The effect of N-(2-hydroxyethyl)-palmitamide (Impulsin, Spofa)--an active endogenous compound which is recommended for preventing virus infection of the respiratory tract--on interferon production in mice stimulated with double stranded RNA and on the course of disease caused by encephalomyocarditis virus (EMC) was studied. Impulsin itself did not stimulate interferon production in mice treated per os or intravenously. But repeated application of this drug per os induced a macrophage activation, reflected by enhanced interferon production in vitro. When the interferon stimulation was delayed until 4 to 10 days after the first dose of Impulsin, interferon response to ds-RNA was slightly increased. After this phase of enhanced activity a decreased production of interferon was observed. Impulsin was not significantly effective in protecting mice from lethal dose of EMC virus. Application of this drug had an inhibitory effect on the toxicity of ds-RNA. A possible explanation of the mechanism by which Impulsin decreased the toxicity of virus in the organism is discussed.