- - - UPDATE ON VACCINE DERIVED POLIOVIRUS

Saturday, 1st of June 2013

UPDATE ON VACCINE DERIVED POLIOVIRUSES

Editorial note below; full text is at http://www.who.int/wer/2012/wer8738.pdf

WHO convened a meeting in May 2012 to review current understanding of VDPVs. This meeting was promptedby: the prolonged large cVDPV2 outbreaks in Nigeria

and DRC; the multiple emergences of cVDPV2 lineages in these and other countries; the new cVDPV outbreaks in Madagascar, Mozambique and Yemen; the increased

detection of iVDPV infections in developing countries; and the continued detection of aVDPVs that resembled cVDPVs and iVDPVs as reported here and earlier. The

following key points were reaffirmed.

1. The clinical signs and severity of paralysis associatedwith VDPV and WPV infections are indistinguishable.

2. cVDPVs pose the same public health threat asWPVs and require the same control measures.

3. Surveillance for WPVs and VDPVs should continueto be strengthened.

4. Environmental surveillance to detect VDPV and WPV infections can serve as an important, sensitive supplement to AFP surveillance in many settings.

5. Persons with prolonged iVDPV infections may transmit poliovirus to others, raising the risk of VDPV circulation in settings of low population immunity to the corresponding poliovirus serotype.

6. Prolonged iVDPV excretion is uncommon among persons with PID exposed to OPV.

7. The prevalence of long-term iVDPV excretors may, however, be higher than suggested by existing surveillance of persons with primary immunodeficiencies.

The development of treatments for prolonged iVDPV infections may facilitate detection of and access to infected individuals.

Detection of genetically related VDPVs from different individuals who are not close contacts, and even if none of the infected persons had AFP, is evidence of VDPV circulation, as described here for Madagascar. Such events should prompt the same response as detection of VDPVs in AFP patients or WPV in individuals or the environment. Key risk factors for cVDPV emergence and spread are: (i) development of immunity gaps arising from low rates of poliovirus vaccine coverage; (ii) prior elimination of the corresponding WPV serotype; (iii) low rates of routine immunization coverage with tOPV coupled with emphasis on use in SIAs of monovalent OPV (mOPV) and bivalent OPV (bOPV, types 1 and 3);8 and (iv) insensitive AFP surveillance. Many of these factors exist in areas of insecurity. In this context it was recognized that VDPV2s present the greatest threat for emergence. It was emphasized that routine immunization should be strengthened and, in the immediate future, regular SIAs using tOPV conducted to close the any immunity gaps.

Because all cases of poliomyelitis since 1999 involving PV2 have been associated with use of tOPV– primarily in the context of low poliovirus vaccine coverage –, the Strategic Advisory Group of Experts advising the GPEI has recommended coordinated simultaneous global cessation of tOPV use in both routine immunization and SIAs, with a switch to bOPV as soon as it is safe to do so.9 Prerequisites for such a switch include strong evidence of cessation of all cVDPV2 transmission based on sensitive poliovirus surveillance, maintenance of high population immunity in all settings, wider use of inactivated poliovirus vaccine to maintain immunity to all 3 serotypes, strategic deployment of OPV stockpiles and maintenance and enhancement of global poliovirus surveillance.