Oncogenicity of non-transforming mutants of avian sarcoma viruses.

Abstract

For practical purposes avian RNA tumour viruses have been divided into sarcoma and leukosis viruses. Sarcoma viruses have the ability to transform chick embryo fibroblasts in vitro and to induce fibro-sarcomas in vivo after a latent period of about 7 to 21 days. Leukosis viruses do not transform chick embryo fibroblasts, although they replicate in them, and in vivo most wild strains induce principally lymphoid leukosis after a latent period of over 90 days. They also frequently induce erythroid leukosis (erythroblastosis) and osteopetrosis, and occasionally other tumours. Non-transforming mutants of sarcoma viruses, which have all the in vitro properties of leukosis viruses, have been produced experimentally by exposure to ultraviolet light (Toyoshima, Friis & Vogt, 1970), by γ-irradiation (Goldé, 1970) and by treatment with chemicals (Graf et al. 1971). These results suggest that leukosis viruses may originate from sarcoma viruses, perhaps by loss of genetic material either by mutation or by segregation of subgenomic components (Toyoshima et al. 1970; Graf et al. 1971; Martin & Duesberg, 1972). It has been suggested that non-transforming mutants arise spontaneously when cloned strains of Rous sarcoma viruses are grown (Vogt, 1971). However, regardless of whether such non-transforming viruses arise spontaneously or are produced experimentally, it is necessary to know whether they are oncogenic in vivo and behave like wild-type leukosis viruses.