Molecular mechanisms of zika virus pathogenesis: An update.
Molecular mechanisms of zika virus pathogenesis: An update.
复制标题
寨卡病毒致病的分子机制研究进展
DOI：
10.4103/ijmr.ijmr_169_20
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发表时间：
2021-03
影响因子：
4.2
通讯作者：
Seth, Pankaj
中科院分区：
文献类型：
--
作者：
Bhagat, Reshma;Kaur, Guneet;Seth, Pankaj
关键词：
寨卡病毒（ZIKV）属于黄病毒属黄病毒科（Flaviviridae）的成员，是节肢动物传播的病毒。已知ZIKV会导致新生儿严重的先天性出生缺陷。由于ZIKV在世界范围内的大量爆发和相关的神经系统并发症，世界卫生组织于2016年2月1日宣布进入公共卫生紧急状态。该病毒表现出嗜神经性，并对发育中的大脑的神经前体细胞具有特定的倾向。在子宫内ZIKV感染导致发育中的大脑中的大量细胞死亡，导致新生儿的各种运动和认知障碍。该病毒在几个水平上调节细胞机制以复制自身，并抑制toll样受体-3信号传导，解除microRNA回路的调节，并在受影响的细胞中诱导慢性炎症反应。在了解神经发病机制及其预防和治疗方面取得了一些重大进展。本综述提供了ZIKV诱导的各种脑细胞功能改变的细胞和分子机制的最新信息。
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.