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中国安徽省由肠道病毒 6 引起的无菌性脑膜炎爆发。

An aseptic meningitis outbreak caused by echovirus 6 in Anhui province, China.

机构信息

WHO WPRO Regional Reference Measles Lab and State Key Laboratory for Molecular Virology and Genetic Engineering, National Institute for Viral Disease Control and Prevention, Chinese Centers for Disease Control and Prevention, Beijing, People's Republic of China.

出版信息

J Med Virol. 2010 Mar;82(3):441-5. doi: 10.1002/jmv.21707.

DOI:10.1002/jmv.21707
PMID:20087933
Abstract

An outbreak of aseptic meningitis (AM) occurred in Jinzhai County in Anhui province from April to July in 2005. Totally, 97 children aged 3-15 years were hospitalized. To identify the etiologic agent, 77 cerebrospinal fluid specimens (CSF) and 5 fecal specimens were collected from the patients and cultured by human rhabdomyosarcoma (RD) cell line. Thirty isolates of human echovirus 6 (E6) from 27 CSF and 3 fecal specimens were confirmed by neutralization assay and sequencing analysis of the VP1 gene. The homology of VP1 gene among Anhui isolates was 99.7-100.0% and it indicated that this AM outbreak probable caused by a single transmission link of E6. Phylogenetic analysis based on all the available complete VP1 sequences indicated that E6 could be divided into clusters A, B, and C with at least 15% diversity between clusters and the C cluster could be further divided into C1, C2, C3, and C4. The Anhui isolates most resembled a 2005 strain from Russia (25465 Tambov) and belong to C4. This is the first report that E6 was responsible for an outbreak of AM in China. J. Med. Virol. 82:441-445, 2010. (c) 2010 Wiley-Liss, Inc.

摘要

2005 年 4 月至 7 月,安徽省金寨县发生无菌性脑膜炎(AM)爆发。共有 97 名 3-15 岁的儿童住院。为了确定病原体,从患者中采集了 77 份脑脊液(CSF)和 5 份粪便标本,并通过人横纹肌肉瘤(RD)细胞系进行培养。通过中和试验和 VP1 基因测序分析,从 27 份 CSF 和 3 份粪便标本中确认了 30 株人肠道病毒 6(E6)分离株。安徽分离株的 VP1 基因同源性为 99.7-100.0%,表明此次 AM 爆发可能是由 E6 的单一传播链引起的。基于所有可用的完整 VP1 序列的系统进化分析表明,E6 可分为 A、B 和 C 簇,簇间至少有 15%的差异,C 簇可进一步分为 C1、C2、C3 和 C4。安徽分离株与 2005 年来自俄罗斯的一株(25465 Tambov)最为相似,属于 C4。这是首次报道 E6 引起中国 AM 的爆发。J. Med. Virol. 82:441-445, 2010.(c)2010 Wiley-Liss, Inc.

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