Identification of a contemporary human parechovirus type I by VIDISCA and characterisation of its full genome

Identification of a contemporary human parechovirus type I by VIDISCA and characterisation of its full genome
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DOI:
10.1186/1743-422x-5-26
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发表时间:
2008-02-12
期刊:
影响因子:
4.8
通讯作者:
Drosten, Christian
Drosten, Christian
中科院分区:
医学3区
文献类型:
--
作者:
Luna, Luciano Kleber de Souza;Baumgarte, Sigrid;Drosten, Christian

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背景:肠炎是由一系列病毒引起的,这些病毒很可能没有被完全描述。当用细胞培养法检测粪便样本时,有时会得到无法用现有方法分型的病毒分离物。在这项研究中,我们使用了一种尚未广泛应用的病毒鉴定方法VIDISCA对这种未分型的病毒分离物进行鉴定。结果:发现1株人类parechovirus (HPeV),毒株编号:BNI-788st。由于没有当代HPeV1的基因组,我们确定了其完整的基因组序列。我们发现,新菌株可能是现代HPeV1菌株祖先的结构蛋白基因与来自未知祖先的非结构蛋白基因重组的结果,这些基因与HPeV3最密切相关。与其他HPeV原型株的非结构蛋白基因相比,BNI-788st和HPeV3原型株的非结构蛋白基因在bootscan分析中与其他原型株的非结构蛋白基因没有共分离。结论:HPeV3非结构蛋白基因可能在循环的HPeV非结构蛋白基因池中形成一个独特的元素。需要对复杂的HPeV进化进行更多的研究,以将病毒生态学与人类疾病模式联系起来。
Background: Enteritis is caused by a spectrum of viruses that is most likely not fully characterised. When testing stool samples by cell culture, virus isolates are sometimes obtained which cannot be typed by current methods. In this study we used VIDISCA, a virus identification method which has not yet been widely applied, on such an untyped virus isolate.Results: We found a human parechovirus (HPeV) type I (strain designation: BNI-788st). Because genomes of contemporary HPeV1 were not available, we determined its complete genome sequence. We found that the novel strain was likely the result of recombination between structural protein genes of an ancestor of contemporary HPeV1 strains and nonstructural protein genes from an unknown ancestor, most closely related to HPeV3. In contrast to the non-structural protein genes of other HPeV prototype strains, the non-structural protein genes of BNI-788st and HPeV3 prototype strains did not co-segregate in bootscan analysis with that of other prototype strains.Conclusion: HPeV3 nonstructural protein genes may form a distinct element in a pool of circulating HPeV non-structural protein genes. More research into the complex HPeV evolution is required to connect virus ecology with disease patterns in humans.