12 Genetic Transmission of RNA Tumour Viruses

Abstract

The idea that cancer induces viruses is not new. Andrewes (1939) speculated on the possible activation of latent virus infections in cancerous tissues and it was postulated by Darlington (1948) that such viruses could arise from cellular genetic elements, which he named “proviruses.” Gross (1958) and Lieberman and Kaplan (1959) observed that lymphoid tumours induced in mice by X rays contained murine leukemia virus (called RadLV), which induced similar tumours when inoculated into unirradiated mice. More recently the induction of RNA tumour viruses following treatment of animals (usually mice) with physical or chemical carcinogens has been reported many times (see Gross, 1970). Apparently mice and other animals are commonly infected with, or at least contain genetic elements capable of developing into, RNA tumour viruses, but these viruses normally remain latent in the host.

There are two chief ways in which carcinogenic agents probably cause these latent viruses to become active. First, it is well known that the immunological mechanisms of the host are particularly sensitive to carcinogens, and under immunosuppressed conditions any latent virus infections would have an increased probability of becoming virulent. Second, it was suggested (Lwoff, 1960; Latarjet and Duplan, 1962; Bentvelzen et al., 1968) that the viruses may exist in a proviral state that can be activated by carcinogens or X rays in the same way that temperate bacteriophages are activated in lysogenic bacteria. Recently chemical evidence for the presence of proviruses has been obtained, and murine and avian C-type RNA viruses have been induced from cultures.