When mice were inoculated intravenously with Newcastle disease virus, interferon was formed, and the mice were protected against the lethal effects of a subsequent intravenous injection of a toxic strain of influenza A virus. Mice were similarly protected when injected intravenously with a suspension of mouse macrophages which had been stimulated to produce interferon by treatment with Newcastle disease virus. It is known that the reticuloendothelial system has a role in the production of interferon and in the development of non-specific resistance to virus infections. When this system was blocked completely by a thorotrast injection, or partially as the result of splenectomy, there was a sharp decrease both in the amounts of interferon formed in mice in response to an injection of Newcastle disease virus and in their resistance to the toxic effects of influenza virus.


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