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This strategy has reduced the incidence of polio worldwide by over 99% since the start of the global eradication program in 1988, and has restricted wild PV circulation to countries in western and central Africa and southern Asia [2].However, replication of OPV in humans is frequently accompanied by genetic changes in the vaccine, are major human pathogens causing the acute paralytic disease poliomyelitis.The human enteroviruses (HEV) are classified into five species, HEV-A to -D, and the PV species (PV-1 to −3).This indicates that co-circulation of HEV-C and OPV strains is associated with evolution by recombination, resulting in unexpectedly extensive viral diversity in small human populations in some tropical regions.This probably contributed to the emergence of recombinant VDPVs.The species HEV-C includes several serotypes of coxsackie A virus, and segregates in the same phylogenetic cluster (cluster C) as the PV species [1].

The first outbreak of poliomyelitis (21 cases) associated with VDPVs, was reported in 2000–2001, in the Dominican Republic and Haiti [12].We looked for other VDPVs and for circulating enteroviruses in 316 stools collected from healthy children living in the small area where most of the AFP cases occurred.We found vaccine PVs, two VDPVs similar to those found in AFP cases, some echoviruses, and above all, many serotypes of coxsackie A viruses belonging to HEV-C, with substantial genetic diversity.The single large coding region of the genome is flanked by 5′- and 3′-UTR.The coding region is translated as a single polyprotein that is processed by viral proteases to yield the mature viral proteins including the capsid proteins VP1 to VP4 and non-structural proteins including proteases and the RNA-dependent RNA polymerase 3D.

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