The treatment of experimental herpes simplex virus keratitis with cortisone or corticotropin locally or systemically has been uniformly unfavorable or ineffective in the experience of several groups of investigators.* This is not peculiar to the herpes simplex virus, because the same undesirable results have occurred in the treatment of experimental poliomyelitis5 and in Coxsackie,6 influenza,† and mumps8 virus infections. Presumably, these infections have a minimal hypersensitivity factor, since it is in the control of the latter that cortisone excels. Several other effects, however, on tissue resistance and immunity have been ascribed to cortisone. As Leopold9 has pointed out, these actions are generally inhibitory in that there is a decrease not only in allergic responses but also in inflammatory responses to topical injury, in granuloma formation, and in resistance to certain infections. According to Selye,10 in distinct contrast to cortisone, the somatotropic hormone (STH), the so-called