Inhibition of Gross Leukemia Virus-Induced Plaque Formation in XC Cells by 3-Deazauridine2

Publisher Website
Google Scholar
Abstract
3-Deazauridine (deaza UR), an analogue of the pyrimidine nucleoside uridine with reported antitumor, antibacterial, and antiviral activity, was evaluated for possible inhibitory activity against Gross murine leukemia virus in vitro by means of a UV-XC plaque-reduction assay procedure. The compound significantly inhibited Gross leukemia virus-induced plaque formation in rat XC cells and virus replication in NIH strain Swiss mouse embryo (NIH-ME) cells at concentrations between 6.4 and 200 µg/ml. Deaza UR was not obviously cytotoxic at concentrations which inhibited virus replication and plaque formation, nor was host cell protein synthesis affected by treatment of NIH-ME cell cultures with the drug at these active concentrations. Although deaza UR had potent cytostatic properties, the synthesis of cellular DNA and RNA was only partially inhibited by the compound at concentrations above 32 µg/ml and was not inhibited at all at concentrations of 10 µg/ml or below, i.e., drug levels at which virus inhibitory effects were still observed. While the compound displayed some selective inhibitory activity against the virus, the mechanism of action of deaza UR against Gross leukemia virus appears to be primarily via its inhibitory effect on cell division per se, a process known to be required for RNA tumor virus replication. The importance of developing selective antiviral agents with activity against the RNA tumor viruses for possible clinical application is discussed.

This publication has 0 references indexed in Scilit: