在Aedes aegypti蚊子中的寨卡病毒传染性进化增强
Yang Liu1,2,3, Jianying Liu1,3, Senyan Du1
1Tsinghua-Peking Center for Life Sciences, School of Medicine, Tsinghua University, Beijing 100084, China.
Nature
|May 18, 2017
概括
寨卡病毒 (ZIKV) 非结构蛋白1 (NS1) 的突变增加了NS1抗原,增强了蚊子的寨卡病毒感染力. 这种演变可能促进了近期流行病中ZIKV的快速传播.
科学领域:
- 病毒学
- 分子生物学
- 流行病学
背景情况:
- 在法属波利尼西亚和南美洲爆发的寨卡病毒 (ZIKV) 突显了它的出现.
- 遗传学研究确定了非洲和亚洲的ZIKV血统,亚洲血统与美国的流行病有关.
- 导致ZIKV从亚洲迅速传播到美洲的机制尚不完全理解.
研究的目的:
- 调查非结构性蛋白1 (NS1) 抗原在ZIKV感染性和传播者蚊子中的作用.
- 将最近的ZIKV临床分离物与老菌株的传染性进行比较.
- 在流行病菌株中确定增强ZIKV感染性的分子决定因素.
主要方法:
- 对来自美洲的ZIKV临床分离物和古老的柬埔寨菌株 (FSS13025) 的蚊子感染性进行比较分析.
- 在感染宿主中量化NS1抗原血症.
- 在ZIKV NS1中引入氨酸替代氨酸残留物的局部定向突变.
- 感染AG6小鼠 (缺少I型和II型干扰素受体) 并随后食埃及蚊.
主要成果:
- 与FSS13025菌株相比,来自美洲的临床ZIKV隔离物在埃及蚊子中具有显著更高的传染性.
- 流行性ZIKV菌株呈现出较高的NS1抗原,这归因于NS1中的188残留物中的氨酸与氨酸的替代.
- 在被感染的AG6小鼠养的蚊子中,这种NS1突变被引入到FSS13025菌株中,增强了它的传染性.
结论:
- ZIKV在其NS1蛋白中发生了自发突变,导致NS1抗原的增加.
- 增加的NS1抗原增加了蚊子中的ZIKV感染力和流行率.
- 这种分子适应可能在最近的ZIKV流行病的爆炸性传播动态中发挥了关键作用.
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