Abstract
Wild poliovirus has remained endemic in northern Nigeria because of low coverage achieved in the routine immunization program and in supplementary immunization activities (SIAs). An outbreak of infection involving 315 cases of type 2 circulating vaccine-derived poliovirus (cVDPV2; >1% divergent from Sabin 2) occurred during July 2005–June 2010, a period when 23 of 34 SIAs used monovalent or bivalent oral poliovirus vaccine (OPV) lacking Sabin 2. In addition, 21 “pre-VDPV2” (0.5%–1.0% divergent) cases occurred during this period. Both cVDPV and pre-VDPV cases were clinically indistinguishable from cases due to wild poliovirus. The monthly incidence of cases increased sharply in early 2009, as more children aged without trivalent OPV SIAs. Cumulative state incidence of pre-VDPV2/cVDPV2 was correlated with low childhood immunization against poliovirus type 2 assessed by various means. Strengthened routine immunization programs in countries with suboptimal coverage and balanced use of OPV formulations in SIAs are necessary to minimize risks of VDPV emergence and circulation.
Highlights
The cornerstone of the Global Polio Eradication Initiative is immunization of children with multiple doses of oral poliovirus vaccine (OPV), via both routine immunization (RI) and supplementary immunization activities (SIAs) [1]
To more efficiently stop wild poliovirus type 1 (WPV1) and WPV3 transmission, monovalent OPV type 1 was regularly used in SIAs starting in March 2006, and mOPV3 was intermittently used starting in July 2007 [12, 13]
In August 2006, virologic investigations detected a cluster of acute flaccid paralysis (AFP) cases associated with Sabin type 2 (Sabin 2)-related isolates in northern Nigeria; sequence analysis revealed that the isolates were vaccine-derived polioviruses (VDPVs) [17]
Summary
The cornerstone of the Global Polio Eradication Initiative is immunization of children with multiple doses of oral poliovirus vaccine (OPV), via both routine immunization (RI) and supplementary immunization activities (SIAs) [1]. VDPVs are operationally defined as OPV-related isolates having .1% nucleotide (nt) sequence divergence from the parental OPV strain in the 900-nt region encoding the major capsid surface protein, VP1 [4, 5]. This arbitrary demarcation represents 1 year of poliovirus (PV) replication after administration of the initiating OPV dose [7], substantially longer than the normal postvaccination excretion period of 4–6 weeks [2, 8]. In August 2006, virologic investigations detected a cluster of acute flaccid paralysis (AFP) cases associated with Sabin 2-related isolates in northern Nigeria; sequence analysis revealed that the isolates were VDPVs [17]. We found an additional 21 cases with ‘‘pre-VDPV2’’ isolates (0.5%–1% VP1 divergent from Sabin 2), sporadically found in settings of high OPV coverage
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