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Variations in polyoma virus genotype in relation to tumor induction in mice. Characterization of wild type strains
Abstract:
The authors have explored the effects of variations in mouse polyoma virus genotype on patterns of tumor formation in the mouse. Four "wild type" virus strains were surveyed. Two were highly oncogenic, inducing multiple tumors of epithelial and mesenchymal origin, at high frequency and with short latency. The other two strains were weakly oncogenic, inducing fewer tumors, solely of mesenchymal origin, and after a long latency. These sharply contrasting tumor profiles were reproduced with virus stocks derived from molecularly cloned viral genomes. Though vastly different in their oncogenic properties, these cloned viruses proved equally effective in transforming established rat fibroblasts in culture and showed the same patterns of tumor antigen expression in cultured mouse cells. Complexes of polyoma middle T antigen and pp60c-src were demonstrated in extracts of epithelial tumors induced by a highly oncogenic virus strain. It is concluded that polyoma viral genetic determinants for tumor induction in the mouse are more complex than those previously defined by the use of cell transformation systems.
Insights
Mouse polyoma virus genotype significantly impacts tumor formation, with distinct strains causing varied tumor types and frequencies. Viral genetic factors influencing oncogenesis are more complex than cell transformation studies suggest.
Area of Science:
- Virology
- Oncology
- Molecular Biology
Background:
- Mouse polyoma virus (MPyV) is a well-studied oncogenic virus.
- Understanding MPyV genotype-specific oncogenic properties is crucial for cancer research.
- Previous studies often relied on cell transformation assays, which may not fully reflect in vivo tumor development.
Purpose of the Study:
- To investigate the influence of different mouse polyoma virus genotypes on tumor formation in mice.
- To compare the oncogenic potential of various wild-type and cloned MPyV strains.
- To elucidate the genetic determinants of MPyV-induced tumorigenesis.
Main Methods:
- Surveyed four wild-type mouse polyoma virus strains for oncogenic activity.
- Utilized molecularly cloned viral genomes to confirm tumor profiles.
- Assessed viral transformation of rat fibroblasts in culture.
- Analyzed tumor antigen expression in cultured mouse cells.
- Detected complexes of polyoma middle T antigen and pp60c-src in tumor extracts.
Main Results:
- Two MPyV strains were highly oncogenic, inducing frequent epithelial and mesenchymal tumors with short latency.
- Two other strains were weakly oncogenic, causing fewer, mesenchymal-only tumors after long latency.
- Cloned viruses reproduced these contrasting tumor profiles.
- All cloned viruses equally transformed rat fibroblasts and showed similar antigen expression in vitro.
- Complexes of polyoma middle T antigen and pp60c-src were found in tumors from highly oncogenic strains.
Conclusions:
- Mouse polyoma virus genotype is a critical determinant of tumor type, frequency, and latency in vivo.
- In vitro cell transformation assays do not fully predict the complex oncogenic behavior of MPyV in mice.
- MPyV genetic determinants for in vivo tumor induction are more intricate than previously understood from cell-based systems.