1947年首次分离出寨卡病毒（ZIKV）。自分离出病毒至2007年，ZIKV引起的症状较为有限（例如发烧、荨麻疹和头痛），然而，在2014年的巴西流行期间，ZIKV感染导致成年人出现吉兰-巴雷综合症，而在感染期间怀孕的妇女的胎儿和婴儿中，则导致小头畸形。使用神经前体细胞（NPCs）、脑器官样结构、神经元和星形胶质细胞研究了ZIKV的神经毒性。NPCs和星形胶质细胞似乎是中枢神经系统最易感染ZIKV的细胞。我们的目标是从人类NPC细胞系中分离出星形胶质细胞培养物。我们分析了ZIKV对人类星形胶质细胞的影响，证明了1）ZIKV感染会减少细胞存活率，增加产生活性氧（ROS）的量，并导致高病毒滴度；2）进入细胞的基因表达发生变化；3）参与谷氨酸能系统稳态的基因表达发生变化；4）线粒体和脂滴的超微结构发生变化，与病毒颗粒的产生有关。我们的研究发现了ZIKV如何危害星形胶质细胞的新证据，这有助于理解与ZIKV相关的先天性疾病的病理生理机制。版权所有：© 2023 Rubio-Hernández等人。本文是根据知识共享许可证发布，允许在任何媒介上自由使用、分发和复制原创作者和出处。

Zika virus (ZIKV) was first isolated in 1947. From its isolation until 2007, symptoms of ZIKV-caused disease were limited (e.g., fever, hives, and headache); however, during the epidemic in Brazil in 2014, ZIKV infection caused Guillain-Barré syndrome in adults and microcephaly in fetuses and infants of women infected during pregnancy. The neurovirulence of ZIKV has been studied using neural progenitor cells (NPCs), brain organoids, neurons, and astrocytes. NPCs and astrocytes appear to be the most susceptible cells of the Central Nervous System to ZIKV infection. In this work, we aimed to develop a culture of astrocytes derived from a human NPC cell line. We analyze how ZIKV affects human astrocytes and demonstrate that 1) ZIKV infection reduces cell viability, increases the production of Reactive Oxygen Species (ROS), and results in high viral titers; 2) there are changes in the expression of genes that facilitate the entry of the virus into the cells; 3) there are changes in the expression of genes involved in the homeostasis of the glutamatergic system; and 4) there are ultrastructural changes in mitochondria and lipid droplets associated with production of virions. Our findings reveal new evidence of how ZIKV compromises astrocytic functionality, which may help understand the pathophysiology of ZIKV-associated congenital disease.Copyright: © 2023 Rubio-Hernández et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.