Rabies, caused by rabies virus (RABV), is one of the most important neurotropic zoonoses and poses a severe threat to human and animal health. Exploration of its mechanism of neural transmission is meaningful but still insufficient. Here, we described the effects of microtubule-depolymerizing drugs and inhibitors of microtubule motor proteins on RABV infection. Colchicine, a microtubule-depolymerizing drug, significantly impeded RABV production in N2a cells. Overexpression of CC1 or p50 attenuated viral infection through the functional disruption of cytoplasmic dynein, which was consistent with the inhibitory effect of Na₃VO₄, a dynein activity inhibitor. Moreover, transfection with Flag-KHCct impaired RABV infection, as cytoplasmic kinesin-based motility was blocked. These results demonstrated that RABV can infect N2a cells in a manner that depends on microtubule integrity as well as dynein and kinesin function.

由狂犬病病毒（RABV）引起的狂犬病是最重要的嗜神经性人畜共患病之一，对人类和动物健康构成严重威胁。探索其神经传递机制是有意义的，但仍是不够的。在这里，我们描述了微管解聚药物和微管运动蛋白抑制剂对 RABV 感染的影响。秋水仙碱是一种微管解聚药物，可显着阻碍 N2a 细胞中 RABV 的产生。CC1 或 p50 的过表达通过细胞质动力蛋白的功能破坏减弱病毒感染，这与 Na ₃ VO ₄的抑制作用一致，一种动力蛋白活性抑制剂。此外，转染 Flag-KHCct 会损害 RABV 感染，因为基于细胞质驱动蛋白的运动被阻断。这些结果表明，RABV 可以以依赖于微管完整性以及动力蛋白和驱动蛋白功能的方式感染 N2a 细胞。