Abstract
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.
Highlights
Enterovirus 71 (EV-A71) belongs to the genus Enterovirus in the family Picornaviridae and is classified as a human enterovirus species A (HEV-A) based on its genome sequence
We look into the different types of recombination between poliovirus and non-polioenteroviruses and how they affected the evolution of RNA viruses such as EV-A71
EV-A71 is an enterovirus that is currently responsible for many large-scale outbreaks of HFMD
Summary
Enterovirus 71 (EV-A71) belongs to the genus Enterovirus in the family Picornaviridae and is classified as a human enterovirus species A (HEV-A) based on its genome sequence. In 2015, a total of 2,014,999 cases of HFMD including 124 deaths were reported in China. A large number of HFMD-associated fatal cases were recorded in Malaysia, Taiwan and China. In April to June 1997, 2628 EV-A71 cases were recorded in Sarawak, East Malaysia [9] During this outbreak, 889 children were hospitalized and 39 developed aseptic meningitis, leading to acute flaccid paralysis. The ORF comprising 6579 nucleotides can be classified into three polyprotein regions, namely, P1, P2 and P3. They encode for structural proteins (VP1 to VP4) in the P1 region and non-structural proteins in the P2 (2A-2C) and P3 regions (3A-3D) following proteolytic cleavage (Figure 1) [5]. The interaction between mutation and recombination enables viruses to benefit from the advantages of having a few beneficial mutations without being affected by many deleterious mutations
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