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UPDATE ON VACCINE DERIVED POLIOVIRUSES

Monday, 20th of August 2012 Print
  •  UPDATE ON VACCINE DERIVED POLIOVIRUSES

Editorial Note below; full text is at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6025a3.htm

The three categories of VDPVs differ in their public health importance. First, cVDPVs [Circulating vaccine derived polioviruses] have recovered the biologic properties of WPVs and have the potential to circulate for years in settings where polio vaccination coverage to prevent that particular type is low. In addition, for each case detected, another 100--1,000 asymptomatic infections occur among susceptible children, as is the case for WPVs (10). Second, iVDPVs [immunodeficient vaccine derived polioviruses]can be excreted for many years by persons with certain primary immunodeficiencies, and some chronic infections are latent. Many persons with prolonged iVDPV infections either spontaneously clear the infections or die from the complications of immunodeficiency. Nonetheless, in the absence of effective antiviral therapy, persons infected with iVDPVs without paralysis are at risk for developing paralytic poliomyelitis and might infect others with poliovirus, posing a risk for outbreaks in areas with low polio vaccination coverage. Third, aVDPVs [ambiguous vaccine derived polioviruses]are heterogeneous; some represent the initial isolates from cVDPV outbreaks, especially in areas with type-specific immunity gaps, and aVDPVs isolated during cVDPV outbreaks of the same serotype might be cVDPVs whose progenitors or progeny were not detected. Other aVDPVs, such as those detected in sewage in Estonia, Finland, and Israel, probably are iVDPVs from latent chronic infections. Still other aVDPVs, especially those with limited divergence, might represent limited spread of OPV virus or the upper limit of OPV divergence in a single normal vaccine recipient or contact.

The detection in Nigeria of numerous isolates with <1% divergence that were ancestral to cVDPV2 lineages (7) prompted a redefinition of VDPV2 for purposes of reporting by the Global Polio Laboratory Network to include isolates with >0.6% divergence and was applied beginning in 2010.

The increased frequency of VDPV detection compared with the previous reporting period (3) is attributable partly to increased surveillance sensitivity and improved laboratory methods. However, for cVDPVs, the most important factor is the growth of type-specific immunity gaps in areas with low routine vaccination, arising from the intensive use of mOPV1 and bOPV in SIAs. These alternative OPV formulations, by eliminating interference from the type 2 OPV strain, are more effective than tOPV in inducing higher levels of population immunity to WPV1 and WPV3. Their use in endemic and outbreak countries has facilitated WPV control. In settings of inadequate routine vaccination coverage with tOPV, conditions develop that favor multiple independent VDPV2 emergences, as occurred in DRC, India, Nigeria, and Somalia. Emergence of cVDPV3 appears to be rare but occurred in areas of low tOPV coverage in Ethiopia after a cVDPV2 emergence in 2008 (3).

Current and past experiences underscore the importance of robust routine vaccination with tOPV (or, alternatively, inactivated poliovirus vaccine) to prevent VDPV emergence and spread as well as to prevent WPV transmission. In countries with low routine vaccination coverage, closing the immunity gaps to all three poliovirus serotypes by periodic but regular use of tOPV in SIAs is essential to prevent cVDPV emergence (3). Maintenance of sensitive AFP surveillance also is crucial; any temporal and geographic clustering of vaccine-related isolates of the same serotype should prompt further investigation.

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