Herpes simplex virus ribonucleotide reductase mutants are hypersensitive to acyclovir.
Two mutants defective in herpes simplex virus-encoded ribonucleotide reductase activity exhibited the novel phenotype of hypersensitivity to acyclovir, aphidicolin, and to a lesser extent, phosphonoacetic acid. These results have implications for acyclovir resistance and the development of drugs that potentiate acyclovir action by inhibition of viral ribonucleotide reductase.
Coen
D M
DM
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115.
Goldstein
D J
DJ
Weller
S K
SK
D000212:Acyclovir / Q000494:pharmacology*; D000998:Antiviral Agents / Q000494:pharmacology; D016590:Aphidicolin; D004224:Diterpenes / Q000494:pharmacology; D004357:Drug Synergism; D009154:Mutation; D010641:Phenotype; D012264:Ribonucleotide Reductases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D018139:Simplexvirus / Q000187:drug effects / Q000201:enzymology* / Q000235:genetics
D000998:Antiviral Agents; D004224:Diterpenes; D016590:Aphidicolin; D012264:Ribonucleotide Reductases; D000212:Acyclovir