Glaus T, Griot C, Richard A, Althaus U, Herschkowitz N, Vandevelde M
Institute of Animal Neurology, University of Berne, Switzerland.
Acta Neuropathol. 1990;80(1):59-67. doi: 10.1007/BF00294222.
To study the pathomechanism of demyelination in canine distemper (CD), dog brain cell cultures were infected with virulent A75/17-CD virus (CDV) and examined ultrastructurally. Special attention was paid to the oligodendrocytes, which were specifically immunolabelled. In addition, cerebroside sulfotransferase (CST), an enzyme specific for oligodendrocyte activity was assayed during the course of the infection. Infection and maturation as well as CDV-induced changes were found in astrocytes and brain macrophages. Infection of oligodendrocytes was rarely seen, although CST activity of the culture markedly decreased and vacuolar degeneration of these cells occurred, resulting in their complete disappearance. We concluded that the degeneration of oligodendrocytes and demyelination is not due to direct virus-oligodendrocyte interaction, but due to CDV-induced events in other glial cells.
为研究犬瘟热(CD)脱髓鞘的发病机制,用强毒A75/17 - CD病毒(CDV)感染犬脑细胞培养物并进行超微结构检查。特别关注了经特异性免疫标记的少突胶质细胞。此外,在感染过程中检测了一种少突胶质细胞活性特异性酶——脑苷脂磺基转移酶(CST)。在星形胶质细胞和脑巨噬细胞中发现了感染、成熟以及CDV诱导的变化。虽然培养物中少突胶质细胞的CST活性显著降低且这些细胞出现空泡变性并最终完全消失,但少突胶质细胞的感染却很少见。我们得出结论,少突胶质细胞的变性和脱髓鞘并非由于病毒与少突胶质细胞的直接相互作用,而是由于CDV在其他神经胶质细胞中诱导的事件所致。