According to news reports and the Center for Disease Control and Prevention (CDC), there were three new outbreaks of vaccine-derived polioviruses reported since late 2010.
Poliovirus isolates are grouped into three categories, based on the extent of divergence of the major viral surface protein (VP1) nucleotide region compared with the corresponding OPV strain: 1) VRPVs (<1% divergent [types 1 and 3] or <0.6% divergent [type 2]); 2) VDPVs or Vaccine-derived polio virus (VRPVs that are >1% divergent [types 1 and 3] or >0.6% divergent [type 2] from the corresponding OPV strain); and 3) Wild polioviruses (WPV) (no genetic evidence of derivation from any vaccine strain).
VDPVs are further categorized as 1) cVDPVs, defined as evidence of person-to-person transmission in the community; 2) immunodeficiency-associated VDPVs (iVDPVs), which is when the virus is isolated from people with primary immunodeficiencies who have prolonged VDPV infections; and 3) ambiguous VDPVs (aVDPVs), defined as either clinical isolates from people with no known immunodeficiency or sewage isolates whose source is unknown, according to the CDC.
The three new outbreaks of circulating VDPVs (cVDPVs) ranged in size from six to 16 cases and were reported in Afghanistan, Ethiopia and India. The previously reported outbreaks in Nigeria, Democratic Republic of Congo (DRC) and Somalia continued through late 2010 or into 2011 and resulted in a total of 405 cases. In addition, two countries experienced importations of cVDPVs from Nigeria and nine people living in seven middle-income and developing countries who were newly identified as paralyzed were found to excrete VDPVs. VDPVs were also found among people and environmental samples in 15 countries. The emerging cVDPVs were type 2 in all but one country, according to a recent report in Morbidity and Mortality Weekly Report.
The three categories of VDPVs differ in their public health importance, according to the CDC report.
First, cVDPVs are made of 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 to 1,000 asymptomatic infections occur among susceptible children, which is also true for WPVs.
Second, iVDPVs can be excreted for many years by people with specific primary immunodeficiencies and some chronic infections are latent. Many people with prolonged iVDPV infections either spontaneously clear the infections or die from the complications of immunodeficiency. Even so, in the absence of effective antiviral therapy, those infected with iVDPVs without paralysis are at risk for developing paralytic poliomyelitis and may potentially infect others with the virus.
Third, aVDPVs are heterogeneous. Some represent the initial isolates from cVDPV outbreaks, especially in areas with type-specific immunity gaps. The authors of the report stress that aVDPVs isolated during cVDPV outbreaks of the same serotype might be cVDPVs whose progenitors or progeny were not detected.
Other aVDPVs are likely iVDPVs from latent chronic infections, while 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 authors wrote.
The increased frequency of VDPV detection compared with the previous reporting period in 2009 is attributable partly to increased surveillance sensitivity and improved laboratory methods. The increase in cVDPVs is mostly a result of increasing type-specific immunity gaps in areas with low routine vaccination, arising from the intensive use of monovalent OPV type 1 and bivalent OPV in mass immunization campaigns, according to the report.
According to Infectious Disease News, the CDC is now using this information to encourage the importance of receiving the trivalent oral poliovirus vaccination to prevent both wild-type and vaccine-derived poliovirus outbreaks.
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