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It is well known that disease is not necemsarily associated with experimentally induced or naturally occurring viral infection. Indeed, in recent years, considerable attention has been directed to the possible lack of direct relationship between viral multiplication and the formation of lesions. Sugg (1949) found that eggpropagated but mouse-unadapted influenza virus produced pneumonia in mice on primary inoculation, but despite active viral multiplication in the lung, lesions were not produced on subsequent passage in mice. He later showed (Sugg, 1950) that the production of pneumonia correlated with the infective titer of virus present in the lung. Extensive studies with pneumonia virus of mice (Horsfall and Ginsberg, 1951) and influenza A virus (Ginsberg and Horsfall, 1952) showed that gross lesions appeared only after extensive viral multiplication and that the rate of production of pulmonary lesions was slower than the rate of production of new virus particles. Ginsberg (1951) and Davenport (1952), independently, studied the nontransmissible pneumonia induced in mice by Newcastle disease virus (NDV) and concluded that this pulmonary lesion resulted solely from the injurious or toxic action of a large amount of virus. Selective inhibition by xerosin of pneumonia produced in mice by the pneumotoxicity of Newcastle disease virus (Group6, et al., 1953) and by mouse unadapted (Ginsberg, 1955) and mouse adapted influenza virus (Group6, et al., 1952) in the absence of demonstrable anti-viral effects provided additional evidence pertinent to the role of viral toxicity in the development of 1 These investigations were supported in part by Grants-in-aid from The National Microbiological Institute, National Institute of Health (E-811), the Roche Anniversary Fund, and by funds provided by the Rutgers Research and Endowment Foundation. lesions. The fact that xerosin was also found to suppress pneumonia induced in mice by a chemical irritant such as the capsular polysaccharide of Klebsiella pneumoniae (Ginsberg, 1955) led to the investigation of the anti-inflammatory properties of xerosin. Waksman and Group6 (1956) showed that xerosin was, indeed, a potent anti-inflammatory agent that suppressed the tuberculin reaction, inflammation induced by turpentine or urease, and the diffusion of die in guinea pig skin but that it did not affect the histamine wheal and flare. These activities were shown to be strikingly similar to those of cortisone and its derivatives. However, cortisone has been found to be ineffective against pneumonia produced in mice by Newcastle disease virus or mouse unadapted influenza virus (Ginsberg, 1955) and generally to decrease resistance of the host to viral infection (Kass and Finland, 1953). The data presented in this report concern certain comparative anti-inflammatory properties of hydrocortisone, xerosin, and a derived pyridopyrimidine (DPP) which was found by Selitto and Randall (1956) to suppress yeast-induced inflammation in the rat ankle. In the interest of brevity and clarity the toxic factors associated with Newcastle disease virus and influenza virus will be referred to tentatively as NDV pneumotoxin and influenza neurotoxin.

COMPARATIVE EFFECTS OF HYDROCORTISONE, A DERIVED PYRIDO-PYRIMIDINE, AND XEROSIN ON PNEUMONIA PRODUCED IN MICE BY VIRAL AND BACTERIAL TOXIN