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NEW THIS WEDNESDAY: EMERGENCY OF VACCINE-DERIVED POLIOVIRUSES, DEMOCRATIC REPUBLIC OF CONGO

Monday, 23rd of September 2013 Print
  • EMERGENCE OF VACCINE-DERIVED POLIOVIRUSES, DEMOCRATIC REPUBLIC OF CONGO, 2004–2011

From the discussion section of this article: ‘The origin of circulating VDPV2 in DRC was probably the result of low population immunity to PV because of a combination of low vaccination coverage in some communities (39) and the prior elimination of the indigenous WPV of the same serotype (20). Because WPV2 has not circulated anywhere globally since 1999, immunity to PV type 2 is not being stimulated through virus circulation. Routine vaccination coverage is low in many regions of DRC; estimated OPV3 coverage was 73% (40). Additional factors that probably facilitated circulation of VDPVs in some communities were poor hygiene, inadequate sanitation, and tropical climate. Because similar conditions exist elsewhere, ongoing high-quality surveillance will be essential for eliminating polio in Africa. The need for vigilance was confirmed by the detection of circulating VDPV2 and circulating VDPV3 in Ethiopia (Gumede et al., unpub. data), circulating VDPV2 in Chad, and circulating VDPV2 in Somalia (20). The occurrence of WPV outbreaks in DRC emphasizes the need to maintain high vaccine coverage and acute flaccid paralysis surveillance to minimize the risk for emergence of VDPVs or circulation of imported WPVs.’

Abstract and introduction below; article, with figures and technical appendices, at http://wwwnc.cdc.gov/eid/article/19/10/13-0028_article.htm

Volume 19, Number 10—October 2013

Research 

Nicksy Gumede  , Olivia Lentsoane, Cara C. Burns, Mark Pallansch, Esther de Gourville, Riziki Yogolelo, Jean Jacques Muyembe-Tamfum, Adrian Puren, Barry D. Schoub, and Marietjie Venter

Author affiliations: National Institute for Communicable Diseases, Johannesburg, South Africa (N. Gumede, O. Lentsoane, A. Puren, B.D. Schoub, M. Venter); University of Witwatersrand, Johannesburg (N. Gumede, B.D. Schoub); University of Pretoria, Pretoria, South Africa (M. Venter); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (C.C. Burns, M. Pallansch); World Health Organization, Geneva, Switzerland (E. de Gourville); National Institute for Biomedical Research, Kinshasa/Gombe, Democratic Republic of Congo (R. Yogolelo, J.J. Muyembe-Tamfum)

 

Abstract

Polioviruses isolated from 70 acute flaccid paralysis patients from the Democratic Republic of Congo (DRC) during 2004–2011 were characterized and found to be vaccine-derived type 2 polioviruses (VDPV2s). Partial genomic sequencing of the isolates revealed nucleotide sequence divergence of up to 3.5% in the viral protein 1 capsid region of the viral genome relative to the Sabin vaccine strain. Genetic analysis identified at least 7 circulating lineages localized to specific geographic regions. Multiple independent events of VDPV2 emergence occurred throughout DRC during this 7-year period. During 2010–2011, VDPV2 circulation in eastern DRC occurred in an area distinct from that of wild poliovirus circulation, whereas VDPV2 circulation in the southwestern part of DRC (in Kasai Occidental) occurred within the larger region of wild poliovirus circulation.

Indigenous wild-type poliovirus (WPV) remains endemic to 3 countries: Nigeria, Afghanistan, and Pakistan (1). Poliovirus (PV) circulation has been sustained in several African countries after importation from a PV-endemic country, resulting in reestablished virus transmission. Worldwide, the number of cases decreased by 50% from 2010 to 2011 (2). In developing countries, live attenuated oral PV vaccine (OPV) is still the vaccine of choice. However, the virus can revert to virulence during OPV replication in humans, resulting in person-to-person spread and circulation of vaccine-derived PVs in areas with low rates of vaccination coverage (3). Substantial sequence drift occurs in circulating VDPVs (>1% nt difference in types 1 and 3, >0.6% nt difference in type 2), indicating prolonged replication of the vaccine strain in human populations and consequent changes in phenotypic properties of neurovirulence and transmissibility (3,4). Poliomyelitis outbreaks associated with circulating VDPVs have been reported in several countries, including Egypt (1982–1993), Haiti (2000–2001), Dominican Republic (2000–2001), Philippines (2001), Madagascar (2002 and 2005), China (2004), Cambodia (2005–2006), Indonesia (2005), and Nigeria 2005–2010 (411). As a result of accumulating evidence about the emergence and spread of circulating VDPVs, there are plans to stop using OPV and synchronously implement more widespread use of inactivated polio vaccine (1215). A better understanding of VDPV persistence and circulation is crucial for deciding when and how to stop vaccination with OPV after WPVs have been eradicated (1618).

In early 2001, indigenous WPVs were eliminated from DRC, but starting in 2006 and continuing through 2011, WPV was imported into DRC from Angola several times. During 2010−2011 in DRC, 2 genetic clusters of the Southeast Asian PV1 genotype circulated; this genotype was imported twice from India to Angola and subsequently to DRC. Since December 2011, no cases of infection with WPV have been detected in DRC (19).

Monovalent OPV types 1 and 3 and bivalent OPV effectively induce immunity because of a lack of interference by the type 2 component (20). Reliance on monovalent OPV1, monovalent OPV3, and bivalent OPV in supplemental vaccination activities has contributed to the emergence of VDPV2. These alternative OPV formulations are more effective than trivalent OPV at inducing higher levels of population immunity to WPV1 and WPV3 because there is no interference from the type 2 OPV strain. No type 2–specific immunity is induced. To maintain population immunity to type 2 PV, the World Health Organization (WHO) recommends 2 doses of trivalent OPV each year.

We describe the genetic characterization of circulating VDPV2 associated with outbreaks in DRC. During 2004–2011, the same time that extensive circulating VDPV transmission occurred in Nigeria, VDPV2 excretion was found for 70 children with acute flaccid paralysis (10,11). The close genetic relationships among many of the viruses provide evidence for circulation in several regions of DRC.

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