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Author

Olen M. Kew

Bio: Olen M. Kew is an academic researcher from Centers for Disease Control and Prevention. The author has contributed to research in topics: Poliovirus & Poliomyelitis. The author has an hindex of 52, co-authored 113 publications receiving 9265 citations.


Papers
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Journal ArticleDOI
TL;DR: Two other adverse events have been identified more recently: long-term excretion of highly evolved vaccine-derived polioviruses (VDPVs) in persons with primary immunodeficiencies, and polio outbreaks associated with circulating VDPVs in areas with low rates of OPV coverage.
Abstract: As the global eradication of wild poliovirus nears, the World Health Organization (WHO) is addressing challenges unprecedented in public health. The live, attenuated oral poliovirus vaccine (OPV), used for more than four decades to interrupt poliovirus transmission, and the vaccine of choice for developing countries, is genetically unstable. Reversion of the small number of substitutions conferring the attenuated phenotype frequently occurs during OPV replication in humans and is the underlying cause of the rare cases of vaccine-associated paralytic poliomyelitis (VAPP) in OPV recipients and their close contacts. Whereas VAPP has long been recognized, two other adverse events have been identified more recently: (a) long-term excretion of highly evolved vaccine-derived polioviruses (VDPVs) in persons with primary immunodeficiencies, and (b) polio outbreaks associated with circulating VDPVs in areas with low rates of OPV coverage. Developing a posteradication strategy to minimize the risks of VDPV emergence and spread has become an urgent WHO priority.

601 citations

Journal ArticleDOI
12 Apr 2002-Science
TL;DR: An outbreak of paralytic poliomyelitis occurred in the Dominican Republic and Haiti during 2000–2001 and was associated with the circulation of a derivative of the type 1 OPV strain, probably originating from a single OPV dose given in 1998–1999.
Abstract: An outbreak of paralytic poliomyelitis occurred in the Dominican Republic (13 confirmed cases) and Haiti (8 confirmed cases, including 2 fatal cases) during 2000-2001. All but one of the patients were either unvaccinated or incompletely vaccinated children, and cases occurred in communities with very low (7 to 40%) rates of coverage with oral poliovirus vaccine (OPV). The outbreak was associated with the circulation of a derivative of the type 1 OPV strain, probably originating from a single OPV dose given in 1998-1999. The vaccine-derived poliovirus associated with the outbreak had biological properties indistinguishable from those of wild poliovirus.

553 citations

Journal ArticleDOI
TL;DR: Current challenges to the final eradication of paralytic poliomyelitis include the continued transmission of wild polioviruses in endemic reservoirs, reinfection of polio-free areas, outbreaks due to circulating vaccine-derived poliovIRuses, and persistent excretion of vaccine- derived poliovirus by a few vaccinees with B-cell immunodeficiencies.
Abstract: Poliomyelitis has appeared in epidemic form, become endemic on a global scale, and been reduced to near-elimination, all within the span of documented medical history. Epidemics of the disease appeared in the late 19th century in many European countries and North America, following which polio became a global disease with annual epidemics. During the period of its epidemicity, 1900-1950, the age distribution of poliomyelitis cases increased gradually. Beginning in 1955, the creation of poliovirus vaccines led to a stepwise reduction in poliomyelitis, culminating in the unpredicted elimination of wild polioviruses in the United States by 1972. Global expansion of polio immunization resulted in a reduction of paralytic disease from an estimated annual prevaccine level of at least 600,000 cases to fewer than 1,000 cases in 2000. Indigenous wild type 2 poliovirus was eradicated in 1999, but unbroken localized circulation of poliovirus types 1 and 3 continues in 4 countries in Asia and Africa. Current challenges to the final eradication of paralytic poliomyelitis include the continued transmission of wild polioviruses in endemic reservoirs, reinfection of polio-free areas, outbreaks due to circulating vaccine-derived polioviruses, and persistent excretion of vaccine-derived poliovirus by a few vaccinees with B-cell immunodeficiencies. Beyond the current efforts to eradicate the last remaining wild polioviruses, global eradication efforts must safely navigate through an unprecedented series of endgame challenges to assure the permanent cessation of all human poliovirus infections.

343 citations

Journal ArticleDOI
01 Oct 1987-Virology
TL;DR: Comparing 150 bases of genomic sequence information from 62 isolates obtained from poliomyelitis patients in five continents allowed us to identify numerous geographic foci of endemic circulation of wild type 1 polioviruses, reveal previously unsuspected links between cases in distant communities, and recognize the recombinant (vaccine-wild; wild-wild) origins of some epidemic poliovIRuses.

333 citations


Cited by
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Journal ArticleDOI

3,734 citations

Journal ArticleDOI
28 Jul 1988-Nature
TL;DR: A novel mechanism of initiation on poliovirus RNA occurs by binding of ribosomes to an internal sequence within the 5′ noncoding region, which may explain the disparate translation of several other eukaryotic messenger RNAs.
Abstract: Poliovirus RNA is naturally uncapped, therefore its translation must proceed via a cap-independent mechanism. Translation initiation on poliovirus RNA occurs by binding of ribosomes to an internal sequence within the 5' noncoding region. This novel mechanism of initiation may explain the disparate translation of several other eukaryotic messenger RNAs.

1,926 citations

Journal ArticleDOI
26 Mar 1982-Science
TL;DR: RNA viruses show high mutation frequencies partly because of a lack of the proofreading enzymes that assure fidelity of DNA replication, and high rates of replication reflected in rates of RNA genome evolution which can be more than a millionfold greater than the rates of the DNA chromosome evolution of their hosts.
Abstract: RNA viruses show high mutation frequencies partly because of a lack of the proofreading enzymes that assure fidelity of DNA replication. This high mutation frequency is coupled with high rates of replication reflected in rates of RNA genome evolution which can be more than a millionfold greater than the rates of the DNA chromosome evolution of their hosts. There are some disease implications for the DNA-based biosphere of this rapidly evolving RNA biosphere.

1,394 citations

Journal ArticleDOI
01 Sep 1985-Nature
TL;DR: The first atomic resolution structure of an animal virus, human rhinovirus 14, strikingly similar to known icosahedral plant RNA viruses, and four neutralizing immunogenic regions have been identified.
Abstract: We report the first atomic resolution structure of an animal virus, human rhinovirus 14. It is strikingly similar to known icosahedral plant RNA viruses. Four neutralizing immunogenic regions have been identified. These, and corresponding antigenic sequences of polio and foot-and-mouth disease viruses, reside on external protrusions. A large cleft on each icosahedral face is probably the host cell receptor binding site.

1,347 citations