Valacyclovir for the Management of Herpes Viral Infections

A. Chakrabarty, MD; N. J. Anderson, MD; R. Beutner, MD, PhD; S. K. Tyring, MD, PhD, MBA

Disclosures

Skin Therapy Letter. 2005;10(1):1-4. 

In This Article

Mechanism of Action

Acyclovir was the first antiviral drug developed for systemic use that exhibited activity preferentially against herpes virus-infected cells. It is a 2'-deoxyguanosine analogue and requires activation by the viral-encoded thymidine kinase followed by cellular kinases. The final product, acyclovir triphosphate, irreversibly inhibits viral DNA polymerase via competition with deoxyguanosine triphosphate, preventing further chain elongation. Acyclovir triphosphate's meager production in non-infected cells and its reduced affinity for cellular DNA polymerase limits its potential side-effects. However, acyclovir has poor oral bioavailability and requires either higher dosing or intravenous administration for severe manifestations of herpes infections (i.e., neonatal herpes, herpes encephalitis).

Valacyclovir provides a high bioavailability of acyclovir, 3-to 5-fold higher than that obtained with oral acyclovir, and it is equivalent to plasma levels achieved with doses of intravenous acyclovir (see Table 1 ).[1] An L-valine ester of acyclovir, valacyclovir is rapidly metabolized into valine and acyclovir by the enzyme valacyclovir hydrolase in the gastrointestinal tract and liver. Being a prodrug, valacyclovir does not have any antiviral activity until it is biotransformed into acyclovir. The drug may be administered without regard to meals.

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