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. Author manuscript; available in PMC: 2016 Jun 16.
Published in final edited form as: Curr Treat Options Neurol. 2012 Jun;14(3):241–255. doi: 10.1007/s11940-012-0172-y
Mechanism of action Ganciclovir inhibits viral DNA polymerase, and thus prevents viral replication. To exert its antiviral properties, ganciclovir undergoes tri-phosphorylation into the active metabolite, ganciclovir triphosphate. The initial phosphorylation requires the enzyme phosphotransferase, which is expressed by HHV-6.
Standard dosage 5 mg/kg intravenously (IV) every 12 h for 14 to 21 days, followed by 5 mg/kg IV daily. The chronic maintenance dosage is 5 mg/kg/day IV 5 to 7 times weekly and should be continued until immune recovery has taken place and the virus can no longer be detected in the CSF.
Contraindications Hypersensitivity to ganciclovir or acyclovir.
Main drug interactions Generalized seizures may occur with imipenem/cilastatin. The concentrations of drugs excreted renally may increase as ganciclovir may be nephrotoxic. Probenecid can significantly decrease renal clearance of ganciclovir. Foscarnet, piperacillin, or total parenteral nutrition cannot be co-administered with ganciclovir intravenously since they may form a precipitate.
Main side effects Renal toxicity is a major concern and close monitoring of renal function is required. Hematological toxicity is common with anemia being most frequent followed by leucopenia; rarely pancytopenia and thrombocytopenia can also occur. Hepatotoxicity can occur in 20 % of patients.
Special points Some cases of HHV-6 infections may not respond to ganciclovir resulting in fulminant manifestations [17]. This could be due to the differential susceptibilities to ganciclovir between variants HHV-6A and HHV-6B with HHV-6B being less susceptible to ganciclovir when compared to HHV-6A [18]. Furthermore, mutations in the U38 DNA polymerase or the U69 phospho-transferase genes can lead to resistance to ganciclovir.