Neurotropic alphaherpesviruses initiate infection in exposed mucosal tissues and, unlike most viruses, spread rapidly to sensory and autonomic nerves where life-long latency is established¹. Recurrent infections arise sporadically from the peripheral nervous system throughout the life of the host, and invasion of the central nervous system may occur, with severe outcomes². These viruses directly recruit cellular motors for transport along microtubules in nerve axons, but how the motors are manipulated to deliver the virus to neuronal nuclei is not understood. Here, using herpes simplex virus type I and pseudorabies virus as model alphaherpesviruses, we show that a cellular kinesin motor is captured by virions in epithelial cells, carried between cells, and subsequently used in neurons to traffic to nuclei. Viruses assembled in the absence of kinesin are not neuroinvasive. The findings explain a critical component of the alphaherpesvirus neuroinvasive mechanism and demonstrate that these viruses assimilate a cellular protein as an essential proviral structural component. This principle of viral assimilation may prove relevant to other virus families and offers new strategies to combat infection.

嗜神经性α疱疹病毒在暴露的黏膜组织中引发感染，并且与大多数病毒不同，它迅速传播到建立终生潜伏期的感觉和自主神经¹。在宿主的整个生命周期中，外周神经系统偶尔会出现复发性感染，可能会侵犯中枢神经系统，并导致严重后果². 这些病毒直接招募细胞马达沿神经轴突中的微管运输，但如何操纵马达将病毒传递到神经元核尚不清楚。在这里，我们使用 I 型单纯疱疹病毒和伪狂犬病病毒作为模型 alphaherpesviruses，表明细胞驱动蛋白马达被上皮细胞中的病毒粒子捕获，在细胞之间携带，随后在神经元中用于运输到细胞核。在没有驱动蛋白的情况下组装的病毒不是神经侵入性的。这些发现解释了α疱疹病毒神经侵袭机制的一个关键组成部分，并证明这些病毒将细胞蛋白同化为一种重要的前病毒结构成分。这种病毒同化原理可能证明与其他病毒家族有关，并提供了对抗感染的新策略。