Acyclovir

Mechanism of action:
Acyclovir is first phosphorylated by the viral thymidine kinase within virus-infected cells to form acyclovir monophosphate. It is then converted into the diphosphate form by guanylate kinase, and finally transformed into acyclovir triphosphate by various cellular kinases. The active triphosphate form competitively inhibits viral DNA polymerase, and once incorporated into viral DNA, it causes chain termination because it lacks a 3'-OH group required for further elongation. This selective mechanism gives acyclovir stronger inhibitory effects in infected cells while having relatively less impact on normal cells.
Reference(s):
1. Nies AT et al. (2012). Multidrug and toxin extrusion proteins as transporters of antimicrobial drugs. Expert Opin Drug Metab Toxicol.
2. Yonezawa A et al. (2011). Importance of the multidrug and toxin extrusion MATE/SLC47A family to pharmacokinetics, pharmacodynamics/toxicodynamics and pharmacogenomics. Br J Pharmacol.
