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寨卡病毒感染抑制神经发生。

Inhibition of Neurogenesis by Zika Virus Infection.

机构信息

Department of Infectious Disease, Drug Discovery Division, Southern Research, 2000, Ninth Ave, South, Birmingham, AL 35205, United States.

Department of Biochemistry and Molecular Genetics, 845 19th Street South, University of Alabama, Birmingham, AL 35205, United States.

出版信息

CNS Neurol Disord Drug Targets. 2018;17(2):78-86. doi: 10.2174/1871527317666180202115114.

DOI:10.2174/1871527317666180202115114
PMID:29422006
Abstract

BACKGROUND & OBJECTIVE: The link between Zika Virus (ZIKV) epidemic and neurological disorder has raised an urgent global alarm. The current epidemic of ZIKV has triggered quick responses in the scientific world. The first case of ZIKV was reported in 2015 from Brazil and now has spread over 30 countries. Nearly four hundred cases of traveler associated ZIKV infection have also been reported in the United States. ZIKV is primarily transmitted by mosquito belonging to the genus Aedes that are widely distributed throughout the world. Additionally, the virus can also be transmitted from male to female by sexual contact. The epidemiological investigations during the current outbreak found a causal link between infection in pregnant women and the development of microcephaly (MCPH) in their unborn babies. This finding is a cause of grave concern since MCPH is a serious neural developmental disorder that can lead to significant post-natal developmental abnormalities and disabilities. Recently, published data indicates that ZIKV infection severely affects the growth of fetal neural progenitor cells and cerebral neurons resulting in malformation of cerebral cortex leading to MCPH. Recently, it has been reported that ZIKV infection deregulates the signaling pathway of neuronal cell and inhibits the neurogenesis.

CONCLUSION

In this review, we discussed the information about cellular and molecular mechanisms of neurodegeneration of human neuronal cells and inhibition of neurogenesis. The provided information in this review will be very useful further not only in neuro-scientific research but also in the desig and development of management strategies for MCPH and other mosquito-borne diseases.

摘要

背景与目的

寨卡病毒(ZIKV)流行与神经疾病之间的联系引起了全球紧急警报。ZIKV 的当前流行在科学界引发了快速反应。首例 ZIKV 于 2015 年在巴西报告,现已传播到 30 多个国家。美国也报告了近 400 例与旅行者相关的 ZIKV 感染病例。ZIKV 主要通过属于伊蚊属的蚊子传播,这些蚊子在世界各地广泛分布。此外,该病毒也可以通过性接触从男性传播给女性。当前疫情的流行病学调查发现,孕妇感染与未出生婴儿小头畸形(MCPH)之间存在因果关系。这一发现令人严重关切,因为 MCPH 是一种严重的神经发育障碍,可导致严重的产后发育异常和残疾。最近发表的数据表明,ZIKV 感染严重影响胎儿神经祖细胞和大脑神经元的生长,导致大脑皮层畸形导致 MCPH。最近有报道称,ZIKV 感染会使神经元细胞的信号通路失调并抑制神经发生。

结论

在这篇综述中,我们讨论了人类神经元细胞神经退行性变和神经发生抑制的细胞和分子机制的信息。本文提供的信息不仅在神经科学研究中,而且在 MCPH 和其他蚊媒疾病的管理策略的设计和开发中都将非常有用。

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Inhibition of Neurogenesis by Zika Virus Infection.寨卡病毒感染抑制神经发生。
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Zika virus infection disrupts neurovascular development and results in postnatal microcephaly with brain damage.寨卡病毒感染会破坏神经血管发育,并导致出生后小头畸形及脑损伤。
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