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11 Replication of Nondefective RNA Tumour Viruses


Unlike the papova viruses and adenoviruses, the RNA tumour viruses do not usually kill the cells in which they replicate, and replication and transformation are often concomitant events.

In 1958 Temin and Rubin reported a focus assay for the transformation by Rous sarcoma virus of chick embryo fibroblasts growing in culture. This was the first assay of transformation in vitro to be devised for any tumour virus, and since 1958 most quantitative studies of the mechanism of replication of the RNA tumour viruses have involved the use of RSV and cultivated chick fibroblasts. The adsorption and penetration of Rous sarcoma viruses (and avian leukosis viruses) are governed by the availability of suitable cell surface receptors and the absence of interfering viruses (see Chapter 10). Once within a susceptible fibroblast, which survives the infection, the nondefective sarcoma virus is uncoated and its genome causes the transformation of the cell as it replicates infectious progeny virus. Many of the newly acquired properties of the RSV-transformed chick fibroblast resemble those acquired by mammalian fibroblasts transformed by papova or adenoviruses (compare Tables 6.1 and 11.1).

By contrast, avian leukosis viruses do not transform susceptible fibroblasts but will replicate and produce progeny virions, usually without killing the host cell. Under certain conditions, however, leukosis viruses of subgroups B and D do cause cell lysis and they can therefore be assayed by plaque formation formation (Graf, 1972; Kawai and Hanafusa, 1972). Leukosis viruses, such as avian myeloblastosis virus, will transform certain differentiated cell types growing in...

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