Abstract
Under normal circumstances, a compatible relationship exists between the mouse and the extensive family of endogenous retroviruses present in the mouse genome. These retroviruses are present as proviruses in all somatic and germline cells and are inherited according to Mendelian expectations [1]. The expression of either infectious virus, or more commonly expression of certain viral proteins, is regulated to various degrees in different mouse strains. Whether the presence of these retroviruses is simply tolerated or whether they serve some selective advantage to the host is yet to be determined. Suffice it to say, however, that in certain circumstances, the compatible relationship breaks down, resulting in leukemia. Evidence now suggests that leukemia results from recombination between otherwise innocuous, endogenous viruses, to produce a virus with oncogenic potential. The following is a synopsis of our understanding of this phenomenon as well as an attempt to outline possible mechanisms by which virus-induced transformation can occur.
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© 1984 Springer-Verlag New York Inc.
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Elder, J.H. (1984). On the Role of Recombinant Retroviruses in Murine Leukemia. In: Notkins, A.L., Oldstone, M.B.A. (eds) Concepts in Viral Pathogenesis. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-5250-4_13
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DOI: https://doi.org/10.1007/978-1-4612-5250-4_13
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