Abstract
As mouse embryos develop they become susceptible to infection by the small DNA oncogenic viruses, simian virus 40 and polyoma1,2. Recently, the mouse teratocarcinoma, an alternative model system for the study of early development3,4, was used in an approach to understanding how differentiation affects host–virus interaction (ref. 5 and M.B. and F.K., unpublished). Several differential teratocarcinoma lines were shown to be fully permissive to polyoma virus and could be transformed by SV40, therefore reacting to viral infection like most commonly used mouse cells. In contrast, the multipotential embryonal carcinoma cells were resistant to both viruses and the block seems to lie early in the lytic cycle, after penetration of the virus, but before synthesis of the viral T antigen. Adenoviruses have much in common with the papovaviruses but are larger and more complex. We therefore examined the susceptibility of teratocarcinoma cells to these viruses. Here we report that both embryonal carcinoma cells and cells from a differentiated teratocarcinoma line are susceptible to adenovirus type 2.
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KELLY, F., BOCCARA, M. Susceptibility of teratocarcinoma cells to adenovirus type 2. Nature 262, 409–411 (1976). https://doi.org/10.1038/262409a0
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DOI: https://doi.org/10.1038/262409a0
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