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1型脊髓灰质炎病毒所致神经损伤的分子发病机制

Molecular pathogenesis of neural lesions induced by poliovirus type 1.

作者信息

Couderc T, Christodoulou C, Kopecka H, Marsden S, Taffs L F, Crainic R, Horaud F

机构信息

Virologie Médicale, Institut Pasteur, Paris, France.

出版信息

J Gen Virol. 1989 Nov;70 ( Pt 11):2907-18. doi: 10.1099/0022-1317-70-11-2907.

Abstract

Using in situ hybridization techniques for viral RNA and employing a specific riboprobe, we have detected virus in neural cells of monkeys infected with poliovirus type 1 (PV-1) by the intraspinal route. In monkeys paralysed after inoculation of a neurovirulent revertant of PV-1/Sabin strain, viral RNA was detected in motor neurons and their processes, and in polymorphonuclear and small neural cells. Quantitative in situ hybridization provided evidence of viral replication in individual cells suggesting that the death of motor neurons was due to the direct effect of poliovirus replication in these cells. The histological study of neural lesions of monkeys paralysed after infection with the attenuated Sabin strain of PV-1 revealed two major differences compared to monkeys infected with a virulent strain: (i) the number of destroyed motor neurons was reduced and limited to the site of inoculation and (ii) the inflammatory reaction was localized but more intense. An account is given of the difference in histopathology induced by virulent and attenuated strains of PV-1 in the central nervous system.

摘要

我们运用针对病毒RNA的原位杂交技术并采用特异性核糖探针,通过脊髓内途径在感染1型脊髓灰质炎病毒(PV-1)的猴子神经细胞中检测到了病毒。在接种PV-1/萨宾株神经毒力回复株后出现麻痹的猴子中,在运动神经元及其突起以及多形核和小神经细胞中检测到了病毒RNA。定量原位杂交提供了病毒在单个细胞中复制的证据,表明运动神经元的死亡是脊髓灰质炎病毒在这些细胞中复制的直接结果。对感染PV-1减毒萨宾株后出现麻痹的猴子神经损伤的组织学研究显示,与感染强毒株的猴子相比有两个主要差异:(i)被破坏的运动神经元数量减少且局限于接种部位;(ii)炎症反应局限但更强烈。本文阐述了PV-1强毒株和减毒株在中枢神经系统中引起的组织病理学差异。

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