Abstract
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.
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