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Theiler's virus infection in mice: an unusual biphasic disease process leading to demyelination.

机译:小鼠泰勒氏病毒感染:一种异常的双相性疾病,导致脱髓鞘。

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An unusual biphasic central nervous system disease developed in 3-week-old Swiss outbred mice after intracerebral inoculation of the DA strain of Theiler's murine encephalomyelitis virus. Nine to 20 days postinfection 86% of mice became paralyzed, and approximately one-half of these animals survived. During this period neuronal necrosis and microglial proliferation were seen in thalamus, brainstem, and spinal cord. There was an initial phase of virus growth in spinal cord followed by persistent infection at a lower concentration. Virus antigen was readily found in the cytoplasm of neurons by immunofluorescent staining early in the course of infection, whereas after 30 days there was a paucity of cells containing virus antigen which were present only in the spinal cord white matter. Between 1 and 5 months, an intense mononuclear inflammatory cell lesion evolved in the spinal cord leptomeninges and white matter, which coincided with a mild gait disturbance in some surviving mice, and patchy demyelination was found in areas of inflammation. The acute gray matter pathology would appear to be the result of direct virus lytic effect. Although the late white matter lesion culminating in demyelination probably represents a cytocidal infection similar to the situation that exists in certain picornavirus carrier culture systems, a virus-induced immunopathological process merits further study.
机译:脑内接种Theiler鼠脑脊髓炎病毒DA株后,在3周龄的瑞士远亲小鼠中发展出一种不寻常的双相中枢神经系统疾病。感染后9至20天,有86%的小鼠瘫痪,其中约有一半的动物存活。在此期间,丘脑,脑干和脊髓可见神经元坏死和小胶质细胞增生。脊髓中有病毒生长的初始阶段,随后以较低浓度持续感染。在感染过程的早期,通过免疫荧光染色可以很容易地在神经元细胞质中发现病毒抗原,而在30天后,只有很少的脊髓白质中含有少量的病毒抗原细胞。在1到5个月之间,脊髓软脑膜和白质中出现了强烈的单核炎性细胞病变,在一些存活的小鼠中出现了轻度步态紊乱,并且在炎症区域发现了斑状脱髓鞘。急性灰质病理似乎是病毒直接溶解作用的结果。尽管晚期白质病病变最终达到脱髓鞘,可能代表与某些小核糖核酸病毒载体培养系统中存在的情况相似的杀细胞感染,但病毒诱导的免疫病理过程值得进一步研究。

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