Analysis of Enterovirus 68 Strains from the 2014 North American Outbreak Reveals a New Clade, Indicating Viral Evolution.
Analysis of Enterovirus 68 Strains from the 2014 North American Outbreak Reveals a New Clade, Indicating Viral Evolution.
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对 2014 年北美爆发的肠道病毒 68 株的分析揭示了一个新分支，表明病毒进化。
DOI：
10.1371/journal.pone.0144208
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Yu XF
中科院分区：
文献类型：
--
作者：
Du J;Zheng B;Zheng W;Li P;Kang J;Hou J;Markham R;Zhao K;Yu XF
肠道病毒68(EVD68)会引起呼吸道疾病，主要发生在儿童身上。尽管报告的传播水平较低，但最近在全球范围内发生的几次疫情，包括2014年在北美爆发的疫情，引起了人们对EVD68的发病和演变的关注。为了阐明EVD68的系统发育特征和2014年暴发的可能原因，从Genbank检索到216株EVD68毒株序列，其中22株来自2014年暴发。对这22株病毒建立了多个地理和基因类型来源，其中19株被归类为B分支。在这19株病毒中，17株表现出与宿主-受体相互作用和/或病毒抗原性有关的蛋白残基的随后聚集和变异。在VP1中检测到大约18个分支间变异，这导致在EVD68株中鉴定出一个新的分支D。这一新支系的分类也通过在系统发育分析中重建的邻接树得到了验证。此外，我们的结果表明，在VP1蛋白残基中含有高度特异性改变的B分支成员是2014年美国疫情的最主要贡献者。宿主-受体相互作用和/或宿主免疫识别的改变可能解释了EVD68的进化以及该病毒的全球出现和持续适应。
Enterovirus 68 (EVD68) causes respiratory illness, mostly in children. Despite a reported low-level of transmission, the occurrence of several recent outbreaks worldwide including the 2014 outbreak in North America has raised concerns regarding the pathogenesis and evolution of EVD68. To elucidate the phylogenetic features of EVD68 and possible causes for the 2014 outbreak, 216 EVD68 strain sequences were retrieved from Genbank, including 22 from the 2014 outbreak. Several geographic and genotypic origins were established for these 22 strains, 19 of which were classified as Clade B. Of these 19 strains, 17 exhibited subsequent clustering and variation in protein residues involved in host-receptor interaction and/or viral antigenicity. Approximately 18 inter-clade variations were detected in VP1, which led to the identification of a new Clade D in EVD68 strains. The classification of this new clade was also verified by the re-construction of a Neighbor-Joining tree during the phylogenetic analysis. In addition, our results indicate that members of Clade B containing highly specific alterations in VP1 protein residues were the foremost contributors to the 2014 outbreak in the US. Altered host-receptor interaction and/or host immune recognition may explain the evolution of EVD68 as well as the global emergence and ongoing adaptation of this virus.