Virus proliferation in hypoxic mice and chick embryos.

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.

Endocrines and their relation to influenza virus infection.

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.