Tsiang H, Lycke E, Ceccaldi P E, Ermine A, Hirardot X
Department of Virology, Pasteur Institute, Paris, France.
J Gen Virol. 1989 Aug;70 ( Pt 8):2075-85. doi: 10.1099/0022-1317-70-8-2075.
We have previously described the capacity of neurites extending from cultured rat sensory dorsal root ganglia (DRG) neurons to transport rabies virus through axoplasm in the retrograde direction. Here we report the infection of cultured neurons derived from the DRG and the subsequent anterograde transport of rabies virus from the infected cell somas through the extending neurites to its release into the culture supernatant. Viral transport was monitored by titration of the virus yield in the external compartment. Both early and late transport mechanisms of rabies virions were identified. The first one occurred a few hours post-infection and was undetectable 6 h later, before the initiation of viral replication. The velocity of this first wave of infective virions was in the range of 100 to 400 mm/day. The early viral transport was probably the result of a direct translocation of infective virions from the somatic site of entry to the neuritic extensions and subsequent release into the culture medium without replication in the cellular perikaryon. The second virus transport peak was detected 48 h post-infection. In this case, the virions detected in the neuritic compartment were presumably the progeny of the inoculated virus which had replicated in the perikaryon before the viral transport occurs. Using a four-compartment culture device we were able to demonstrate, simultaneously, retrograde and anterograde transport of the virus. The presence of antirabies serum in contact with the exposed neurites did not inhibit either the retrograde or the anterograde transport mechanisms. The viral release from the neuritic extensions after the fast anterograde transport was evaluated to be in the range of 150 to 300 infectious virions per bundle of neurites per day.
我们之前曾描述过，从培养的大鼠感觉背根神经节（DRG）神经元延伸出的神经突能够将狂犬病毒通过轴浆逆行运输。在此，我们报告了源自DRG的培养神经元的感染情况，以及随后狂犬病毒从被感染的细胞体通过延伸的神经突进行顺行运输并释放到培养上清液中的过程。通过滴定外部隔室中的病毒产量来监测病毒运输。确定了狂犬病毒粒子的早期和晚期运输机制。第一种机制在感染后数小时出现，6小时后在病毒复制开始前无法检测到。这第一波感染性病毒粒子的速度在每天100至400毫米范围内。早期病毒运输可能是感染性病毒粒子从体细胞进入部位直接转运到神经突延伸部位，随后释放到培养基中，而不在细胞周核中复制的结果。第二个病毒运输峰值在感染后48小时检测到。在这种情况下，在神经突隔室中检测到的病毒粒子大概是接种病毒在病毒运输发生前在周核中复制产生的后代。使用四隔室培养装置，我们能够同时证明病毒的逆行和顺行运输。与暴露的神经突接触的抗狂犬病血清既不抑制逆行运输机制也不抑制顺行运输机制。快速顺行运输后神经突延伸部位的病毒释放量估计为每天每束神经突150至300个感染性病毒粒子。
