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兔眼内注射I型单纯疱疹病毒后脱髓鞘的机制

Mechanism of demyelination after HSV type I intraocular injection in rabbits.

作者信息

Narang H K

出版信息

J Neurol Sci. 1980 Feb;45(1):109-22. doi: 10.1016/s0022-510x(80)80012-8.

Abstract

Intraocular injection of herpes simplex virus (HSV) type I into the vitreous body of 18-day-old rabbits induced, on the 7th day post-inoculation, neurological signs with marked head jerking and atazia. Examination of semi-serial 1-micrometers thick sections of the whole lengths of right and left optic nerves and chiasma of 4--64 days post-inoculated rabbits revealed a small lesion, restricted to the medial side, which had extended 2--3 mm, during the first 4 days, along the optic nerve. Ahead of the developing lesion marked chromatin changes of neuroglial cells were noticed followed by cuffing of blood vessels, infiltration by macrophages, demyelination and remyelination. The present study indicated that demyelination occurred following the infection of the myelinating cells. It appeared that virus did not become latent and many cells survived the viral attack. Repeated episodies of viral activity caused further damage while repair did not keep pace.

摘要

将I型单纯疱疹病毒(HSV)眼内注射到18日龄兔的玻璃体中,在接种后第7天诱发神经症状,表现为明显的头部抽搐和共济失调。对接种后4 - 64天的兔的左右视神经全长和视交叉进行半连续1微米厚切片检查,发现一个小病变,局限于内侧,在最初4天内沿视神经延伸了2 - 3毫米。在病变发展之前,观察到神经胶质细胞有明显的染色质变化,随后是血管套叠、巨噬细胞浸润、脱髓鞘和再髓鞘化。本研究表明,髓鞘形成细胞感染后发生了脱髓鞘。似乎病毒没有潜伏,许多细胞在病毒攻击下存活下来。病毒活性的反复发作造成了进一步的损害,而修复未能跟上。

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Peripheral nervous system demyelination with herpes simplex virus.
J Neuropathol Exp Neurol. 1986 Jul;45(4):419-25. doi: 10.1097/00005072-198607000-00004.

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