Induced Resistance in Mice to Intravenous Toxicity of Influenza Virus. ∗

Summary

Sublethal quantities of homologous and heterologous influenza virus, mumps virus, and Newcastle disease virus injected intravenously in mice produced a state of resistance to the toxic effects of large quantities of intravenously injected PR-8 influenza A virus. Virus heated sufficiently to destroy infectivity was less effective in inducing resistance than was fully active virus; destruction of hemagglutinin caused complete loss of resistance inducing activity. Injection of sublethal doses of virus was followed by a lag period, which varied with the virus injected, before resistance became demonstrable, and resistance waned after 3-4 days. No increase in resistance to influenza toxicity was demonstrable after pre-challenge injection of feline pneumonitis virus, R. prowazeki, or typhoid vaccine. A preparation of receptor destroying enzyme (RDE) was effective in inducing increased resistance but its effect could not be attributed to its capacity for destruction of mucoprotein receptors since heat destruction of this activity did not completely destroy its resistance inducing effect.