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由副流感I(6/94)病毒引起的乳鼠实验性全脑炎。III. 超微结构研究。

Experimental panencephalitis induced in suckling mice by parainfluenza I (6/94) virus. III. Ultrastructural studies.

作者信息

Wolinsky J S, Gilden D H, Rorke L B

出版信息

J Neuropathol Exp Neurol. 1976 May;35(3):271-86. doi: 10.1097/00005072-197605000-00005.

Abstract

Intracerebral inoculation of newborn mice with Parainfluenza I (6/94) virus produces a chronic panencephalitis. Electron microscopic studies were carried out over 125 days of the infection. Productive infection of choroidal and ependymal epithelial cells was seen from postinoculation days 2nd to the 8th. Fusion of adjacent choroid and ependymal cells resulted in giant cell formation. Completed virions were seen adsorbed to circulating macrophages and these cells replicated intracytoplasmic nucleocapsids. Neuronal infection was evident on the 3rd postinoculation day, was widespread by the 6th day postinoculation and persisted to the 35th day postinoculation. Nucleocapsid alignment and budding from neuronal plasma membranes was never seen. An initially intense mononuclear cell infiltrate subsided by the 35th day but residual inflammation persisted throughout the study. Late in the course of the infection, vacuolation of the neuropil and a periventricular and deep cerebral spongiform change was seen which could not be directly associated with local viral replication. These ultrastructural findings are correlated with prior light microscopic, virological and immunofluorescent studies of the infection and compared to other experimental models of myxovirus central nervous system infections.

摘要

用I型副流感病毒(6/94)对新生小鼠进行脑内接种可引发慢性全脑炎。在感染的125天内进行了电子显微镜研究。从接种后第2天至第8天可见脉络膜和室管膜上皮细胞的增殖性感染。相邻脉络膜和室管膜细胞融合导致巨细胞形成。可见完整的病毒体吸附在循环巨噬细胞上,这些细胞在胞质内复制核衣壳。接种后第3天可见神经元感染,接种后第6天广泛存在并持续至接种后第35天。从未见过核衣壳排列以及从神经元质膜出芽的情况。最初强烈的单核细胞浸润在第35天消退,但整个研究过程中残留炎症持续存在。在感染后期,可见神经纤维网空泡化以及脑室周围和深部脑海绵状改变,这些改变与局部病毒复制无直接关联。这些超微结构发现与先前该感染的光学显微镜、病毒学和免疫荧光研究结果相关,并与黏液病毒中枢神经系统感染的其他实验模型进行了比较。

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