The interference with viral synthesis which is induced by large quantities of non-infective influenza B virus is inhibited or negated with small quantities of cortisone and other C-21 steroids. The specificity of this effect is attested by the inactivity of 11-alpha hydroxy epimers of highly active compounds. Maximal activity in negation of interference is associated with the presence of oxygen at the C-11 position of the steroid molecule.
In view of the demonstration that negation of interference can occur, it is concluded that the phenomenon of multiplicity reactivation of non-infective virus is not primarily influenced by cortisone. Rather, it is suggested that the reactivation phenomenon is unmasked by cortisone through its inhibiting effect on the autointerference intrinsic in multiplicity infection.
If it is accepted that influenza virus infections in ovo are self-limited in part by viral autointerference, present evidence is consistent with the view that negation of this autointerference is the mechanism by which cortisone induces definitively increased yields of virus.
