Department of Cellular & Molecular Neuroscience, National Brain Research Centre, Manesar, Gurgaon, India; Department of Genetics, Washington University in Saint Louis, Missouri, United States of America.
Department of Cellular & Molecular Neuroscience, National Brain Research Centre, Manesar, Gurgaon, India.
Indian J Med Res. 2021 Mar;154(3):433-445. doi: 10.4103/ijmr.IJMR_169_20.
Zika virus (ZIKV), member of the family Flaviviridae belonging to genus Flavivirus, is an arthropod-borne virus. The ZIKV is known to cause severe congenital birth defects in neonates. Due to a large number of worldwide outbreaks and associated neurological complications with ZIKV, a public health emergency was declared by the World Health Organization on February 1, 2016. The virus exhibits neurotropism and has a specific propensity towards neural precursor cells of the developing brain. In utero ZIKV infection causes massive cell death in the developing brain resulting in various motor and cognitive disabilities in newborns. The virus modulates cell machinery at several levels to replicate itself and inhibits toll like receptors-3 signalling, deregulates microRNA circuitry and induces a chronic inflammatory response in affected cells. Several significant advances have been made to understand the mechanisms of neuropathogenesis, its prevention and treatment. The current review provides an update on cellular and molecular mechanisms of ZIKV-induced alterations in the function of various brain cells.
寨卡病毒（ZIKV）属于黄病毒科黄病毒属的虫媒病毒。已知寨卡病毒可导致新生儿严重的先天性出生缺陷。由于该病毒在世界范围内大量爆发，并伴有与寨卡病毒相关的神经并发症，世界卫生组织于 2016 年 2 月 1 日宣布该病毒为公共卫生紧急事件。该病毒具有神经趋向性，对发育中大脑的神经前体细胞具有特殊的倾向性。寨卡病毒宫内感染可导致发育中大脑的大量细胞死亡，导致新生儿出现各种运动和认知障碍。该病毒通过多个层面来调节细胞机制以自我复制，并抑制 toll 样受体-3 信号通路，扰乱 microRNA 通路，并在受感染的细胞中诱导慢性炎症反应。目前已经取得了一些重要进展，以了解神经发病机制、预防和治疗的机制。本综述提供了寨卡病毒引起各种脑细胞功能改变的细胞和分子机制的最新进展。
