寨卡病毒（Zika virus，ZIKV）属于蚊媒传播病毒，感染后可引起严重的神经系统症状。至今尚不清楚ZIKV感染的致病机制，以及感染早期病毒与宿主蛋白的相互作用关系。哺乳动物雷帕霉素靶蛋白（mammalian target of rapamycin，mTOR）作为调控细胞生长和分解代谢的核心分子，其信号通路的下游分子通过调节蛋白翻译和细胞自噬影响ZIKV复制，上游分子Akt激酶活性在ZIKV感染过程也发挥重要作用。此文从ZIKV的结构与复制、mTOR复合物的结构和信号通路以及mTOR信号通路调节ZIKV复制3个方面，详细阐述了mTOR信号通路与ZIKV感染复制的作用机制。

Zika virus (ZIKV), a mosquito-borne virus, may cause severe neurological symptoms upon infection. To date, the knowledge of pathogenesis underlying the early stages of ZIKV infection and its interaction with host cells is limited. The mammalian target of rapamycin (mTOR) plays an essential part in cell growth and catabolism. The downstream molecules of its signaling pathway regulate protein translation and cell autophagy to affect ZIKV replication,and its upstream Akt kinase activity also plays crucial role in virus infection process. This paper reviews the mechanism between the mTOR signaling pathway and ZIKV infection and replication from three aspects: ZIKV structure and replication, mTOR complex structure and signaling pathway, and the regulation of mTOR signaling pathway on ZIKV replication.