Key result
Poliovirus mutants from persistently infected neuroblastoma cells accumulated 31 point mutations compared to the parental strain, including clustered missense mutations in capsid proteins.
Population
Poliovirus mutants selected in persistently infected human neuroblastoma cells
Comparison
Nucleotide sequence analysis vs Parental lytic Sabin 1 poliovirus strain
Design
Preclinical
Authors
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Cell culture models of poliovirus persistence warrant clinical caution; leaves open the role of capsid mutations and RNA structure in vivo.
Both missense and silent mutations are selected during persistent poliovirus infection of neuroblastoma cells, suggesting RNA secondary structure in the coding region may play a role in viral infection.
Borzakian et al. (1993) studied Poliovirus infection. Persistent infection in neuroblastoma cells vs. Parental lytic Sabin 1 poliovirus strain was evaluated on Nucleotide sequence mutations. Poliovirus mutants from persistently infected neuroblastoma cells accumulated 31 point mutations compared to the parental strain, including clustered missense mutations in capsid proteins.
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