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大鼠长期冠状病毒感染诱发的脱髓鞘性脑脊髓炎。初步报告。

Demyelinating encephalomyelitis induced by a long-term corona virus infection in rats. A preliminary report.

作者信息

Nagashima K, Wege H, Meyermann R, ter Meulen V

出版信息

Acta Neuropathol. 1979 Mar 15;45(3):205-13. doi: 10.1007/BF00702672.

Abstract

About 30% of weanling rats inoculated with JHM virus developed a subacute demyelinating encephalomyelitis (SDE) 3 weeks after inoculation (a.i.). From the remaining animals, 5% displayed overt neurological signs 3, 6, and 8 months a.i. Animals with and without clinical signs 6-8 months a.i. were morphologically examined. Fresh demyelinating lesions could be demonstrated in paralyzed animals. Viral antigen was demonstrated and infectious JHM virus could be recovered from one animal which developed clinical signs at 3 months a.i. In one animal with clinical onset of 8 months a.i. completely remyelinated areas as well as recent demyelinating lesions were observed, suggesting a recurrence of the disease process. Remyelinated areas were also found in 40% of clinically silent animals. The morphology of the late onset of the demyelination was similar to that occurring in SDE. Remyelination consisted of both CNS and PNS-type. This animal model offers the possibility to investigate the virus-host relationship which is responsible for the induction of a demyelinating process after a long incubation period.

摘要

接种JHM病毒的断奶大鼠中,约30%在接种后3周(接种后)出现亚急性脱髓鞘性脑脊髓炎(SDE)。在其余动物中,5%在接种后3、6和8个月出现明显的神经学症状。对接种后6 - 8个月有和没有临床症状的动物进行了形态学检查。在瘫痪动物中可发现新鲜的脱髓鞘病变。在接种后3个月出现临床症状的一只动物中证实了病毒抗原,并从中分离出了具有传染性的JHM病毒。在一只接种后8个月出现临床症状的动物中,观察到了完全再髓鞘化区域以及近期的脱髓鞘病变,提示疾病过程复发。在40%无临床症状的动物中也发现了再髓鞘化区域。迟发性脱髓鞘的形态与SDE中出现的相似。再髓鞘化包括中枢神经系统和外周神经系统类型。该动物模型为研究病毒 - 宿主关系提供了可能性,这种关系在长时间潜伏期后负责诱导脱髓鞘过程。

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