Structures of guanosine and<unk>  compared Mechanisms (HSV DNA polymerase inhibition and HSV DNA incorporation) of<unk>  action<unk>  is converted by viral thymidine kinase to<unk>  monophosphate, which is then converted by host cell kinases to<unk>  triphosphate <unk> -TP, also known as aciclo-GTP).<unk> -TP is a very potent inhibitor of viral DNA replication.<unk> -TP competitively inhibits and inactivates the viral DNA polymerase. Its monophosphate form also incorporates into the viral DNA, resulting in chain termination. Resistance Resistance to<unk>  is rare in people with healthy immune systems, but is more common (up to 10%) in people with immunodeficiencies on chronic antiviral prophylaxis (transplant recipients, people with acquired immunodeficiency syndrome due to HIV infection). Mechanisms of resistance in HSV include deficient viral thymidine kinase; and mutations to viral thymidine kinase or DNA polymerase, altering substrate sensitivity. Microbiology Varicella zoster virus-produced plaques in monolayers of MRC5 cells. When the virus was reproducing each well contained different amounts of the antiviral drug<unk> . By counting the plaques (holes formed by the virus in the layer of cells) the potency of the<unk>  to the virus was calculated.<unk>  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) *Human cytomegalovirus (HCMV) – least activity
Aciclovir
Penciclovir
Valganciclovir
Famciclovir
Ganciclovir
Alcaftadine
Benzylpenicillin
Amantadine