RABIES VIRUS-INFECTION OF CULTURED RAT SENSORY NEURONS
RABIES VIRUS-INFECTION OF CULTURED RAT SENSORY NEURONS
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DOI：
10.1128/jvi.61.9.2733-2741.1987
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发表时间：
1987-09-01
影响因子：
5.4
通讯作者：
TSIANG, H
中科院分区：
文献类型：
--
作者：
LYCKE, E;TSIANG, H
本文研究了狂犬病病毒（固定病毒攻毒株）在分化的大鼠胚胎背根神经节细胞中的轴突运输。此外，我们还观察到狂犬病病毒对神经元延伸的附着以及受感染神经元的病毒产生。使用了一个区室化的细胞培养系统，允许感染和操纵神经元延伸，而不将神经索马暴露于病毒。培养物由60%的大神经元细胞组成，其延伸表现出神经丝结构。狂犬病病毒表现出高结合亲和力的无髓神经突起，所建议的病毒吸附和免疫荧光研究的测定。病毒的轴浆运输速率为12至24 mm/天，包括病毒内化到神经突中所需的时间。细胞松弛素B、长春碱和秋水仙碱可阻断病毒转运，一旦感染建立，这些药物均不会对细胞中病毒的产生产生负面影响。得出的结论是，狂犬病病毒从外周神经突起逆行转移到神经元索马，微管蛋白和肌动蛋白的结构的完整性是必不可少的。大鼠感觉神经元的特点是许可的，中度敏感，但狂犬病毒的低生产者。这些神经元能够长时间携带狂犬病病毒，并且能够将病毒释放到培养基中而不显示任何形态学改变。 参与狂犬病病毒的发病机制，无论是在病毒运输和作为一个网站的持续性病毒感染的感觉神经元，进行了讨论。
The axonal transport of rabies virus (challenge virus strain of fixed virus) was studied in differentiated rat embryonic dorsal root ganglion cells. In addition, we observed the attachment of rabies virus to neuronal extensions and virus production by infected neurons. A compartmentalized cell culture system was used, allowing infection and manipulation of neuronal extensions without exposing the neural soma to the virus. The cultures consisted of 60% large neuronal cells whose extensions exhibited neurofilament structures. Rabies virus demonstrated high binding affinity to unmyelinated neurites, as suggested by assays of virus adsorption and immunofluorescence studies. The rate of axoplasmic transport of virus was 12 to 24 mm/day, including the time required for internalization of the virus into neurites. The virus transport could be blocked by cytochalasin B, vinblastine, and colchicine, none of which negatively affected the production of virus in cells once the infection was established. It was concluded that, for the retrograde transfer of rabies virus by neurites from the periphery to the neuronal soma, the integrity of tubulin- and actin-containing structures is essential. The rat sensory neurons were characterized as permissive, moderately susceptible, but low producers of rabies virus. These neurons were capable of harboring rabies virus for long periods of time and able to release virus into the culture medium without showing any morphological alterations. The involvement of sensory neurons in rabies virus pathogenesis, both in viral transport and as a site for persistent viral infection, is discussed.