Acyclovir-resistant, pathogenic herpesviruses.
In herpes simplex virus, the simplest path to resistance to the drug acyclovir is a mutation that knocks out the enzyme thymidine kinase. Such mutants are highly attenuated in mouse models of viral pathogenesis, but have been reported to be associated with severe disease in immunocompromised patients. This review discusses possible resolution of this paradox.
Coen
D M
DM
Dept of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.
D000212:Acyclovir / Q000494:pharmacology*; D000818:Animals; D004352:Drug Resistance, Microbial / Q000235:genetics; D006561:Herpes Simplex / Q000821:virology*; D006801:Humans; D007121:Immunocompetence; D016867:Immunocompromised Host; D051379:Mice; D016513:Mice, SCID; D009154:Mutation / Q000235:genetics; D018139:Simplexvirus / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics / Q000472:pathogenicity*; D013937:Thymidine Kinase / Q000235:genetics* / Q000378:metabolism
D013937:Thymidine Kinase; D000212:Acyclovir