Abstract
Vaccine derived poliovirus (VDPV) type 2 strains strongly divergent from the corresponding vaccine strain, Sabin 2, were repeatedly isolated from sewage in Slovakia over a period of 22 months in 2003–2005. Cell cultures of stool specimens from known immune deficient patients and from an identified putative source population of 500 people failed to identify the potential excretor(s) of the virus. The occurrence of VDPV in sewage stopped without any intervention. No paralytic cases were reported in Slovakia during the episode. According to a GenBank search and similarity plotting-analysis, the closest known relative of the first isolate PV2/03/SVK/E783 through all main sections of the genome was the type 2 poliovirus Sabin strain, with nucleotide identities in 5′UTR, P1, P2, P3, and 3′UTR parts of the genome of 88.6, 85.9, 87.3, 88.5, and 94.0 percent, respectively. Phenotypic properties of selected Slovakian aVDPV strains resembled those of VDPV strains isolated from immune deficient individuals with prolonged PV infection (iVDPV), including antigenic changes and moderate neurovirulence in the transgenic mouse model. One hundred and two unique VP1 coding sequences were determined from VDPV strains isolated from 34 sewage specimens. Nucleotide differences from Sabin 2 in the VP1 coding region ranged from 12.5 to 15.6 percent, and reached a maximum of 9.6 percent between the VDPV strains under study. Most of the nucleotide substitutions were synonymous but as many as 93 amino acid positions out of 301 in VP1 showed substitutions. We conclude that (1) individuals with prolonged poliovirus infection are not as rare as suggested by the studies on immune deficient patients known to the health care systems and (2) genetic divergence of VDPV strains may remain extensive during years long replication in humans.
Highlights
The trivalent oral poliovirus vaccine containing the attenuated Sabin strains of the three serotypes of poliovirus (Species Human enterovirus C, genus Enterovirus, family Picornaviridae) has been the central tool in the success of the Global Polio Eradication Initiative (GPEI)
While iVDPV strains usually are much more drifted from the corresponding parental Sabin strain than circulating vaccine derived poliovirus (cVDPV) strains, they are genetically of monotypic origin or recombinants of two or three Sabin strains, in contrast to the cVDPV strains which almost always have a part of the non-capsid coding region of the genome derived from one or more unidentified strain(s) of the Human enterovirus C (HEV-C) species [3]
In this paper we have described details of a previously reported episode of extended occurrence of neurovirulent type 2 vaccine derived poliovirus (VDPV) strains in environmental specimens collected in Slovakia
Summary
The trivalent oral poliovirus vaccine (tOPV) containing the attenuated Sabin strains of the three serotypes of poliovirus (Species Human enterovirus C, genus Enterovirus, family Picornaviridae) has been the central tool in the success of the Global Polio Eradication Initiative (GPEI). The high efficacy of OPV has traditionally overweighed its rare complication, the vaccine associated paralytic poliomyelitis (VAPP) occurring at an incidence of about 1 per half a million primary vaccinations [1,2,3] Another rare complication known for decades is the capacity of the OPV strains to institute prolonged infection in the tissues of persons with a deficiency in the humoral immune systems (reviewed in [1]). In the absence of the corresponding wild virus serotype and with decreasing OPV coverage, OPV-derived poliovirus strains can circulate in the human population, lose their attenuation and cause paralytic poliomyelitis referred to as outbreaks due to circulating vaccine derived poliovirus (cVDPV), first of its kind discovered in 2000 in the island of Hispaniola [5,6]. While iVDPV strains usually are much more drifted from the corresponding parental Sabin strain than cVDPV strains, they are genetically of monotypic origin or recombinants of two or three Sabin strains, in contrast to the cVDPV strains which almost always have a part of the non-capsid coding region of the genome derived from one or more unidentified strain(s) of the Human enterovirus C (HEV-C) species [3]
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