神经发育蛋白质Musashi-1与寨卡基因组相互作用并促进病毒复制
Pavithra L Chavali1, Lovorka Stojic1, Luke W Meredith2
1Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Robinson Way, Cambridge CB2 0RE, UK.
Science (New York, N.Y.)
|June 3, 2017
概括
寨卡病毒感染通过与大脑发育至关重要的蛋白质Musashi-1 (MSI1) 相互作用来准神经前体. 这种相互作用会破坏神经干细胞的正常功能,这可能解释了寨卡病毒爆发期间的小头症.
科学领域:
- 神经科学
- 病毒学
- 遗传学
背景情况:
- 巴西寨卡病毒爆发与新生儿小头症的增加有关.
- 大脑神经前体中的寨卡病毒神经变性尚不清楚.
研究的目的:
- 调查寨卡病毒神经变的机制.
- 确定涉及寨卡病毒复制和病变的宿主因素.
主要方法:
- 研究了寨卡病毒基因组与Musashi-1 (MSI1) 之间的相互作用.
- 评估了寨卡病毒感染对MSI1结合内源点的影响.
- 在人类胚胎大脑神经祖先中检查MSI1表达.
- 分析了自体逆性初级小头症患者的MSI1突变.
主要成果:
- 穆沙希-1 (MSI1) 与寨卡病毒基因组相互作用,促进病毒复制.
- 寨卡病毒感染会破坏MSI1与正常目标的结合,从而改变神经干细胞的基因表达.
- 在人类胚胎神经原始体中MSI1的表达很高.
- 在初级小头症病例中发现MSI1突变.
结论:
- 穆沙希-1 (MSI1) 是一个关键的宿主因子,可使寨卡病毒在神经前体中复制.
- 寨卡病毒对MSI1功能的破坏导致神经发育缺陷,如小头症.
- 神经前体中的MSI1选择性表达解释了它们对寨卡感染的脆弱性.
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