寨卡病毒（Zika virus，ZIKV）感染孕妇后可导致胎儿流产或小头畸形，且与成年人吉兰-巴雷综合征密切相关。细胞表面的黏多糖和C型凝集素受体在ZIKV入侵细胞时发挥黏附、募集作用。ZIKV通过其表达的多种蛋白抑制免疫应答通路，或过度激活宿主的抗原模式识别受体以破坏固有免疫应答，引发病理效应。IFN-α介导的固有免疫应答能阻止ZIKV早期感染，细胞免疫和体液免疫在宿主清除ZIKV时均发挥重要作用。针对病毒与宿主细胞表面结合的相关受体、病毒复制周期中的关键酶或宿主细胞内病毒增殖相关靶点的治疗药物研究已有报道，并经体外及动物实验显示有效，但有待进一步临床试验证实。此文对ZIKV感染机制及相关治疗药物的最新研究进展做一综述。

Zika virus (ZIKV) has been closely associated with miscarriage and infant microcephaly in infected  pregnant women, and Guillain-Barré syndrome in adults. The entry of ZIKV into target cells is mediated by glycosaminoglycans or C-type lectin receptors that adhere and/or recruit virus onto cell surface. ZIKV encodes multiple proteins to inhibit the immune response pathway or excessively activate host antigen pattern recognition receptors, in order to destroy the innate immune response and cause pathological effect. Innate immune response mediated by IFN-α could prevent early ZIKV infection, and cellular and humoral immunity plays an important role in the clearance of ZIKV. ZIKV therapeutic drugs in research aiming at receptors related to virus interaction with the host cell surface, key enzyme in viral replication cycle, and host intracellular targets related to virus reproduction have been reported effective in vitro and in animal trials. They need further clinical trials

to confirm. This article reviews the mechanisms of ZIKV infection and relevant therapeutic drugs.