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Updated: Jul 20, 2026
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Particle Agglutination Method for Poliovirus Identification
Published on: April 20, 2011
Will the polio niche remain vacant?
E Rieder1, A E Gorbalenya, C Xiao
1Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, 11794-5222, USA.
Developments in Biologicals
|January 5, 2002
Summary
C-Cluster enteroviruses (C-CEVs) show diverse disease patterns, with Coxsackie A viruses (C-CAVs) causing respiratory illness and polioviruses (PVs) causing poliomyelitis. This study explores how receptor specificity, particularly ICAM-1 for C-CAVs and CD155 for PVs, drives these differences and suggests PVs may have evolved from C-CAVs.
Area of Science:
- Virology
- Molecular Biology
- Evolutionary Biology
Background:
- C-Cluster enteroviruses (C-CEVs), including Coxsackie A viruses (C-CAVs) and polioviruses (PVs), are grouped by genomic sequences but exhibit distinct human disease syndromes.
- C-CAVs cause respiratory diseases, similar to major group rhinoviruses (magHRV), utilizing ICAM-1 as their cellular receptor.
- PVs invade the central nervous system (CNS) to cause poliomyelitis, uniquely employing CD155 as their receptor.
Purpose of the Study:
- To investigate the molecular basis for the phenotypic diversity observed in C-CEVs, focusing on cellular receptor specificity.
- To understand the evolutionary relationship between C-CAVs and PVs, particularly how PVs might have emerged from C-CAV ancestors.
- To explore the potential for genetic manipulation of C-CEVs to switch receptor affinity, altering their pathogenic potential.
Main Methods:
- Phylogenetic analysis of non-structural proteins to determine evolutionary relationships between C-CAVs and PVs.
- Studies on virion structure and virion/receptor interactions.
- Investigation into the genetics and molecular biology of C-CEVs.
Main Results:
- Phylogenetic analysis reveals that certain C-CAVs (11, 13, 17, 18) are evolutionarily interleaved with PV serotypes, suggesting PVs may have evolved from a C-CAV pool.
- PVs uniquely use CD155, while C-CAVs and magHRVs use ICAM-1, indicating receptor specificity as a key determinant of pathogenesis.
- The study highlights the potential for C-CEVs to genetically switch receptor affinity (e.g., PVs from CD155 to ICAM-1, C-CAVs from ICAM-1 to CD155).
Conclusions:
- Differences in pathogenesis between C-CAVs and PVs are primarily governed by their distinct cellular receptor specificities (ICAM-1 vs. CD155).
- PVs may have originated from C-CAVs through the evolution of unique receptor specificity.
- In an environment free of PVs and neutralizing antibodies, C-CAVs could potentially evolve into new polio-like viruses by switching to CD155.
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