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Ultraviolet (UV) irradiation of SV40 and polyoma virus (R. I. Carp and R. B. Gilden, Virology 27:639, 1965; V. Defendi, F. Jensen, and G. Sauer, p. 645, in J. S. Colter and W. Paranchych [ed.], The Molecular Biology of Viruses, Academic Press, Inc., New York, 1967) and adenovirus type 12 (Z. Gilead and H. S. Ginsberg, J. Bacteriol. 92:1853, 1966) inactivated their capacity to induce a new complementfixing antigen (T antigen) at a rate that was one-third to one-fourth the rate of inactivation of virus infectivity. In addition, the capacity of polyoma virus to transform cultured cells was n.ore resistant to inactivation by UVand 'y-irradiation than was the capacity to initiate plaques (T. L. Benjamin, Proc. Natl. Acad. Sci. U.S. 54:121, 1965; C. Basilico and D. di Mayorca, Proc. Natl. Acad. Sci. U.S. 54:125, 1965; R. Laterjet, R. Cramer, and L. Montagnier, Virology 33:104, 1967). The experiments reported here demonstrate that the radiation-sensitive region of the virus responsible for transformation by an adenovirus is also smaller than the region responsible for plaque formantion. The source and passage history of the simian adenovirus, SA7, and the methods for the preparation of cell cultures, virus assays, and transformation of hamster embryo cells have been described elsewhere (B. Casto, J. Virol. 2:376, 1968). The SA7 virus used in this study was propagated in BSC-1 cells and had a titer of 5 x 107 plaque-forming units (PFU) /ml in primary African green monkey kidney cell cultures. In the two experiments reported here, 3and 5-ml virus samples, contained in 60or 100-mm plastic petri dishes (Falcon Plastics, Inc., Los Angeles, Calif.), respectively, were irradiated on a rotary shaker at a distance of 10 cm from the UV-light source (two Sylvania G15T8 lamps). Immediately after irradiation, the samples were frozen at -60 C;

Effects of ultraviolet irradiation on the transforming and plaque-forming capacities of simian adenovirus SA7