An emerging and expanding clade accounts for the persistent outbreak of Coxsackievirus A6-associated hand, foot, and mouth disease in China since 2013

Enterovirus (EV)-A71 and Coxsackievirus (CV)-A16 have historically been the major pathogens of hand, foot, and mouth disease (HMFD) in China; however, CV-A6, which had previously received little attention, became the predominant pathogen in 2013, and has remained one of the common pathogens since th...

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Published inVirology (New York, N.Y.) Vol. 518; pp. 328 - 334
Main Authors He, Shuizhen, Chen, Mengyuan, Wu, Wenhui, Yan, Qiang, Zhuo, Zhihao, Su, Xiaosong, Zhang, Shiyin, Ge, Shengxiang, Xia, Ningshao
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.05.2018
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Summary:Enterovirus (EV)-A71 and Coxsackievirus (CV)-A16 have historically been the major pathogens of hand, foot, and mouth disease (HMFD) in China; however, CV-A6, which had previously received little attention, became the predominant pathogen in 2013, and has remained one of the common pathogens since then. In this work, we conducted a molecular epidemiology study of CV-A6-associated HFMD in Xiamen from 2009 to 2015. The data showed CV-A6 pandemics had a certain periodicity rather than occurring randomly. Evolution analysis based on near-complete VP1 nucleotide sequences showed subgenotype D5 lineage 4 strains account for the persistent outbreak of CV-A6-associated HFMD in China since 2013. Alignment analysis revealed eight candidate amino acid substitutions in VP1, which may provide useful information for the research of CV-A6 virulence enhancement. This study contributed to elucidating the circulation patterns and genetic characteristics of CV-A6 in China; however, further surveillance and intervention in CV-A6 epidemics is recommended. •CV-A6 became the primary pathogen in China in 2013 and 2015.•D5.4 Lineage strains were responsible for CV-A6 epidemics since 2013 in China.•Eight VP1 candidate substitutions were identified between different CV-A6 lineage strains.
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ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2018.03.012