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Persistent circulation of genotype D coxsackievirus A2 in mainland of China since 2008

Coxsackievirus A2 (CV-A2) has emerged as an important etiological agent in the hand, foot, and mouth disease and herpangina pathogen spectrum because of its high global prevalence. In the present study, we investigated the evolutionary dynamics of CV-A2 circulating in China. We analyzed a total of 1...

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Detalles Bibliográficos
Autores principales: Yang, Qian, Gu, Xinrui, Zhang, Yong, Wei, Haiyan, Li, Qi, Fan, Huan, Xu, Yi, Li, Jie, Tan, Zhaolin, Song, Yang, Yan, Dongmei, Ji, Tianjiao, Zhu, Shuangli, Xu, Wenbo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6147602/
https://www.ncbi.nlm.nih.gov/pubmed/30235342
http://dx.doi.org/10.1371/journal.pone.0204359
Descripción
Sumario:Coxsackievirus A2 (CV-A2) has emerged as an important etiological agent in the hand, foot, and mouth disease and herpangina pathogen spectrum because of its high global prevalence. In the present study, we investigated the evolutionary dynamics of CV-A2 circulating in China. We analyzed a total of 163 entire VP1 sequences of CV-A2, including 74 sequences generated from the present study and 89 sequences collected from the GenBank database. Phylogenetic analysis based on the entire VP1 nucleotide sequences confirmed the persistent circulation of the predominant genotype D in mainland of China since 2008. Cluster analysis grouped the sequences into two distinct clusters, clusters 1 and 2, with most grouped under cluster 2. After 2012, cluster 1 was gradually replaced by cluster 2. Results of Bayesian Markov chain Monte Carlo analysis suggested that multiple lineages of genotype D were transmitted in mainland of China at an estimated evolutionary rate of 6.32×10(−3) substitutions per site per year, which is consistent with the global evolutionary rate of CV-A2 (5.82×10(−3) substitutions per site per year). Continuous transmission and evolution of CV-A2 resulted in the genetic polymorphism.