Sheahan B J, Barrett P N, Atkins G J
Acta Neuropathol. 1981;53(2):129-36. doi: 10.1007/BF00689993.
Twelve of 34 weanling mice (35%) developed lesions in the brain and spinal cord following i.p. infection with 10(2) 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.
34只断奶小鼠中有12只(35%)经腹腔注射10² 个空斑形成单位(p.f.u.)的塞姆利基森林病毒(SFV)突变体后,在脑和脊髓出现病变。感染后13天(p.i.)检查的12只小鼠中有6只出现脑膜脑脊髓炎,在灰质和白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。感染后21天检查的6只小鼠中只有1只,感染后28天检查的6只小鼠中也只有1只出现病变,病变包括白质中的反应性和营养不良性改变。此时未见到海绵状病变和固缩核。在疾病早期,在假定坏死的少突胶质细胞中可见病毒核衣壳。未见到成熟病毒颗粒。这与感染强毒野生型SFV的小鼠形成对比,后者的病变更严重,且伴有大量未成熟和成熟病毒颗粒。提示感染突变体SFV的小鼠脱髓鞘主要是由突变病毒对少突胶质细胞的选择性破坏所致。