This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Borzakian, S Articles by Colbere-Garapin, F Search for Related Content PubMed PubMed Citation Articles by Borzakian, S Articles by Colbere-Garapin, F

 Previous Article  |  Next Article 

J Virol. 1993 May; 67(5): 2914-2917

Precise missense and silent point mutations are fixed in the genomes of poliovirus mutants from persistently infected cells.

Unité de Virologie Médicale, Institut Pasteur, Paris, France.

ABSTRACT

Poliovirus mutants selected in persistently infected human neuroblastoma cells have a modified cell tropism and can establish a secondary persistent infection in nonneural cells, such as HEp-2c cells. Nucleotide sequence analysis revealed that the genome of a persistent mutant, S11, differed from that of the parental lytic Sabin 1 poliovirus strain by 31 point mutations. Three mutations occurred in the noncoding regions. The other mutations resulted in 12 amino acid substitutions; 1 substitution occurred in a nonstructural protein (3A), while the other 11 substitutions were clustered in the capsid proteins VP2 and VP1. The same missense mutations, as well as many of the silent mutations that we observed in mutant S11, also accumulated in the genome of two other persistent viruses isolated from independent infections. This finding indicates that both missense and silent mutations are selected during the persistent infection of neuroblastoma cells and suggests that the secondary structure of RNA in the coding region may play a role in viral infection.

This article has been cited by other articles:

• Zhang, J., Timoney, P. J., MacLachlan, N. J., McCollum, W. H., Balasuriya, U. B. R. (2008). Persistent Equine Arteritis Virus Infection in HeLa Cells. J. Virol. 82: 8456-8464 [Abstract] [Full Text]  
• Herrera, M., Grande-Perez, A., Perales, C., Domingo, E. (2008). Persistence of foot-and-mouth disease virus in cell culture revisited: implications for contingency in evolution. J. Gen. Virol. 89: 232-244 [Abstract] [Full Text]  
• Tam, P. E., Messner, R. P. (1999). Molecular Mechanisms of Coxsackievirus Persistence in Chronic Inflammatory Myopathy: Viral RNA Persists through Formation of a Double-Stranded Complex without Associated Genomic Mutations or Evolution. J. Virol. 73: 10113-10121 [Abstract] [Full Text]