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Evolutionary enhancement of Zika virus infectivity in Aedes aegypti mosquitoes

机译：埃及伊蚊对寨卡病毒感染性的进化增强

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摘要

Zika virus (ZIKV) remained obscure until the recent explosive outbreaks in French Polynesia (2013-2014) and South America (2015-2016)(1-3). Phylogenetic studies have shown that ZIKV has evolved into African and Asian lineages. The Asian lineage of ZIKV was responsible for the recent epidemics in the Americas(1,3). However, the underlying mechanisms through which ZIKV rapidly and explosively spread from Asia to the Americas are unclear. Non-structural protein 1 (NS1) facilitates flavivirus acquisition by mosquitoes from an infected mammalian host and subsequently enhances viral prevalence in mosquitoes(4). Here we show that NS1 antigenaemia determines ZIKV infectivity in its mosquito vector Aedes aegypti, which acquires ZIKV via a blood meal. Clinical isolates from the most recent outbreak in the Americas were much more infectious in mosquitoes than the FSS13025 strain, which was isolated in Cambodia in 2010. Further analyses showed that these epidemic strains have higher NS1 antigenaemia than the FSS13025 strain because of an alanine-to-valine amino acid substitution at residue 188 in NS1. ZIKV infectivity was enhanced by this amino acid substitution in the ZIKV FSS13025 strain in mosquitoes that acquired ZIKV from a viraemic C57BL/6 mouse deficient in type I and II interferon (IFN) receptors (AG6 mouse). Our results reveal that ZIKV evolved to acquire a spontaneous mutation in its NS1 protein, resulting in increased NS1 antigenaemia. Enhancement of NS1 antigenaemia in infected hosts promotes ZIKV infectivity and prevalence in mosquitoes, which could have facilitated transmission during recent ZIKV epidemics.
机译：直到最近法属波利尼西亚（2013-2014）和南美（2015-2016）（1-3）爆发爆发之前，寨卡病毒（ZIKV）仍然不为人所知。系统发育研究表明，ZIKV已进化为非洲和亚洲谱系。 ZIKV的亚洲血统是导致美洲最近流行的原因（1,3）。但是，ZIKV从亚洲迅速扩散到美洲的基本机制尚不清楚。非结构蛋白1（NS1）有助于蚊子从感染的哺乳动物宿主中捕获黄病毒，从而提高了蚊子中的病毒流行率（4）。在这里，我们显示，NS1抗原血症在其蚊媒埃及伊蚊（Aedes aegypti）中决定了ZIKV的感染性，该蚊子通过血粉获得ZIKV。来自美洲最近一次疫情的临床分离株比2010年在柬埔寨分离的FSS13025株在蚊子中的感染性高得多。进一步的分析表明，由于丙氨酸转化为丙二醛，这些流行株比FSS13025株具有更高的NS1抗原血症。 -NS1中第188位残基的-缬氨酸氨基酸取代。通过从缺乏I型和II型干扰素（IFN）受体的病毒C57BL / 6小鼠（AG6小鼠）获得ZIKV的蚊子中ZIKV FSS13025菌株中的这种氨基酸取代，可增强ZIKV的感染力。我们的研究结果表明ZIKV进化为获得其NS1蛋白的自发突变，从而导致NS1抗原血症增加。感染宿主中NS1抗原血症的增强会促进ZIKV的感染性和蚊子的流行，这可能有助于在最近的ZIKV流行期间传播。

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  • 来源
    《Nature》 |2017年第7655期|482-486|共5页
  • 作者

    Liu Yang; Liu Jianying; Du Senyan; Shan Chao; Nie Kaixiao; Zhang Rudian; Li Xiao-Feng; Zhang Renli; Wang Tao; Qin Cheng-Feng; Wang Penghua; Shi Pei-Yong; Cheng Gong;

  • 作者单位

    Tsinghua Univ, Sch Med, Tsinghua Peking Ctr Life Sci, Beijing 100084, Peoples R China|Tsinghua Univ, Sch Life Sci, Beijing 100084, Peoples R China|Shenzhen Ctr Dis Control & Prevent, SZCDC SUSTech Joint Key Lab Trop Dis, Shenzhen 518055, Guangdong, Peoples R China;

    Tsinghua Univ, Sch Med, Tsinghua Peking Ctr Life Sci, Beijing 100084, Peoples R China|Shenzhen Ctr Dis Control & Prevent, SZCDC SUSTech Joint Key Lab Trop Dis, Shenzhen 518055, Guangdong, Peoples R China;

    Tsinghua Univ, Sch Med, Tsinghua Peking Ctr Life Sci, Beijing 100084, Peoples R China;

    Univ Texas Med Branch, Dept Biochem & Mol Biol, Dept Pharmacol & Toxicol, Galveston, TX 77555 USA|Univ Texas Med Branch, Sealy Ctr Struct Biol & Mol Biophys, Galveston, TX 77555 USA;

    Tsinghua Univ, Sch Med, Tsinghua Peking Ctr Life Sci, Beijing 100084, Peoples R China;

    Tsinghua Univ, Sch Med, Tsinghua Peking Ctr Life Sci, Beijing 100084, Peoples R China|Tsinghua Univ, Sch Life Sci, Beijing 100084, Peoples R China;

    Beijing Inst Microbiol & Epidemiol, State Key Lab Pathogen & Biosecur, Beijing 100071, Peoples R China;

    Shenzhen Ctr Dis Control & Prevent, SZCDC SUSTech Joint Key Lab Trop Dis, Shenzhen 518055, Guangdong, Peoples R China;

    Shenzhen Ctr Dis Control & Prevent, SZCDC SUSTech Joint Key Lab Trop Dis, Shenzhen 518055, Guangdong, Peoples R China|Southern Univ Sci & Technol, Dept Biol, Shenzhen 518055, Guangdong, Peoples R China;

    Beijing Inst Microbiol & Epidemiol, State Key Lab Pathogen & Biosecur, Beijing 100071, Peoples R China;

    New York Med Coll, Sch Med, Dept Microbiol & Immunol, Valhalla, NY 10595 USA;

    Univ Texas Med Branch, Dept Biochem & Mol Biol, Dept Pharmacol & Toxicol, Galveston, TX 77555 USA|Univ Texas Med Branch, Sealy Ctr Struct Biol & Mol Biophys, Galveston, TX 77555 USA;

    Tsinghua Univ, Sch Med, Tsinghua Peking Ctr Life Sci, Beijing 100084, Peoples R China|Shenzhen Ctr Dis Control & Prevent, SZCDC SUSTech Joint Key Lab Trop Dis, Shenzhen 518055, Guangdong, Peoples R China;

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