Abstract
The effect of ITSC, a highly specific antiviral agent, on some of the biochemical parameters of vaccinia virus replication in HeLa cell monolayers has been studied. At concentrations which completely inhibited infectious virus production this compound did not affect the previously observed enhancement of thymidine-H3 incorporation, and the inhibition of valine-C14 incorporation in infected cells, nor did it affect these reactions in control cells. There was a typical cytoplasmic accumulation of thymidine-H3 at virus-synthesizing sites in presence of the drug. In kinetic experiments, ITSC prevented virus formation only in proportion to the part of the virus replication cycle during which it was present, and independent of the absolute time in the cycle at which it was first added. The implications of these results on the mode of action of ITSC are discussed.