Biological activity of polyoma viral DNA in mice and hamsters (original) (raw)
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The synthesis of viral- and cellular-DNA in mammalian cells exposed to polyoma virus
Archiv f�r die gesamte Virusforschung, 1972
Various mammalian cell cultures were examined for their ability to support polyoma virus DNA replication, and for induction of cellular DNA synthesis, as a result of infection by polyoma virus. Viral DNA synthesis was measured by the technique of DNA-DNA hybridization which allowed its detection at a level of 0.2 ~ of that occurring during optimum viral DNA replication in mouse cells. All those cultures which failed to produce significant yields of infectious virus were also negative for viral DNA synthesis, indicating that restriction operates at an early stage in the infection cycle; and also were not induced to synthesize cellular DNA. The only exception was the BHK-21 cell line, in which polyoma virus infection stimulated the incorporation of labelled thymidine into DNA, in the absence of detectable viral DNA synthesis. Polyoma transformed hamster cells, known to harbor viral genetic information, were not induced to synthesize viral DNA following a variety of "rescue" attempts, in contrast to cultures of SV 40 (Simian virus 40)-transformed cells in which SV 40 DNA replication could be measured after analogous treatments. Thus in all of the non-murine cultures examined, polyoma virus gene expression was restricted at a stage prior to viral DNA replication.
Journal of Virology
The interaction of polyoma virus with a continuous line of rat cells was studied. Infection of these cells with polyoma did not cause virus multiplication but induced transformation. Transformed cells did not produce infectious virus, but in all clones tested virus was rescuable upon fusion with permissive mouse cells. Transformed rat cells contained, in addition to integrated viral genomes, 20 to 50 copies of nonintegrated viral DNA equivalents per cell (average). "Free" viral DNA molecules were also found in cells transformed by the ts-a and ts-8 polyoma mutants and kept at 33 C. This was not due to a virus carrier state, since the number of nonintegrated viral DNA molecules was found to be unchanged when cells were grown in the presence of antipolyoma serum. Recloning of the transformed cell lines produced subclones, which also contained free viral DNA. Most of these molecules were supercoiled and were found in the nuclei of the transformed cells. The nonintegrated viral DNA is infectious. Its specific infectivity is, however, about 100-fold lower than that of polyoma DNA extracted from productively infected cells, suggesting that these molecules contain a large proportion of defectives.
Journal of virology, 1971
The multiplication of polyoma virus in a mouse-hamster (3T3 x BHK) somatic hybrid line (10A), which, although permissive for viral multiplication, produces very low amounts of virus, has been studied. In this cell line, the efficiency of productive infection is high, but the yield of infectious virus is on the order of 0.5% of that of 3T3 cells. The amount of viral deoxyribonucleic acid (DNA) synthesized by these cells upon infection is about 5% of that of 3T3 cells. An examination of the virus produced in hybrid 10A revealed that it was only one-tenth as infectious as the virus grown in 3T3. Although the viral DNA synthesized in the infected 10A cells is normal, the DNA extracted from purified virus grown in 10A consists of approximately 10% of normal, supercoiled polyoma DNA molecules and of approximately 90% linear DNA molecules with a sedimentation coefficient of 14 to 16S. These DNA molecules appear to be of cellular origin but contain a limited amount of viral DNA sequences. T...
The American journal of pathology, 1987
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 determ...
Virology, 1992
It is widely believed that infection with various DNA viruses stimulates quiescent host cells to divide in preparation for virus replication. To examine this issue, the effects of acute polyoma virus infection on cellular DNA synthesis are observed in newborn mice. Using rH]thymidine incorporation and fluorography of whole mouse sagittal sections, we observed clear, high-resolution images of organ-specific patterns of cellular DNA synthesis in newborn animals. No alteration in these patterns was observed during acute polyoma virus infection. Other methods, including measurements of [3H]thymidine-labeled DNA-specific activities in various tissues and in situ autoradiography, also failed to detect virus-induced alterations in cellular DNA synthesis. These results indicate that newborn animals have high endogenous levels of DNA synthesis and imply that acute polyoma virus infection may not be associated with further induced levels of cellular DNA synthesis.
Journal of Virology
The interaction of polyoma virus with a continuous line of rat cells was studied. Infection of these cells with polyoma did not cause virus multiplication but induced transformation. Transformed cells did not produce infectious virus, but in all clones tested virus was rescuable upon fusion with permissive mouse cells. Transformed rat cells contained, in addition to integrated viral genomes, 20 to 50 copies of nonintegrated viral DNA equivalents per cell (average). "Free" viral DNA molecules were also found in cells transformed by the ts-a and ts-8 polyoma mutants and kept at 33 C. This was not due to a virus carrier state, since the number of nonintegrated viral DNA molecules was found to be unchanged when cells were grown in the presence of antipolyoma serum. Recloning of the transformed cell lines produced subclones, which also contained free viral DNA. Most of these molecules were supercoiled and were found in the nuclei of the transformed cells. The nonintegrated viral DNA is infectious. Its specific infectivity is, however, about 100-fold lower than that of polyoma DNA extracted from productively infected cells, suggesting that these molecules contain a large proportion of defectives.
In vitro polyoma DNA synthesis: characterization of a system from infected 3T3 cells
Journal of virology, 1974
A lysate from hypotonically swollen polyoma-infected BALB/3T3 cells incorporated labeled deoxynucleotide triphosphates into both viral and cellular DNAs. The incorporation was stimulated by the presence of ATP, deoxynucleotide triphosphates, thiols, and magnesium ions. Strong inhibition of incorporation was observed with thiol reagents and arabinosyl nucleotide triphosphates. The rate of in vitro synthesis increased with the temperature of incubation as expected. Incorporation into cellular DNA for up to 2 h was observed in lysates from virus-infected and serum-stimulated cells but not from resting cells. Synthesis in the system, therefore, appeared to reflect the physiological state of the cells before preparation of the lysate. Incorporation into viral DNA stopped far sooner than that into cellular DNA. During the initial phase of the in vitro incubation, incorporation occurred into viral replicative intermediates (RI). These RIs had identical properties to those isolated after in...