Abstract
The deoxyguanosine analogue, acyclovir, represents a singularly important advance in antiviral therapy because it is an antiherpes drug which requires a viral-specific enzyme to form an active inhibitor of viral DNA replication. As discussed by Richards et al. in this issue of the Journal (p. 378), acyclovir is a preferred substrate for herpesvirus thymidine kinase (TK) which phosphorylates acyclovir to acyclovir monophosphate (Elion et aI., 1978). Cellular guanylate kinase then leads to the formation of acyclovir triphosphate (Miller and Miller, 1980). Acyclovir triphosphate is a substrate for the herpesvirus DNA polymerase; it is a competitive inhibitor for DNA polymerase activity, and appears to be a chain terminator of elongating herpesvirus DNA (Derse et aI., 1981; Furman et aI., 1979). Acyclovir triphosphate inhibits viral DNA polymerase 30 times more preferentially than any cellular polymerase (Elion et aI., 1978).
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