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From the Department of Bacteriology, Hygiene and Preventive Medicine and the Department of Pharmacology, The George Washington University School of Medicine, Washington 5, D. C.
Abstract
Twelve compounds were found to inhibit the PR8 strain of influenza A virus in embryonated eggs, and six of these also inhibited the Lee strain of influenza B. Four of the inhibitors were virucidal as shown by in vitro tests at concentrations similar to those existing in the allantoic cavity. At high concentrations, only two compounds were without virucidal activity. Three compounds showed inhibitory effects when given by the yolk sac, a route different from that of the virus. The possibility that some of these compounds do not reach the site of viral growth when injected into the yolk sac is suggested.
When tested at various time intervals after the infectious process had started, four compounds were found to be ineffective when given only 1 hour after the virus. The other compounds were effective when given at intervals which ranged from 3 to 12 hours after infection. Polymerised sodium salts of substituted benzoid sulfonic acids, one of the most effective compounds tested, prevented multiplication up to 12 hours after injection of virus.
Thirty-seven naturally occurring substances were tested for ability to reverse the inhibition caused by six of the compounds. Several sudstances were antagonistic to the virus inhibitors. Tryptophane reversed the inhibition caused by minimal concentrations of polymerized sodium salts of substituted benzoid sulfonic acids, but it did not affect higher concentrations. Riboflavin caused reversal of inhibition by Congo red, but only at low concentrations of the drug. Thiamin hydrochloride also reversed the inhibition caused by Congo red, apparently due to a direct combination of the drug with the antagonist, making the drug unavailable for virustatic action.
None of the compounds tested against influenza A infections in mice was found to have any effect in preventing infection.
Footnotes
1 These studies were carried out under a contract (N7onr-419) with the Office of Naval Research.
2 Present address: National Microbiological Institute, National Institutes of Health, Bethesda 14, Maryland.
3 Part of this material is from a dissertation presented by Kenneth K. Takemoto in partial fulfillment of the requirements for the Ph.D. degree.
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