Key result
EV-A71 genetic recombination and mutations drive increased viral virulence and severe outbreak strains.
This review provides insights into the evolution patterns of EV-A71, focusing on its recombination history and the effect of spontaneous mutations on virulence.
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May inform EV-A71 genomic surveillance; leaves open whether recombination drives outbreaks pending prospective validation.
Enterovirus 71 (EV-A71) is a major etiological agent of hand, foot and mouth disease (HFMD) that mainly affects young children less than five years old. The onset of severe HFMD is due to neurological complications bringing about acute flaccid paralysis and pulmonary oedema. In this review, we address how genetic events such as recombination and spontaneous mutations could change the genomic organization of EV-A71, leading to an impact on viral virulence. An understanding of the recombination mechanism of the poliovirus and non-polio enteroviruses will provide further evidence of the emergence of novel strains responsible for fatal HFMD outbreaks. We aim to see if the virulence of EV-A71 is contributed solely by the presence of fatal strains or is due to the co-operation of quasispecies within a viral population. The phenomenon of quasispecies within the poliovirus is discussed to reflect viral fitness, virulence and its implications for EV-A71. Ultimately, this review gives an insight into the evolution patterns of EV-A71 by looking into its recombination history and how spontaneous mutations would affect its virulence.
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Mandary et al. (2018) conducted a review in Enterovirus 71 (EV-A71) infection and Hand, foot and mouth disease (HFMD). EV-A71 genomic recombination and spontaneous mutations was evaluated. Recombination and spontaneous mutations in the EV-A71 genome significantly impact viral virulence, adaptation, and fitness, driving the emergence of novel strains responsible for severe outbreaks.
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