The presence of the gene results in a greater interferon (IFN)-mediated antiviral resistance in cells challenged by orthomyxovirus. In the absence of IFN no difference in influenza virus yield was detected in -bearing () or non-bearing (+/+) mouse embryo fibroblasts. Although the putative product of the gene has been suggested to act in concert with IFN it is not clear whether was itself induced by IFN. Binucleate heterokaryons were formed by the fusion of an cell and an IFN-treated +/+ cell. Results show that no constitutive activity was present in the cell that was not IFN-treated, which was capable of enhancing the marginal anti-influenza virus resistance characteristic of the IFN-treated +/+ cell. Heterokaryons between +/+ cells and IFN-treated cells, however, showed resistance characteristic of the -containing cell. Hybrids of fusions between IFN-pretreated +/+ cells and cells that had been IFN-treated for 1 to 2 h revealed a graded response to influenza virus growth inhibition. Resistance in such hybrids increased commensurate with the development of the anti-influenza virus state in the donor. No synergistic enhancement of influenza virus growth inhibition was observed. These data suggest that the product of the gene is induced by IFN. Cybrids, constructed between nucleated +/+ or cells and enucleated cytoplasts, when subsequently treated with IFN and challenged with influenza virus, showed resistance characteristic only of the nucleated cell donor. Thus, no cytoplasmic component present in -bearing cytoplasts is able to cooperate with the nuclear elements of a +/+ cell to induce a state of high influenza virus resistance. The simplest interpretation of these data is that specific resistance is not the result of modifications of virus growth or IFN activities but probably occurs by the IFN-mediated induction of the gene , the product of which directly, or indirectly, interferes with orthomyxovirus replication.


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