Roles of the T Antigens in Transformation by SV40 (original) (raw)

  1. R. G. Martin*,
  2. V. P. Setlow*,
  3. A. B. Chepelinsky*,
  4. R. Seif*,
  5. A. M. Lewis, Jr.†,
  6. C. D. Scher‡,
  7. C. D. Stiles§, and
  8. J. Avila**
  9. * Laboratory of Molecular Biology, National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda, Maryland 20205; †Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20205; ‡Department of Hematology-Oncology, Sidney Farber Cancer Institute, and Children's Hospital Medical Center, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115; §Laboratory of Tumor Biology, Sidney Farber Cancer Institute, and Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115; **Centro de Biologia Molecular, Universidad Autonoma de Madrid, Facultad de Ciencias, Canto Blanco, Madrid 34, Spain

Excerpt

The following discussion of transformation by SV40 stresses the alternation of host DNA synthesis induced by the virus because other aspects of transformation are discussed elsewhere in this volume.

Establishment of Transformation

In 1966, Todaro and Green (1966, 1967) demonstrated that the efficiency of transformation of resting cells by SV40 could be greatly enhanced if the cells were replated at low cell densities immediately after adsorption of the virus. This result implied that the virus was inefficient in its ability to establish the transformed phenotype in resting cells. Data now suggest that the initial events leading to stable integration of SV40 into the host genome can be divided into three steps.

Step 1: Stimulation of resting cells through a first round of DNA synthesis. SV40 can stimulate resting monkey, human, hamster, mouse, and rat cells through at least one cycle of DNA replication and cell division (Sauer and Defendi 1966;...