Scientific Publications by FDA Staff

Virology 2008 Jan 20;370(2):343-51

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

Murata H, Peden K, Lewis AM Jr

Lewis AM (reprint author), US FDA, Lab DNA Viruses, Div Viral Products, CBER, Bldg 29A,Room 1B10,29 Lincoln Dr, Bethesda, MD 20892 USA US FDA, Lab DNA Viruses, Div Viral Products, CBER, Bethesda, MD 20892 USA NCI, Canc Prevent Fellowship Program, Off Prevent Oncol, Div Canc Prevent,NIH, Bethesda, MD 20892 USA US FDA, Lab Retrovirus Res, Div Viral Products, CBER, 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.