The adverse effects of corticosteroids on resistance to viral infections have been recognized for a long time [1, p. 108; 2; 3]. In order to shed light on the mechanisms responsible for this enhanced susceptibility, studies were conducted to determine the effect of cortisone on interferon, an antiviral factor, the importance of which in resistance to viral infections is becoming widely accepted [4]. In the initial studies, Newcastle disease virus (NDV) was employed as the inducer of interferon [5]. NDV, which does not go through a complete cycle of replication in the mouse and which produces no pathology unless given in toxic amounts [6, 7], was thought to be particularly suitable for this study, since the ancillary effects of the steroid on viral replication per se would be circumvented. It was found that pretreatment of mice with cortisone prior to induction of interferon by NDV led to a significant suppression of the response to interferon. Titers of interferon in the cortisone-pretreated mice were 10-fold lower than those in the control animals at the time of the maximal inter-
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