Penney J B, Wolinsky J S
Lab Invest. 1979 Mar;40(3):324-30.
Newborn ICR mice were infected by intracerebral inoculation of 10(5.3) LD50 of the WW strain of Theiler's virus and examined serially by virologic and ultrastructural methods. Maximal titers of 10(6) LD50 developed in the brain by day 8 when 90 per cent of the animals were dead or moribund. The virus first appeared and was most prominent in the thalamus, basal ganglia, and midbrain. It spread from these areas throughout the cortex, brainstem, and spinal cord but spared the cerebellar cortex. Both neurons and oligodendroglia were infected. Infected cells first showed dispersion of polyribosomes, accumulation of vesicles, and widening of perinuclear cisternae. Normal cytoplasmic organelles and the nucleus were displaced by an accumulation of viral crystals, membranous profiles, and fibrillar material. Within degenerating cells the nuclear chromatin became clumped and marginated and the cytoplasm was filled either with vesicles or masses of paracrystalline viral arrays. These changes were accompanied by a vigorous inflammatory response of lymphocytes, plasma cells, macrophages, neutrophils, and eosinophils. Lysis of oligodendroglia during acute infection with the WW strain of Theiler's virus may provide a stimulus for the late autoimmune demyelination that has been described in animals that survive the acute encephalitis.
新生ICR小鼠通过脑内接种10(5.3)半数致死剂量（LD50）的泰勒病毒WW株进行感染，并通过病毒学和超微结构方法进行连续检查。到第8天，当90%的动物死亡或濒死时，脑内病毒滴度达到最高10(6) LD50。病毒首先出现在丘脑、基底神经节和中脑，且最为显著。它从这些区域扩散到整个皮质、脑干和脊髓，但小脑皮质未受影响。神经元和少突胶质细胞均被感染。被感染的细胞首先表现为多核糖体分散、囊泡积聚和核周池增宽。正常的细胞质细胞器和细胞核被病毒晶体、膜性结构和纤维状物质的积聚所取代。在退化细胞内，核染色质聚集并边缘化，细胞质充满囊泡或大量副晶状病毒阵列。这些变化伴随着淋巴细胞、浆细胞、巨噬细胞、中性粒细胞和嗜酸性粒细胞的强烈炎症反应。泰勒病毒WW株急性感染期间少突胶质细胞的裂解可能为急性脑炎存活动物中描述的迟发性自身免疫性脱髓鞘提供刺激。
