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SummaryAntiherpetic activity of AME was demonstrated in in vitro inactivation tests and in cell culture systems against herpes zoster and five strains of herpes simplex virus.The recently reported activity of water-soluble amphotericin B methyl ester (AME) against lipid-bound viruses (2, 3) suggested the potential use of this polyene antibiotic for topical treatment of herpetic infections. Extensive studies in our laboratories have shown significant antiherpetic activity with AME, as evidenced by the inactivation in vitro and by the inhibition in cell cultures of herpes zostervaricella and five strains of herpes simplex virus. Activity was independent of type or strain relationships among the viruses tested. Since host-cell membrane components of the lipid viral envelope have been proposed as the site of interaction with AME (3), it was essential for these comparative studies to prepare all strains of herpesviruses in the same host-cell line, the host of choice being MA-184 human newborn foreskin cells. The minimum effective concentration of AME necessary for maximum virueidal activity was limited by and directly related to the size of the virus population. While quantitative sensitivities were similar in most cases, a comparative analysis using two strains of herpes simplex virus showed different kinetics of inactivation for each strain. The present report deals ~dth these findings.Amphoteriein B methyl ester (AME) is a semisynthetie antifungal agent produced by esterification with diazomethane of the heptaene macrolide antibiotic, amphotericin B (5). Chemically, AME is a base which easily forms watersoluble salts with mineral and organic acids. In contrast, the parent compound Arch. ¥iroL 48/4 27

The presence of high concentrations of lysozyme in the stools of patients with ulcerative colitis has been demonstrated by a number of observers. It has been suggested that this enzyme may play a fundamental role in causing destruction of the colonic mucosa. Recent observations, showing that a high concentration of lysozyme is present also in granulation tissue and in leukocytes, have cast doubt on this hypothesis and suggest that the large amount of the enzyme in the feces of patients with ulcerative colitis is a result rather than a cause of the inflammatory process.The present report summarizes a series of studies designed to elucidate the source of lysozyme in the stools in ulcerative colitis. Our observations lead us to believe that the enzyme content of the feces is derived predominantly from the white blood cells present in the intestinal wall and stools in this disease. REVIEW OF LITERATUREIn 1922 Fleming (1) drew attention to a powerful bacteriolytic agent, which he named "Lysozyme," present in many body tissues and secretions of man and animals. He noted the high levels of this enzyme in tears, nasal secretion, egg white and leukocytes. Since then, many investigators have helped to clarify the nature of this enzyme, and it is now known to be a protein of low molecular weight capable of depolymerizing certain muco-polysaccharides. Meyer and Hahnel (2) contributed much toward the fundamental knowledge of this enzyme and devised an excellent viscosimetric technique for its quantitation in tissues and secretions, using as a substrate a mucopolysaccharide obtained from the micrococcus lysodeikticus.

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of reducing agents, and 0.001 M diisopropylphosphofluoridate reduced proteolysis partially. The enzymes from both strains were inactivated fairly quickly a t 70°C.1. Rogers, C. H., A m .

The instillation of Escherichia coli endotoxin (lipopolysaccharide) intranasally into mice produced severe lung lesions and a substantial increase in lung weight. Lung inflammation was maximal about 3 days after endotoxin instillation. Intraperitoneal injection of prednisone, cortisone and hydrocortisone sharply suppressed the lung inflammation. Five milligrams of prednisone produced a maximal anti-inflammatory effect when injected 24 and 48 hours after the endotoxin. Administration of large doses of Butazolidin also produced a modest effect on the lung inflammation. It is suggested that locally applied endotoxin alters blood vessel permeability of the lungs, resulting in hemorrhage, edema and exudation. The anti-inflammatory steroids reverse or inhibit this effect, perhaps by maintaining the integrity of the capillaries. Possible use and significance of this experimental anti-inflammatory system is discussed.

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