Abstract
Acyclovir-resistant varicella–zoster virus (VZV) selected in the presence of acyclovir was 3–20 times more sensitive to nucleoside analogues with arabinosyl configuration than the parent virus. Their sensitivity in comparison with a thymidine kinase-deficient mutant to anti-herpetic drugs and sensitivity to phosphonoacetic acid suggested that recognition by altered mutants' DNA polymerase might result in their novel sensitivity to nucleoside analogues. Information on the unique sensitivity of these acyclovir-resistant mutants may be useful in designing chemotherapeutic agents against VZV.
