A perspective on resistance to acyclovir in herpes simplex virus.
Herpes simplex virus can acquire resistance to acyclovir by mutation leading to change in either of the two virus-specified enzymes involved in the mode of action of the drug. Thymidine kinase may be completely lost yet the virus is able to replicate normally, at least in vitro. Resistant variants arise readily in tissue culture but, in contrast, resistance does not emerge quickly in experimentally infected animals or in man undergoing chemotherapy. Thymidine kinase defective mutants are generally attenuated but have accounted for several cases of resistance in immunosuppressed patients. While resistance does not appear to be a clinical problem at the moment, consideration of the properties of laboratory mutants suggests that eventually resistance may be encountered among human infections.
D000212:Acyclovir / Q000494:pharmacology*; D000818:Animals; D004259:DNA-Directed DNA Polymerase / Q000378:metabolism; D004352:Drug Resistance, Microbial; D006801:Humans; D009154:Mutation; D018139:Simplexvirus / Q000187:drug effects* / Q000235:genetics; D013937:Thymidine Kinase / Q000378:metabolism
D013937:Thymidine Kinase; D004259:DNA-Directed DNA Polymerase; D000212:Acyclovir