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Identification of a mutation in the SV40 capsid protein VP1 that influences plaque morphology, vacuolization, and
Haruhiko Murata1, Keith Peden, Andrew M Lewis
1Cancer Prevention Fellowship Program, Office of Preventive Oncology, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
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.
Insights
A Simian Virus 40 (SV40) variant, SV40-LP(KT), shows a VP1 mutation impacting plaque formation and cellular interactions. This genetic change influences key SV40 phenotypes, offering insights into viral adaptation.
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- SV40 is a well-studied polyomavirus with historical significance.
- SV40 variants can exhibit distinct biological properties.
- Understanding viral mutations is key to deciphering viral behavior.
Purpose of the Study:
- To characterize a specific SV40 plaque variant, SV40-LP(KT).
- To identify genetic determinants responsible for observed phenotypic differences.
- To analyze the impact of a VP1 mutation on SV40 biology.
Main Methods:
- Molecular cloning of the SV40-LP(KT) genome.
- DNA sequence analysis of the viral genome.
- Comparative analysis with known SV40 isolates.
Main Results:
- SV40-LP(KT) genome is nearly identical to the 777 isolate.
- A specific mutation in the VP1 coding region (H136Y) was identified in SV40-LP(KT).
- This VP1 mutation influences plaque morphology, vacuole formation, and ganglioside receptor usage.
Conclusions:
- The VP1 mutation in SV40-LP(KT) is a critical determinant of its unique phenotypes.
- This finding enhances understanding of structure-function relationships in SV40 VP1.
- The study provides molecular insights into SV40 variant evolution and host interactions.
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