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犬瘟热病毒感染体外培养中的少突胶质细胞病理学

Oligodendroglial pathology in canine distemper virus infection in vitro.

作者信息

Zurbriggen A, Vandevelde M, Dumas M, Griot C, Bollo E

机构信息

Institute of Animal Neurology, University of Berne, Switzerland.

出版信息

Acta Neuropathol. 1987;74(4):366-73. doi: 10.1007/BF00687214.

DOI:10.1007/BF00687214
PMID:3687388
Abstract

Dog brain cell cultures were infected with different canine distemper virus (CDV) strains to study the oligodendrocytes, which were characterized with eight different antibodies to cover the whole oligodendroglial population in the culture. A few weeks after infection all oligodendroglial cell types started to degenerate and disappeared from the culture. However, since no CDV protein could be demonstrated in the degenerating oligodendrocytes with extensive double-labelling studies, this lesion can not be explained as being a result of cytolytic infection. This conclusion was further supported in experiments with plaque-forming CDV, in which viral replication is restricted to the cytolytic areas only; oligodendrocytes also degenerated in virus-free areas between the plaques. The hypothesis of toxic factors released by other infected cell types in the culture leading to secondary damage of the oligodendrocyte could not be confirmed by transferring supernatants from infected to normal cultures. Whereas the presence of toxic factors can not be completely excluded, the possibility of an abortive infection of the oligodendrocytes with no or very limited viral protein synthesis is discussed.

摘要

用不同的犬瘟热病毒(CDV)毒株感染犬脑细胞培养物,以研究少突胶质细胞,用八种不同抗体对其进行表征,以覆盖培养物中的整个少突胶质细胞群体。感染后几周,所有少突胶质细胞类型开始退化并从培养物中消失。然而,由于通过广泛的双重标记研究在退化的少突胶质细胞中未检测到CDV蛋白,因此不能将这种损伤解释为细胞溶解性感染的结果。在形成蚀斑的CDV实验中进一步支持了这一结论,其中病毒复制仅局限于细胞溶解性区域;蚀斑之间的无病毒区域中的少突胶质细胞也发生了退化。将感染培养物的上清液转移到正常培养物中,未能证实培养物中其他受感染细胞类型释放有毒因子导致少突胶质细胞继发性损伤的假说。虽然不能完全排除有毒因子的存在,但讨论了少突胶质细胞发生流产感染且病毒蛋白合成极少或没有的可能性。

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本文引用的文献

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Primary demyelination in experimental canine distemper virus induced encephalomyelitis in gnotobiotic dogs. Sequential immunologic and morphologic findings.无菌犬实验性犬瘟热病毒诱导脑脊髓炎中的原发性脱髓鞘。连续的免疫学和形态学发现。
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Antibody-induced generation of reactive oxygen radicals by brain macrophages in canine distemper encephalitis: a mechanism for bystander demyelination.犬瘟热脑炎中脑巨噬细胞抗体诱导的活性氧自由基生成:旁观者脱髓鞘的一种机制
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Ultrastructural and biochemical findings in brain cell cultures infected with canine distemper virus.感染犬瘟热病毒的脑细胞培养物的超微结构和生化研究结果
Acta Neuropathol. 1990;80(1):59-67. doi: 10.1007/BF00294222.
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Glia. 1991;4(4):408-16. doi: 10.1002/glia.440040409.
新生犬脑源性混合神经胶质细胞培养物的形态学和免疫细胞化学特征
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Myelin-associated glycoprotein is produced before myelin basic protein in cultured oligodendrocytes.在培养的少突胶质细胞中,髓鞘相关糖蛋白比髓鞘碱性蛋白产生得早。
J Neuroimmunol. 1984 Feb;6(1):41-9. doi: 10.1016/0165-5728(84)90041-9.
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IgM in a human neuropathy related to paraproteinemia binds to a carbohydrate determinant in the myelin-associated glycoprotein and to a ganglioside.与副蛋白血症相关的人类神经病变中的IgM与髓鞘相关糖蛋白中的碳水化合物决定簇以及一种神经节苷脂结合。
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Demyelinating lesions due to Theiler's virus are associated with ongoing central nervous system infection.由泰勒氏病毒引起的脱髓鞘病变与中枢神经系统持续感染有关。
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