Identification of a mutation in the SV40 capsid protein VP1 that influences plaque morphology, vacuolization, and receptor usage

Haruhiko Murata; Keith Peden; Andrew M Lewis Jr

doi:10.1016/j.virol.2007.08.040

Identification of a mutation in the SV40 capsid protein VP1 that influences plaque morphology, vacuolization, and receptor usage

Virology. 2008 Jan 20;370(2):343-51. doi: 10.1016/j.virol.2007.08.040. Epub 2007 Oct 22.

Authors

Haruhiko Murata¹, Keith Peden, Andrew M Lewis Jr

Affiliation

¹ Cancer Prevention Fellowship Program, Office of Preventive Oncology, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.

PMID: 17936868
DOI: 10.1016/j.virol.2007.08.040

Abstract

A plaque variant of SV40 that was first isolated in the 1960s, designated SV40-LP(KT), was molecularly cloned and subjected to sequence analysis. The genome of SV40-LP(KT) was found to be nearly identical to the previously described isolate known as 777. However, SV40-LP(KT) contained a mutation in the VP1 coding region resulting in a change of histidine 136 to tyrosine. This VP1 mutation was identified as a genetic determinant influencing a number of phenotypes associated with SV40-LP(KT) such as plaque morphology, intracellular vacuole formation, and ganglioside receptor usage.

Publication types

Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

MeSH terms

Amino Acid Substitution
Animals
Capsid Proteins / chemistry
Capsid Proteins / genetics*
Capsid Proteins / physiology
Cell Line
Cells, Cultured
Chlorocebus aethiops
Gangliosides / physiology
Genes, Viral*
Microscopy, Electron, Transmission
Models, Molecular
Mutagenesis, Site-Directed
Mutation*
Phenotype
Protein Structure, Quaternary
Receptors, Virus / physiology
Simian virus 40 / genetics*
Simian virus 40 / pathogenicity
Simian virus 40 / physiology
Vacuoles / virology
Viral Plaque Assay

Substances

Capsid Proteins
Gangliosides
Receptors, Virus
VP1 protein, polyomavirus