonstration of astrocytes, oligodendrocytes, and CDV antigen. The infection spread slowly with moderate cytolysis and cell fusion. Soon after inoculation, infection of astrocytes was found by means of double immunofluorescent labeling. One week after inoculation, CDV-induced astrocytic fusion and rearrangement of astroglial fibrils became apparent. The astrocytic changes progressed during the observation period. Double immunofluorescent labeling failed to show oligodendroglial infection. Despite clear absence of viral replication within oligodendrocytes at all stages of the experiment, these cells exhibited marked pathologic changes starting at about 20 days after inoculation and progressed to complete cytolysis within 10 days. The degeneration of the oligodendrocytes was thought to be secondary to CDV-induced changes in other cell types of the culture probably through the release of toxic factors in the tissue culture medium. Since little evidence has been found for oligodendroglial infection in demyelinating lesions in canine distemper in vivo, the present tissue culture findings suggest that demyelination in vivo could be the result of indirect oligodendroglial damage caused by CDV-induced changes in other cell types such as astrocytes.
为研究犬瘟热病毒(CDV)感染时脱髓鞘的发病机制,用CDV感染原代犬脑细胞培养物,以检测病毒诱导的特定神经胶质细胞变化。接种后定期收获培养物,并进行免疫染色,以特异性显示星形胶质细胞、少突胶质细胞和CDV抗原。感染传播缓慢,伴有中度细胞溶解和细胞融合。接种后不久,通过双重免疫荧光标记发现星形胶质细胞被感染。接种后一周,CDV诱导的星形胶质细胞融合和星形胶质纤维重排变得明显。在观察期内,星形胶质细胞变化不断进展。双重免疫荧光标记未显示少突胶质细胞感染。尽管在实验的各个阶段少突胶质细胞内均未发现病毒复制,但这些细胞在接种后约20天开始出现明显的病理变化,并在10天内进展为完全细胞溶解。少突胶质细胞的变性被认为可能是由于培养物中其他细胞类型的CDV诱导变化继发所致,可能是通过组织培养基中释放的毒性因子。由于在犬瘟热脱髓鞘病变的体内研究中,几乎没有证据表明少突胶质细胞被感染,因此目前的组织培养结果表明,体内脱髓鞘可能是CDV诱导的其他细胞类型(如星形胶质细胞)变化导致少突胶质细胞间接损伤的结果。