Abstract
Polyoma virus normally establishes a silent persistent infection in its natural host, the mouse, although, in the laboratory, the virus can become a powerful pathogen. Given appropriate selections of virus and host strains, inoculation of newborn mice results in the rapid development of multiple tumors [1,2]. Tumors may arise from any one of a dozen different cell types, and some may appear grossly as early as 6 weeks. In this setting, polyoma virus is probably the most potent, broadly acting experimental oncogen known. Virus replication is also widespread under these experimental conditions. The kidney is the major site of virus amplification, although significant replication can occur in the lung and skin, as well as in the tumors themselves. Histological examination reveals cytopathic effects indicative of replication in as many as 30 different cell types [2].
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Freund, R., Dubensky, T.W., Talmage, D.A., Dawe, C.J., Benjamin, T.L. (1989). Molecular Aspects of Pathogenesis in the Polyoma Virus-Mouse System. In: Notkins, A.L., Oldstone, M.B.A. (eds) Concepts in Viral Pathogenesis III. Springer, New York, NY. https://doi.org/10.1007/978-1-4613-8890-6_5
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DOI: https://doi.org/10.1007/978-1-4613-8890-6_5
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