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THE most widely used drug therapy for herpes simplex virus (HSV) is the nucleoside analogue acyclovir.1 2 3 To inhibit the growth of HSV, acyclovir must first be phosphorylated to the monophosphate form by virus–specific thymidine kinase, followed by phosphorylation to the active triphosphate form by cellular enzymes. The activated triphosphate is a potent inhibitor of herpes-specific DNA polymerase.4 Resistance to acyclovir has occurred infrequently, usually in patients with severe immunodeficiency disorders, and resistance is usually associated with loss of viral thymidine kinase activity.5 6 7 8 9 10 Severe mucocutaneous infections due to acyclovir-resistant herpesvirus infections are now occurring with increasing frequency in patients with the . . .
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Chatis et al. (1989) studied this question.
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