Virus proliferation in hypoxic animals was markedly reduced. Little difference in this respect between influenza virus (PR8) and mouse encephalomyelitis virus (Theiler's GD VII) was observed except that there was a longer depression of the latter virus. The possible mechanisms involved are discussed.
Treatment with testosterone increases proliferation of influenza virus as well as protein anabolism. A relative lack of testosterone caused by castration is associated with a diminished rate of virus growth. When protein catabolism is increased by ACTH or cortisone, the rate of virus proliferation decreases. These results suggest the existence of a correlation between alterations of protein metabolism and virus proliferation.