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Molecular epidemiology and the evolution of human coxsackievirus A6

Research output: Contribution to journalArticle

  • Jiratchaya Puenpa
  • Sompong Vongpunsawad
  • Riikka Osterback
  • Matti Waris
  • Eva Eriksson
  • Jan Albert
  • Sofie Midgley
  • Thea K Fischer
  • Anna M Eis-hübinger
  • María Cabrerizo
  • Eleanor Gaunt
  • Peter Simmonds
  • Yong Poovorawan

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Original languageEnglish
Pages (from-to)3225-3231
JournalJournal of General Virology
Issue number12
Early online date29 Sep 2016
Publication statusPublished - Dec 2016


Coxsackievirus A6 (CV-A6) infection is a major etiologic agent for hand, foot and mouth disease (HFMD) in recent years. HFMD outbreaks associated with CV-A6 results from the evolutionary dynamics of CV-A6 and the appearance of novel recombinant forms (RFs). To examine this, 151 variants collected between 2013 and 2014 from Germany, Spain, Sweden, Denmark, and Thailand were genotyped for the VP1 capsid and 3Dpol genes. Analysis of the VP1 gene showed an increasing likelihood between CV-A6 genome recombination and sequence divergence (estimated substitution rate of 8.1 × 10-3 substitutions/site/year and RFs half-life of 3.1 years). Bayesian phylogenetic analysis showed that recent recombination groups (RF-E, -F, -H, -J and -K) shared a common ancestor (RF-A). Thirty-nine full-length genomes of different RFs revealed recombination breakpoints between the 2A-2C and the 5' untranslated regions. The emergence of new CV-A6 recombination groups has become widespread in Europe and Asia within the last 8 years.

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