Abstract
Cells transformed by DXA viruses do not produce progeny of the virus that caused the transformation. However, Gerber1 and Sabin and Koch2 found that small amounts of SV40 virus are produced if SV40-transformed cells are grown together with cells able to support SV40 multiplication. A clue to the possible mechanism of this activation was provided by Gerber3 and by Koprowski and Jensen,4 who observed that more virus is produced if UV-inactivated Sendai virus is added to the cell mixture. The inactivated Sendai virus promotes cell fusion;5 it is possible, therefore, that SV40 virus is produced by heterokaryons resulting from fusion of transformed cells with virus-susceptible cells.
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Notes
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When this manuscript had been completed, an article by H. Koprowski, F. C. Jensen, and Z. Steplewski (these Proceedings, 58, 127 (1967)) contributed additional evidence on this subject.
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Watkins, J.F., Dulbecco, R. (1976). Production of SV40 Virus in Heterokaryons of Transformed and Susceptible Cells. In: Schiminovich, S. (eds) The Biology of DNA Tumor Viruses. Milestones in Current Research. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-6970-7_13
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DOI: https://doi.org/10.1007/978-1-4684-6970-7_13
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