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关于兰德里-吉兰-巴雷综合征中病毒诱导脱髓鞘的一种理论。

A theory of virus-induced demyelination in the Landry-Guillain-Barré syndrome.

作者信息

Pepose J S

出版信息

J Neurol. 1982;227(2):93-7. doi: 10.1007/BF00313775.

Abstract

The Landry-Guillain-Barré syndrome (LGBS) is a demyelinating disorder of the peripheral nervous system frequently preceded by infection with common viruses. Most prevalent among these agents are herpesviruses, particularly Epstein-Barr virus (EBV) and cytomegalovirus (CMV). The specific role played by antecedent viral infection in the pathogenesis of the LGBS remains obscure. In this regard, recent studies of Marek's disease (MD) neuropathy, an avian herpesvirus-induced experimental model for the LGBS, may provide insight. The autoimmune pattern of demyelination seen in MD neuropathy is histopathologically indistinguishable from that seen in the LGBS. In this paper, a comprehensive theory is discussed regarding the pathogenetic mechanisms that may be operative in the LGBS.

摘要

兰德里-吉兰-巴雷综合征(LGBS)是一种周围神经系统的脱髓鞘疾病,通常在感染常见病毒后发病。其中最常见的病原体是疱疹病毒,尤其是爱泼斯坦-巴尔病毒(EBV)和巨细胞病毒(CMV)。先前的病毒感染在LGBS发病机制中所起的具体作用仍不清楚。在这方面,最近对马立克氏病(MD)神经病变的研究,一种由禽疱疹病毒引起的LGBS实验模型,可能会提供一些见解。MD神经病变中所见的自身免疫性脱髓鞘模式在组织病理学上与LGBS中所见的模式无法区分。本文讨论了关于可能在LGBS中起作用的发病机制的综合理论。

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