Abstract
The influence of araT on the synthesis of HSV of types 1 and 2 including a TK(-) variant, on the activity of the dThd and the dCyd kinases and on the incorporation of radioactivity into insoluble or soluble material after infection was studied. AraT inhibited different parameters of the replication of a TK(-) variant; it is possibly phosphorylated by enzymes other than the deoxypyrimidine kinase and therefore it is less selectively phosphorylated than dThd. The mode of action of araT on herpes replication must be studied in more detail.