Molecular Biology of Friend Viral Erythroleukemia

Publisher Website
Google Scholar
Abstract
Friend virus induces rapid progressive erythroleukemia in susceptible mice. To oncologists and to cell biologists, this disease has provided a fascinating model for analyzing neoplastic progression, the role of host genes in controlling susceptibility to cancer, and the differentiation of erythroid cells in culture. However, to molecular biologists, Friend virus (and the closely related Rauscher and Cas virus complexes) has been generally viewed as a relatively complex anomaly. The virus lacks a classical oncogene of the sort typified by the src gene of Rous sarcoma virus. Such classical viral oncogenes (v-oncs) are modified versions of normal cellular genes (proto-oncogenes or c-oncs) and they are present in all of the other known retroviruses that cause rapidly developing neoplasms (Bishop 1983, 1985; Weinberg 1985). The c-oncs have been highly conserved throughout evolution, and there, is evidence that they perform important cellular functions. Because Friend virus lacks such a modified cellular gene and contains only retroviral-specific nucleic acid sequences, and because it induces a progressively developing neoplasm rather than an immediate cancer, it has been widely assumed that it is relatively “different” and “complex,” perhaps too different to provide general insights and too complex for molecular biological analysis.