The administration of cortisone to chick embryos inoculated with large quantities of inactive influenza B virus results in a rate of viral increase greater than is concommittantly observed with inocula of comparable infectivity which are devoid of inactive particles. Thus, more than a mere negation of autointerference is effected.

It is concluded that in the presence of cortisone reactivation has occurred of non-infective virus to a state in which it can participate in viral synthesis.

Cortisone-induced viral reactivation is dependent upon a high partide/cell ratio and is thus analogous to the previously described phenomenon of "multiplicity reactivation."

Cortisone does not influence either homologous or heterologous viral interference unless reactivation of the inactive interfering virus occurs.

Virus reactivable with cortisone possesses both interfering and enzymatic properties.

Reactivation of virus with cortisone cannot be effected in vitro but is mediated by the host cell.

Two hypotheses concerning the action of cortisone are presented.

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