<unk>  is a prodrug, an esterified version of aciclovir that has greater oral bioavailability (about 55%) than aciclovir. It is converted by esterases to the active drug, aciclovir, and the amino acid valine via hepatic first-pass metabolism. Aciclovir is selectively converted into a monophosphate form by viral thymidine kinase, which is more effective (3000 times) in phosphorylation of aciclovir than cellular thymidine kinase. Subsequently, the monophosphate form is further phosphorylated into a disphosphate by cellular guanylate kinase and then into the active triphosphate form, aciclo-GTP, by cellular kinases. Mechanism of action Aciclo-GTP, the active triphosphate metabolite of aciclovir, is a very potent inhibitor of viral DNA replication. Aciclo-GTP competitively inhibits and inactivates the viral DNA polymerase. Its monophosphate form also incorporates into the viral DNA, resulting in chain termination. It has also been shown that the viral enzymes cannot remove aciclo-GMP from the chain, which results in inhibition of further activity of DNA polymerase. Aciclo-GTP is fairly rapidly metabolized within the cell, possibly by cellular phosphatases. Aciclovir is active against most species in the herpesvirus family. In descending order of activity: *Herpes simplex virus type I (HSV-1) *Herpes simplex virus type II (HSV-2) *Varicella zoster virus (VZV) *Epstein–Barr virus (EBV) *Cytomegalovirus (CMV) The drug is predominantly active against HSV and, to a lesser extent, VZV. It is only of limited efficacy against EBV and CMV. However,<unk>  has been shown to lower or eliminate the presence of the Epstein–Barr virus in subjects afflicted with acute mononucleosis, leading to a significant decrease in the severity of symptoms.<unk>  and acyclovir act by inhibiting viral DNA replication, but as of 2016 there was little evidence that they are effective against Epstein–Barr virus, they are expensive, they risk causing resistance to antiviral agents, and (in 1% to 10% of cases) can cause unpleasant side effects. Acyclovir therapy does prevent viral latency, but has not proven effective at eradicating latent viruses in nerve ganglia. As of 2005, resistance to<unk>  has not been significant. Mechanisms of resistance in HSV include deficient viral thymidine kinase and mutations to viral thymidine kinase and/or DNA polymerase that alter substrate sensitivity. It also is used for herpes B virus postexposure prophylaxis.
Valaciclovir
Umifenovir
Letermovir
Oseltamivir
Balapiravir
Favipiravir
Rovafovir etalafenamide
Coronavir