Mitomycin C enhances measles virus replication in BSC-1 cells, likely due to secondary effects on host cell metabolism rather than interferon repression.
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Mitomycin C may enhance measles virus yields in vitro; leaves open effects on pathogenesis or therapeutic applications.
Summary The replication of both virulent and attenuated strains of measles virus in BSC-1 cells is enhanced by mitomycin C. This enhancement results in larger virus yields, the formation of larger plaques and a decrease in the latent period of the virus in the cells employed. Other inhibitors, including actinomycin D, iododeoxyuridine and cytosine arabinoside, failed to stimulate or inhibit synthesis of the virus. The action of mitomycin C, therefore, does not appear to be due to repression of interferon production but is more likely a secondary consequence of the effect of the antibiotic on the metabolism of the host cells.
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Rapp et al. (1965) studied this question.
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