Vaccine-Derived Polioviruses
I started my scientific career working on vaccine-derived polioviruses. We’ve come a long way since those distant days and we’re slowly getting closer to eradicating polio worldwide, but it’s not all over yet:
In 1988, the World Health Assembly resolved to eradicate poliomyelitis worldwide. Subsequently, the Global Polio Eradication Initiative of the World Health Organization (WHO) reduced the global incidence of polio associated with wild polioviruses (WPVs) from an estimated 350,000 cases in 1988 to 1,998 reported cases in 2006 and reduced the number of countries that have never succeeded in interrupting WPV transmission to four (Afghanistan, India, Nigeria, and Pakistan). However, because vaccine-derived polioviruses (VDPVs) can produce polio outbreaks in areas with low rates of Sabin oral poliovirus vaccine (OPV) coverage and can replicate for years in immunodeficient persons, enhanced strategies are needed to limit emergence of VDPVs and stop all use of OPV once WPV transmission is eliminated. This report updates a summary of VDPV activity published in 2006 and describes VDPVs detected during January 2006-August 2007.
VDPVs can cause paralytic polio in humans and the potential for sustained circulation of poliovirus. VDPVs resemble WPVs biologically and differ from the majority of Sabin vaccine-related poliovirus isolates by having genetic properties consistent with prolonged replication or transmission. Because poliovirus genomes evolve at a rate of approximately 1% per year, Sabin vaccine-related isolates that differ from the corresponding OPV strain by more than 1% of nucleotide positions (usually determined by sequencing the genomic region encoding the major viral surface protein, VP1) are estimated to have replicated for at least 1 year after administration of an OPV dose. This is substantially longer than the normal period of vaccine virus replication of 4-6 weeks.
Poliovirus isolates can be distinguished by their three serotypes: type 1, type 2, and type 3. Isolates also can be divided into three categories, based on the extent of VP1 nucleotide sequence divergence from the corresponding Sabin OPV strain: 1) Sabin vaccine-like viruses (<1% divergent), 2) VDPVs (1%-15% divergent), and 3) WPVs (>15% divergent) (4). VDPVs are further categorized as 1) circulating VDPVs (cVDPVs), which emerge in areas with inadequate OPV coverage; 2) immunodeficient-associated VDPVs (iVDPVs), which are isolated from persons with primary immunodeficiencies who have prolonged VDPV infections after exposure to OPV; and 3) ambiguous VDPVs (aVDPVs), which are either clinical isolates from persons with no known immunodeficiency or environmental isolates whose ultimate source has not been identified.
Related:
- Epidemics to eradication: the modern history of poliomyelitis
- Imaging Poliovirus Entry in Live Cells
Tags: eradication, paralysis, polio, poliomyelitis, poliovirus, Sabin oral poliovirus vaccine, serotypes, vaccination, World Health Organization
Well, I always wondered how someone I know who is in their mid-20′s now (in North Africa) managed to catch polio as a child, even having been vaccinated for it. I guess what he caught must have differed more than one percent from the vaccine he received. Am I understanding that correctly?
Best regards,
Eileen
Not necessarily. No vaccine is 100% effective in all hosts, so it could have been one of the rare cases of vaccine failure. The only way to tell would have been to sequence recovered virus.
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