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单纯疱疹病毒感染与脱髓鞘疾病之间可能存在的关联。

Possible association of herpes simplex virus infection with demyelinating disease.

作者信息

Vahlne A, Edström S, Hanner P, Andersen O, Svennerholm B, Lycke E

出版信息

Scand J Infect Dis Suppl. 1985;47:16-21.

PMID:3868023
Abstract

Administration of herpes simplex virus (HSV) in sublethal doses to experimental animals may cause a relapsing demyelination in the central nervous system (CNS) but will leave the peripheral myelin unimpaired. Demyelination will be followed by remyelination by oligodendroglial cells or by invading Schwann cells. Relapsing episodes of CNS demyelination seen in HSV latently infected animals may be caused either by reactivation of HSV residing in the CNS itself or virus transported to the CNS after reactivation of a latent infection in peripheral sensory or autonomic ganglia. Although HSV is not the only virus known to induce a demyelination in the CNS of experimental animals, the similarities of this HSV induced demyelination and multiple sclerosis (MS) are intriguing, albeit an association of HSV reactivation and MS has not as yet been reported. However, circumstantial evidence for HSV induction of restricted CNS demyelination in man has recently been obtained: Several laboratories have reported on association of HSV with acute idiopathic facial palsy (Bell's palsy). If HSV be the cause of this palsy, the site of a lesion giving the nerve dysfunction should be located in the brain stem of the CNS rather than in the extrapontine part of the facial nerve. Indeed, most of Bell's palsy patients studied had signs of a brain stem disorder revealed by either one or more of the following tests: auditory brain stem response test, trigeminal evoked potential test or extensive clinical neurological examination. Furthermore, 35% of patients with Bell's palsy had increased concentrations of myelin basic protein in the cerebrospinal fluid collected in the acute stage of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

给实验动物注射亚致死剂量的单纯疱疹病毒(HSV)可能会导致中枢神经系统(CNS)出现复发性脱髓鞘,但不会损害周围神经髓鞘。脱髓鞘后,少突胶质细胞或侵入的施万细胞会进行髓鞘再生。在HSV潜伏感染的动物中观察到的中枢神经系统复发性脱髓鞘发作,可能是由于中枢神经系统自身存在的HSV重新激活,或者是外周感觉或自主神经节潜伏感染重新激活后病毒传播至中枢神经系统所致。虽然HSV不是已知唯一能在实验动物中枢神经系统诱发脱髓鞘的病毒,但这种由HSV诱发的脱髓鞘与多发性硬化症(MS)的相似之处很有趣,尽管尚未有HSV重新激活与MS相关联的报道。然而,最近已获得HSV在人类中诱发局限性中枢神经系统脱髓鞘的间接证据:几个实验室报告了HSV与急性特发性面神经麻痹(贝尔氏麻痹)的关联。如果HSV是这种麻痹的病因,导致神经功能障碍的病变部位应位于中枢神经系统的脑干,而非面神经脑桥外部分。事实上,大多数接受研究的贝尔氏麻痹患者通过以下一项或多项测试显示出脑干疾病的迹象:听觉脑干反应测试、三叉神经诱发电位测试或广泛的临床神经学检查。此外,35%的贝尔氏麻痹患者在疾病急性期采集的脑脊液中髓鞘碱性蛋白浓度升高。(摘要截选至250字)

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