Genome analysis of enterovirus 71 strains differing in mouse pathogenicity

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• 作者：Peng Li ; Yingying Yue ; Nannan Song ; Bingqing Li ; Hong Meng ; Guiwen Yang…
• 关键词：Genome ; Enterovirus 71 (EV71) ; Mutation ; Virulence ; 3C proteinase (3Cpro)
• 刊名：Virus Genes
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：52
• 期：2
• 页码：161-171
• 全文大小：941 KB
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• 作者单位：Peng Li (1) (2)
  Yingying Yue (2)
  Nannan Song (2)
  Bingqing Li (2)
  Hong Meng (2)
  Guiwen Yang (1)
  Zhihui Li (2)
  Liguo An (1)
  Lizeng Qin (2)
  
  1. College of Life Science, Shandong Normal University, 88 East Wenhua Road, Jinan, 250014, People’s Republic of China
  2. Key Laboratory of Rare and Uncommon Diseases, Department of Microbiology, Institute of Basic Medicine, Shandong Academy of Medical Sciences, 18877 Jingshi Road, Jinan, 250062, People’s Republic of China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Medical Microbiology
  Virology
  Plant Sciences
  
• 出版者：Springer Netherlands
• ISSN：1572-994X

文摘

Enterovirus 71 (EV71) is a major causative agent of hand, foot, and mouth disease (HFMD) and is occasionally associated with severe neurological diseases. The investigation of virulence determinants of EV71 is rudimentary. Therefore, it is important to understand the relationship between EV71 virulence and genomic information. In this study, a series of analyses about full-length genomic sequence were performed on six EV71 strains isolated from HFMD patients with either severe or mild clinical symptoms. A one-day-old BALB/c mouse model was used to study the infection characteristics. Results showed all six strains were of the subgenogroup C4a. Viral full-length genomic sequence analysis showed that a total of 40 nucleotide differences between strains of highly and low virulence were revealed. Among all mutations, three nucleotide mutations were found in the untranslated region. A mutation, nt115, at internal ribozyme entry site (IRES) caused RNA secondary structural change. The other 37 mutations were all located in the open reading frame resulting in 8 amino acid mutations. Importantly, we discovered that a mutation of amino acid (Asn1617 → Asp1617) in the 3C proteinase (3Cpro) of highly and low pathogenic strains could lead to conformational change at the active center, suggesting that this site may be a virulence determinant of EV71.