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罗斯河病毒诱导的脱髓鞘:II. 超微结构研究。

Ross River virus--induced demyelination: II. Ultrastructural studies.

作者信息

Seay A R, Wolinsky J S

出版信息

Ann Neurol. 1983 Nov;14(5):559-68. doi: 10.1002/ana.410140511.

Abstract

Focal central nervous system demyelination is a prominent feature of Ross River virus encephalitis in mice. The present ultrastructural study shows that oligodendrocytes are a primary site of viral replication. The earliest myelin disruption occurs in association with an inflammatory infiltrate composed primarily of polymorphonuclear leukocytes, which are later replaced by macrophages. Viral particles are found in oligodendrocytes, selected neuronal populations, macrophages, and polymorphonuclear leukocytes through the end of the first week of infection as macrophages remove myelin from normal-appearing axons. Between the second and third weeks of infection, axons within foci of demyelination partially remyelinate with central myelin. Schwann cells are not found within regions of central remyelination. Cyclophosphamide treatment does not prevent or delay demyelination or remyelination. Results of this and previous studies strongly suggest that Ross River virus--induced demyelination is not immune mediated but rather the direct result of viral infection of oligodendrocytes.

摘要

局灶性中枢神经系统脱髓鞘是小鼠罗斯河病毒脑炎的一个显著特征。目前的超微结构研究表明,少突胶质细胞是病毒复制的主要部位。最早的髓鞘破坏与主要由多形核白细胞组成的炎性浸润有关,这些白细胞随后被巨噬细胞取代。在感染的第一周结束前,在少突胶质细胞、特定的神经元群体、巨噬细胞和多形核白细胞中发现病毒颗粒,因为巨噬细胞从外观正常的轴突中清除髓鞘。在感染的第二至第三周之间,脱髓鞘灶内的轴突部分被中枢髓鞘重新髓鞘化。在中枢重新髓鞘化区域未发现施万细胞。环磷酰胺治疗不能预防或延迟脱髓鞘或重新髓鞘化。本研究及以往研究结果强烈表明,罗斯河病毒诱导的脱髓鞘不是免疫介导的,而是少突胶质细胞病毒感染的直接结果。

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