Multiple Independent Emergences of Type 2 Vaccine-Derived Polioviruses during a Large Outbreak in northern Nigeria

Journal of Virology
March 2013, volume 87, issue 6
http://jvi.asm.org/content/current
[No relevant content]

Published ahead of print 13 February 2013, doi: 10.1128/​JVI.02954-12
Multiple Independent Emergences of Type 2 Vaccine-Derived Polioviruses during a Large Outbreak in northern Nigeria
Cara C. Burns1,#, Jing Shaw1, Jaume Jorba1, David Bukbuk3, Festus Adu4, Nicksy Gumede5, Muhammed Ali Pate6, Emmanuel Ade Abanida6, Alex Gasasira7, Jane Iber1, Qi Chen1, Annelet Vincent1, Paul Chenoweth2, Elizabeth Henderson1, Kathleen Wannemuehler2, Asif Naeem8, Rifqiyah Nur Umami8, Yorihiro Nishimura8, Hiroyuki Shimizu8, Marycelin Baba3, Adekunle Adeniji4, A. J. Williams1, David R. Kilpatrick1, M. Steven Oberste1, Steven G. Wassilak2, Oyewale Tomori9, Mark A. Pallansch1 and Olen Kew1

ABSTRACT
Since 2005, a large poliomyelitis outbreak associated with type 2 circulating vaccine-derived poliovirus (cVDPV2) has occurred in northern Nigeria, where immunization coverage with trivalent oral poliovirus vaccine (tOPV) has been low. Phylogenetic analysis of P1/capsid region sequences of isolates from each of the 403 cases reported in 2005–2011 resolved the outbreak into 23 independent VDPV2 emergences, at least seven of which established circulating lineage groups. Virus from one emergence (lineage group 2005-8; 361 isolates) was estimated to have circulated for over six years. The population of the major cVDPV2 lineage group expanded rapidly in early 2009, fell sharply after two tOPV rounds in mid-2009, and gradually expanded again through 2011. The two major determinants of attenuation of the Sabin 2 OPV strain (A481 in the 5’ -untranslated region [5’ -UTR] and VP1-Ile143) had been replaced in all VDPV2 isolates; most A481 5’ -UTR replacements occurred by recombination with other enteroviruses. cVDPV2 isolates representing different lineage groups had biological properties indistinguishable from those of wild polioviruses, including efficient growth in neuronal-derived HEK293 cells, the capacity to cause paralytic disease in both humans and PVR-Tg21 transgenic mice, loss of the temperature-sensitive phenotype, and the capacity for sustained person-to-person transmission. We estimate from the poliomyelitis case count and the paralytic case:infection ratio for type 2 wild poliovirus infections that ∼700,000 cVDPV2 infections have occurred during the outbreak. The detection of multiple concurrent cVDPV2 outbreaks in northern Nigeria highlights the risks of cVDPV emergence accompanying tOPV use at low rates of coverage in developing country settings.