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Review
. 2011 Aug;3(8):1460-84.
doi: 10.3390/v3081460. Epub 2011 Aug 17.

Recombination between poliovirus and coxsackie A viruses of species C: a model of viral genetic plasticity and emergence

Nicolas Combelas  1 , Barbara Holmblat, Marie-Line Joffret, Florence Colbère-Garapin, Francis Delpeyroux
Affiliations
Review

Recombination between poliovirus and coxsackie A viruses of species C: a model of viral genetic plasticity and emergence

Nicolas Combelas et al. Viruses. 2011 Aug.

Abstract

Genetic recombination in RNA viruses was discovered many years ago for poliovirus (PV), an enterovirus of the Picornaviridae family, and studied using PV or other picornaviruses as models. Recently, recombination was shown to be a general phenomenon between different types of enteroviruses of the same species. In particular, the interest for this mechanism of genetic plasticity was renewed with the emergence of pathogenic recombinant circulating vaccine-derived polioviruses (cVDPVs), which were implicated in poliomyelitis outbreaks in several regions of the world with insufficient vaccination coverage. Most of these cVDPVs had mosaic genomes constituted of mutated poliovaccine capsid sequences and part or all of the non-structural sequences from other human enteroviruses of species C (HEV-C), in particular coxsackie A viruses. A study in Madagascar showed that recombinant cVDPVs had been co-circulating in a small population of children with many different HEV-C types. This viral ecosystem showed a surprising and extensive biodiversity associated to several types and recombinant genotypes, indicating that intertypic genetic recombination was not only a mechanism of evolution for HEV-C, but an usual mode of genetic plasticity shaping viral diversity. Results suggested that recombination may be, in conjunction with mutations, implicated in the phenotypic diversity of enterovirus strains and in the emergence of new pathogenic strains. Nevertheless, little is known about the rules and mechanisms which govern genetic exchanges between HEV-C types, as well as about the importance of intertypic recombination in generating phenotypic variation. This review summarizes our current knowledge of the mechanisms of evolution of PV, in particular recombination events leading to the emergence of recombinant cVDPVs.

Keywords: VDPV; emergence; enterovirus; genetic plasticity; live vaccine; poliomyelitis; poliovirus; recombination; vaccine-derived poliovirus.

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Figures

Figure 1.
Figure 1.
Schematic representation of the capsid and genome of poliovirus. (a) The icosahedral capsid of the virus is represented with the three external proteins VP1, -2 and -3 constituting a protomer. The 5-fold, 3-fold and 2-fold axis of symmetry are indicated. The canyon recognized by the cellular viral receptor CD155 is shown. (b) The genome is constituted of a poly-adenylated positive strand RNA genome that is covalently linked to a small viral protein VPg (also named 3B) at the 5′ terminus. The single open-reading frame is flanked by two non-coding regions (5′NC and 3′NC). The single viral polyprotein is cleaved mostly by the viral proteases 2A, 3C and 3CD (triangles indicate cleavage sites). The peptidic precursors P1, P2 and P3 are subsequently cleaved to give the different viral proteins including the capsid proteins (VP1–4) and the non-structural proteins such as the RNA polymerase 3Dpol.
Figure 2.
Figure 2.
Reported poliomyelitis outbreaks due to circulating vaccine-derived polioviruses (cVDPVs) (since 1988). The country, the type of implicated cVDPVs, the year of the outbreak and the number of reported cases are indicated. Data are those available from WHO/HQ on 3 May 2011 [11].
Figure 3.
Figure 3.
Genetic features of recombinant genomes from cVDPVs implicated in different outbreaks. A schematic view of the genetic organization of the poliovirus genome is given (see also Figure 1). The presence of vaccine-derived sequences are indicated above the cVDPV genomes (mutated Sabin 1 or 2 sequences) as well as the non-vaccine sequences derived from other HEV-Cs (HEV-C sequences). Patterns differentiate HEV-C sequences that differed significantly from each other. Data are modified from [83] (Hispaniola), [84] (Philippines), [67] (Egypt) and [85] (Nigeria).
Figure 4.
Figure 4.
Genetic features of recombinant cVDPV genomes from Madagascar. Some cVDPVs isolated in Madagascar in 2002 and 2005 are represented as in Figure 3. Non-vaccine sequences (HEV-C sequences) showing similarity with those of coxsackie A viruses (CV-A11, -A13, -A17) isolated in the same province are indicated. Data are modified from [–90].
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