Abstract
Treatment of Friend leukemia cells with cholera toxin or with its purified B subunit inhibits the interferon (IFN)-induced reduction of Friend virus release and of virus yields after exogenous infection with vesicular stomatitis virus. Likewise, the “enhancement” of erythroid differentiation of DMSO-treated Friend cells induced by low doses of crude or semipurified IFN is completely abolished. These results, confirmed with pure IFN preparations, are in keeping with the hypothesis that an early interaction with the cell membrane is a necessary step for the establishment of these different IFN effects. In addition, they indicate that the increased cyclic AMP levels, induced by the whole toxin, do not play a significant role in these phenomena; rather they may be due to the lectin-like activity of the B subunit. Evaluation of reciprocal dose-response curves of IFN and cholera toxin shows that treatment with toxin concentrations as low as 10 13 M induces a major inhibition of IFN effects. A millionfold higher toxin concentration does not substantially increase the toxin actions. The toxin-induced redistribution of membrane gangliosides is discussed as a possible mechanism of the observed inhibition of IFN activities.
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