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Demyelination in mice resulting from infection with a mutant of Semliki Forest virus

机译:感染Semliki Forest病毒突变体的小鼠脱髓鞘

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摘要

Twelve of 34 weanling mice (35%) developed lesions in the brain and spinal cord following i.p. infection with 10 p.f.u. of a mutant of Semliki Forest virus (SFV). Six of 12 mice examined 13 days post infection (p.i.) showed meningo-encephalomyelitis with focal spongiform lesions in the grey and white matter. The spongiform lesions were characterised by necrosis of putative oligodendrocytes, myelinic vacuolation and mononuclear cell infiltration. Only one of six mice examined 21 days p.i. and one of six mice examined 28 days p.i. showed lesions which comprised reactive and dystrophic changes in the white matter. Spongiform lesions and pycnotic nuclei were not seen at these times. Viral nucleocapsids were seen in the early stages of the disease in putative necrotic oligodendrocytes. Mature virus particles were not seen. This was in contrast to mice infected with virulent wild-type SFV when lesions were more severe and were accompanied by large numbers of immature and mature virus particles. It is suggested that the demyelination in mice infected with mutant SFV results primarily from selective destruction of oligodendrocytes by the mutant virus.
机译:腹腔内麻醉后,有12只(34%)断奶小鼠(12%)出现了大脑和脊髓损伤。感染10 p.f.u.姆利基森林病毒(SFV)的突变体。感染后第13天检查的12只小鼠中有6只(p.i.)显示脑膜脑脊髓炎,灰白色物质中有局灶性海绵状病变。海绵状病变的特征是假定的少突胶质细胞坏死,髓鞘空泡化和单核细胞浸润。六只小鼠中只有一只在下午21天检查。和六只小鼠中的一只在p.i.下午28天检查。显示出包括在白质中反应性和营养不良变化的病变。在这些时间未见海绵状病变和幽门核。在疾病的早期阶段,在假定的坏死少突胶质细胞中发现了病毒核衣壳。没有看到成熟的病毒颗粒。这与感染了严重野生型SFV且病变更为严重并伴有大量未成熟和成熟病毒颗粒的小鼠相反。提示感染SFV突变小鼠的脱髓鞘主要是由突变病毒选择性破坏少突胶质细胞引起的。

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