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乙型流感病毒诱发瑞氏综合征的小鼠模型:脑病的临床、病毒学及形态学研究

The influenza B virus mouse model of Reye's syndrome: clinical, virologic and morphologic studies of the encephalopathy.

作者信息

Davis L E, Blisard K S, Kornfeld M

机构信息

Neurology Service, Veterans Administration Medical Center, Albuquerque, NM 87108.

出版信息

J Neurol Sci. 1990 Jul;97(2-3):221-31. doi: 10.1016/0022-510x(90)90220-h.

Abstract

The influenza B virus mouse model of Reye's syndrome was studied to learn more about the encephalopathy in Reye's syndrome. One to 3 days after intravenous influenza B/Lee virus, Balb/c mice became lethargic, seized and lapsed into a fatal coma. Wide-spread cerebral edema without inflammation developed 1-3 days after virus inoculation. Swollen astrocytic foot processes containing increased glial fibrillary acidic protein were located around capillaries. Viral particles were not seen by electron microscopy and complete viral replication did not occur. Immunohistochemical studies demonstrated influenza B viral antigen within many endothelial cells but not within other brain cells. Qualitative (Evans blue dye) and quantitative (percent brain water and technetium -99 pertechnetate) studies of the blood-brain barrier demonstrated abnormalities. This model reproduced many clinical, virologic and pathologic features of the Reye's syndrome encephalopathy. In addition, a non-permissive viral infection of brain endothelial cells occurred which may be important in the pathogenesis of the mouse encephalopathy and may participate in the encephalopathy of Reye's syndrome.

摘要

对乙型流感病毒所致瑞氏综合征小鼠模型进行了研究,以进一步了解瑞氏综合征中的脑病。静脉注射乙型流感病毒/Lee株1至3天后,Balb/c小鼠变得嗜睡、惊厥并陷入致命昏迷。病毒接种后1至3天出现广泛的脑水肿且无炎症。在毛细血管周围发现含有增加的胶质纤维酸性蛋白的肿胀星形胶质细胞足突。电子显微镜下未见病毒颗粒,也未发生完整的病毒复制。免疫组织化学研究显示许多内皮细胞内有乙型流感病毒抗原,但其他脑细胞内没有。血脑屏障的定性(伊文思蓝染料)和定量(脑含水量百分比和高锝酸盐-99)研究显示存在异常。该模型再现了瑞氏综合征脑病的许多临床、病毒学和病理学特征。此外,发生了脑内皮细胞的非允许性病毒感染,这可能在小鼠脑病的发病机制中起重要作用,并可能参与瑞氏综合征的脑病。

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