Penciclovir microbiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Antiviral Activity: In cell culture studies, penciclovir has antiviral activity against the following herpes viruses: HSV-1 and HSV-2. The antiviral activity of penciclovir against wild type strains grown on human foreskin fibroblasts was assessed with a plaque reduction assay and staining with crystal violet 3 days postinfection for HSV. The median EC50 values of penciclovir against laboratory and clinical isolates of HSV-1 andHSV-2 were 2 µM (range 1.2 to 2.4 µM, n=7) and 2.6 µM (range 1.6 to 11 µM, n=6), respectively.
Resistance: Penciclovir-resistant mutants of HSV can result from mutations in viral thymidine kinase (TK) and DNA polymerase genes. Mutations in the viral TK gene may lead to complete loss of TK activity (TK negative), reduced levels of TK activity (TK partial), or alteration in the ability of viral TK to phosphorylate the drug without an equivalent loss in the ability to phosphorylate thymidine (TK altered). The median EC50 values observed in a plaque reduction assays with penciclovir resistant HSV-1 and HSV-2 were 69 µM (range 14 to 115 µM, n=6) and 46 µM (range 4 to > 395 µM, n=9), respectively. The possibility of viral resistance to penciclovir should be considered in patients who fail to respond or experience recurrent viral shedding during therapy.
Cross-resistance: Cross-resistance has been observed among HSV DNA polymerase inhibitors. The most commonly encountered acyclovir-resistant mutants that are deficient in viral thymidine kinase (TK negative) are also resistant to penciclovir.[1]
References
- ↑ "DENAVIR (PENCICLOVIR) CREAM [PRESTIUM PHARMA, INC.]". Retrieved 6 January 2014.
Adapted from the FDA Package Insert.