Abstract
Infection of L cells with wild-type (L1) vesicular stomatitis virus at high or low multiplicities does not result in the production of interferon; however, infection of L cells with low multiplicities of a small-plaque mutant (S2) results in the synthesis of large amounts of interferon. In chick embryo (CE) cells, both viruses induce synthesis of interferon; there is no significant multiplicity effect in CE cells. The rate and efficiency of shutoff of macromolecular synthesis in the different host cells is a critical factor in determining the ability of the viruses to induce interferon synthesis. If host ribonucleic acid or protein synthesis is shut off by the virus before the required new ribonucleic acid is transcribed or translated, interferon production does not occur. The relative yield of the two viruses in CE and L cells is not related to the effects of interferon produced during the course of infection.
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Selected References
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