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Virology. 2008 Jan 20;370(2):343-51. Epub 2007 Oct 22.

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

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


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.

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