PATHOGENESIS OF EXPERIMENTAL RABIES IN MICE - AN IMMUNOHISTOCHEMICAL STUDY
PATHOGENESIS OF EXPERIMENTAL RABIES IN MICE - AN IMMUNOHISTOCHEMICAL STUDY
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DOI：
10.1007/bf00688204
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发表时间：
1989-01-01
影响因子：
12.7
通讯作者：
REIMER, DL
中科院分区：
文献类型：
--
作者：
JACKSON, AC;REIMER, DL
用狂犬病病毒CVS株固定化毒株，在小鼠后肢足垫和脑内接种后，观察狂犬病病毒在中枢神经系统的传播。所有小鼠均发生麻痹性狂犬病。脑内接种后，早期大脑皮层神经元和海马锥体神经元同时感染，后期扩散至小脑。高剂量脑内接种后，在侧脑室内衬的室管膜细胞和脊髓中央管附近的神经元中存在早期感染，这表明狂犬病病毒至少部分通过脑脊液途径进入CNS。后肢足垫接种后，受累顺序不同。感染在第5天在小脑中建立，在第6天在大脑皮层中建立，在第8天在海马中建立。CA 3最初受到感染，CA 1在2天后受到感染，并且齿状回的受累要少得多。海马感染发生较晚，相对于其余的脑外周接种后，但不是脑内接种后。海马不是检测外周接种后早期脑感染的好位置，尽管当天然狂犬病媒介具有传播感染的能力时，海马可能参与其中。这些发现也对临床狂犬病中观察到的边缘系统功能障碍的机制提出了疑问。
The spread of rabies virus in the central nervous system of mice was examined after hindlimb footpad and intracerebral inoculation of the CVS strain of fixed rabies virus. All mice developed paralytic rabies. After intracerebral inoculation there was early simultaneous infection of neurons in the cerebral cortex and pyramidal neurons of the hippocampus, and later there was spread to the cerebellum. After high-dose intracerebral inoculation there was early infection in ependymal cells lining the lateral ventricles and neurons adjacent to the central canal of the spinal cord, suggesting that rabies virus entry into the CNS occurs, at least in part, by a cerebrospinal fluid pathway. The sequence of involvement was different after hindlimb footpad inoculation. Infection became established in the cerebellum on day 5, in the cerebral cortex on day 6, and in the hippocampus on day 8. CA3 was initially affected, CA1 became infected 2 days later, and there was much less involvement of the dentate gyrus. Hippocampal infection occurred late relative to the rest of the brain after peripheral inoculation, but not after intracerebral inoculation. The hippocampus is not a good location for the detection of early brain infection after peripheral inoculation, although it may be involved when a natural rabies vector has the ability to transmit infection. These findings also raise questions about the mechanisms for the limbic dysfunction observed in clinical rabies.