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实验性1型副流感病毒诱发成年小鼠脑病。中枢神经系统慢性退行性变的发病机制。

Experimental parainfluenza type 1 virus-induced encephalopathy in adult mice. Pathogenesis of chronic degenerative changes in the CNS.

作者信息

Zgorniak-Nowosielska I, Iwasaki Y, Tachovsky T, Tanaka R, Koprowski H

出版信息

Arch Neurol. 1976 Jan;33(1):55-62. doi: 10.1001/archneur.1976.00500010057009.

Abstract

The pathogenicity of the 6/94 strain of parainfluenza type 1 virus, originally isolated from multiple sclerosis brain, was studied in adult mouse brains. Intracerebral inoculation of the virus caused mononuclear cell infiltration in the form of perivascular cuffing and a diffuse exudation into the parenchymal tissue, preferentially in cerebral white matter, that resulted in marked degeneration over a 90-day observation period. Immunofluorescent staining revealed viral antigen in the ependymal lining cells only during the first seven days after infection. No correlation was found between the severity of the brain lesions and the level of circulating antiviral antibody, preexisting or newly produced.

摘要

对最初从多发性硬化症患者大脑中分离出的1型副流感病毒6/94株在成年小鼠大脑中的致病性进行了研究。脑内接种该病毒导致以血管周围套袖形式出现单核细胞浸润,并向实质组织,尤其是脑白质,发生弥漫性渗出,在90天的观察期内导致明显退化。免疫荧光染色显示,仅在感染后的前七天,室管膜衬里细胞中有病毒抗原。在脑损伤的严重程度与预先存在或新产生的循环抗病毒抗体水平之间未发现相关性。

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