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寨卡病毒感染神经系统的病理生理学和机制。

Pathophysiology and Mechanisms of Zika Virus Infection in the Nervous System.

机构信息

Department of Neuroscience and Mahoney Institute for Neurosciences, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; email:

Department of Developmental and Cell Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

出版信息

Annu Rev Neurosci. 2019 Jul 8;42:249-269. doi: 10.1146/annurev-neuro-080317-062231.

Abstract

In 2015, public awareness of Zika virus (ZIKV) rose in response to alarming statistics of infants with microcephaly being born to women who were infected with the virus during pregnancy, triggering global concern over these potentially devastating consequences. Although we have discovered a great deal about the genome and pathogenesis of this reemergent flavivirus since this recent outbreak, we still have much more to learn, including the nature of the virus-host interactions and mechanisms that determine its tropism and pathogenicity in the nervous system, which are in turn shaped by the continual evolution of the virus. Inevitably, we will find out more about the potential long-term effects of ZIKV exposure on the nervous system from ongoing longitudinal studies. Integrating clinical and epidemiological data with a wider range of animal and human cell culture models will be critical to understanding the pathogenetic mechanisms and developing more specific antiviral compounds and vaccines.

摘要

2015 年,寨卡病毒(ZIKV)引起了公众的关注,原因是令人震惊的统计数据显示,孕妇感染该病毒后所生婴儿患有小头症,这引发了全球对这些潜在破坏性后果的关注。尽管自最近爆发以来,我们已经对这种新出现的黄病毒的基因组和发病机制有了很多了解,但我们还有更多的东西需要学习,包括病毒-宿主相互作用的性质以及决定其在神经系统中的嗜性和致病性的机制,而这些反过来又受到病毒的持续进化的影响。不可避免地,我们将从正在进行的纵向研究中了解到更多关于 ZIKV 暴露对神经系统的潜在长期影响。将临床和流行病学数据与更广泛的动物和人类细胞培养模型相结合,对于理解发病机制和开发更具特异性的抗病毒化合物和疫苗至关重要。

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