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Evidence for emergence of diverse polioviruses from C-cluster coxsackie A viruses and implications for global poliovirus eradication
Open accessAbstract
The poliovirus (PV) eradication campaign is conducted on the premise that this virus, because of the lack of a zoonotic reservoir, will not reemerge once eradicated. This report examines the origin of PV using theoretical and experimental approaches. Our rooted phylogenetic analysis suggests a speciation of PV from a C-cluster coxsackie A virus (C-CAV) ancestor through mutation of the capsid that caused a receptor switch from intercellular adhesion molecule-1 to CD155, leading to a change of pathogenicity. This hypothesis is supported experimentally with chimeras generated from three different pairs of PV and C-CAV. Those carrying the PV capsid and the replication proteins of C-CAVs replicated well, whereas their reciprocal counterparts were either debilitated or dead. This phenomenon of asymmetry is observed also in recombinants between PV1 and C-CAV20, selected in tissue culture cells using a previously undescribed protocol. The recombinants are generated at frequencies of 10 −6 typical for PV interserotype recombination. Strikingly, they resemble genetically and phenotypically, including neurovirulence in CD155 transgenic mice, the large majority of circulating vaccine-derived PVs that have caused poliomyelitis outbreaks in different parts of the world. These data provide experimental evidence for C-CAVs being partners to PVs in generating diverse PV progeny by homologous recombination. They support speciation of a novel human pathogen (PV) from a pool of different human pathogens (C-CAVs). In a PV-free world without PV neutralizing antibodies, contemporary C-CAV, like their ancestor(s), could be fertile ground for a PV-like agent to emerge by mutation.
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“and lend support to the proposal that PVs and HEV-C should be considered to be members of a single species [5,36,55,56].”
From Co-Circulation and Evolution of Polioviruses and Species C Enteroviruses in a District of Madagascar (2007) · cites this paper as [55]
In the citing paper
“This hypothesis was recently supported experimentally with recombinant viruses generated from PVs and CA20 or CA21 prototype strains [55].”
From Co-Circulation and Evolution of Polioviruses and Species C Enteroviruses in a District of Madagascar (2007) · cites this paper as [55]
In the citing paper
“The genetic structure resembling that of cVDPV, with a PV capsid, consistently survived much better than did their reciprocal counterparts with a CAV capsid.”
From Recombination between Poliovirus and Coxsackie A Viruses of Species C: A Model of Viral Genetic Plasticity and Emergence (2011) · cites this paper as [111]
In the citing paper
“Interestingly, the PV1/CV-A20 recombinants were nearly as neurovirulent in Tg-PVR mice as wild PV1 [111].”
From Recombination between Poliovirus and Coxsackie A Viruses of Species C: A Model of Viral Genetic Plasticity and Emergence (2011) · cites this paper as [111]
In the citing paper
“This suggested that some CAVs can be recombination partners of PV in nature.”
From Recombination between Poliovirus and Coxsackie A Viruses of Species C: A Model of Viral Genetic Plasticity and Emergence (2011) · cites this paper as [111]
In the citing paper
“A non-functional interaction between the protein VP3 of some CAVs and the protein 2C of PV could explain the defect in multiplication of CAV/PV recombinants [111,112] and their apparent absence in nature [88].”
From Recombination between Poliovirus and Coxsackie A Viruses of Species C: A Model of Viral Genetic Plasticity and Emergence (2011) · cites this paper as [111]
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Metadata
- Authors
- Jiang, P., Faase, J. A. J., Toyoda, H., Paul, A., Wimmer, E., & Gorbalenya, A. E.
- Affiliations
- Stony Brook University (US)
- Leiden University Medical Center (NL)
- Corresponding author
- Wimmer, Eckard
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2007-05-29
- Volume
- 104
- Issue
- 22
- Pages
- 9457-9462
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC1874223
- OpenAlex
- W2026369794
- Cited by
- 105
- References
- 38
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 1 · 2021: 6 · 2020: 1 · 2019: 8 · 2018: 6 · 2017: 3 · 2016: 2 · 2015: 6 · 2014: 12 · 2013: 5 · 2012: 9
- FWCI
- 6.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- European Commission (LSHG-CT-2004-511960)
- National Institutes of Health
- National Cancer Institute
- National Institute of General Medical Sciences (GM 650300)
- National Institute of Allergy and Infectious Diseases (AI-15122, R37AI015122, R01AI015122)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Viral Infections and Immunology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
- Health Sciences › Medicine › Epidemiology › Virology and Viral Diseases
- Keywords
- poliovirus, coxsackievirus A, CD155, ICAM-1, homologous recombination, vaccine-derived poliovirus, polio eradication, neurovirulence, chimeric viruses, poliomyelitis outbreak
- MeSH terms
- Animals, Base Sequence, Membrane Proteins, Mice, Transgenic, Molecular Sequence Data, Phylogeny, Poliomyelitis, Receptors, Virus, Selection, Genetic, Genetic Variation, Poliovirus, Mice
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