双刃剑：武藏1在寨卡病毒复制和小头畸形中的作用
Dual Blades: The Role of Musashi 1 in Zika Replication and Microcephaly.
作者信息
Klein Robyn S
机构信息
Department of Internal Medicine, Washington University School of Medicine, St Louis, MO 63110, USA; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA; Department of Neuroscience, Washington University School of Medicine, St Louis, MO 63110, USA.
出版信息
Cell Host Microbe. 2017 Jul 12;22(1):9-11. doi: 10.1016/j.chom.2017.06.015.
Abstract
Infection with Zika virus (ZIKV) during pregnancy may cause severe developmental defects in the human brain via unknown mechanisms. In a recent issue of Science, Chavali et al. (2017) identified a neural progenitor cell (NPC)-specific RNA binding protein that may underlie the high levels of ZIKV replication and apoptosis observed in these cells during congenital infections.
摘要
孕期感染寨卡病毒（ZIKV）可能通过未知机制导致人类大脑出现严重发育缺陷。在最近一期的《科学》杂志上，查瓦利等人（2017年）鉴定出一种神经祖细胞（NPC）特异性RNA结合蛋白，该蛋白可能是先天性感染期间在这些细胞中观察到的高水平寨卡病毒复制和凋亡的基础。
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本文引用的文献
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Neurodevelopmental protein Musashi-1 interacts with the Zika genome and promotes viral replication.神经发育蛋白Musashi-1与寨卡病毒基因组相互作用并促进病毒复制。
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Zika virus produces noncoding RNAs using a multi-pseudoknot structure that confounds a cellular exonuclease.寨卡病毒利用一种能使细胞外切核酸酶失效的多假结结构来产生非编码RNA。
Science. 2016 Dec 2;354(6316):1148-1152. doi: 10.1126/science.aah3963. Epub 2016 Nov 10.
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Zika Virus Disrupts Neural Progenitor Development and Leads to Microcephaly in Mice.寨卡病毒扰乱神经祖细胞发育，导致小鼠小头畸形。
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Zika Virus Depletes Neural Progenitors in Human Cerebral Organoids through Activation of the Innate Immune Receptor TLR3.寨卡病毒通过激活天然免疫受体TLR3消耗人脑海马体类器官中的神经祖细胞。
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