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    Acyclovir (9-[2-hydroxyethoxymethyl] guanine) is an acyclic nucleoside analogue of guanosine which is a potent and selective antiviral agent. Acycloviris converted to the monophosphate by thymidine kinase the virus-specific form of this enzyme and is subsequently converted to the triphosphate by the host cell kinase. Acyclovir triphosphate inhibits viral DNA-polymerase terminating the chain and is the active form. It is 30 times more potent against the herpes simplex virus enzyme than the host enzyme. Acyclovir triphosphate is fairly rapidly broken down within the host cells by cellular phosphatases. Resistance due to changes in the viral genes coding for thymidine kinase or DNA polymerase cause acyclovir-resistant herpes simplex virus and has been the cause of pneumonia, encephalitis and mucocutaneous infections.
Acyclovir can be administered orally or intravenously. When it is given orally, only 10-20% of the dose is absorbed. Acyclovir is widely distributed throughout the body, reaching concentrations in the cerebrospinal fluid which are 30 to 50% of those in the serum. In neonates, the half-life of acyclovir is about 5 hours, but it is 2.5 hours in children over 3 months old. The herpes simplex virus is transmitted vertically from infected mothers to fetuses and the administration of 400 mg acyclovir orally three times daily from 36 weeks of pregnancy until delivery has been suggested. Alternatively, a cesarean section can be performed to avoid the transmission of the herpes simplex virus to fetuses. The aim of this study is to review the effects and pharmacokinetics of acyclovir in neonates.