- needs to block viral entry/exit from host cell
- or active inside host cell
- hence toxicity relates to intefering host cell function
- viral infection --> replication peaks at/before manisfestation of clinical symptoms
- hence the reason for early initiation of therapy OR prevention of infection (chemoprophylaxis for influenzae A using amantidine)
- stages of viral replication
- adsorption --> enter host cell
- uncoating of viral neucleic acid
- systhesis of early regulatory proteins --> nucleic acid polymerases
- systhesis of RNA/DNA
- systhesis of late, structural proteins
- assembly of viral particles
- release from cell
- acyclovir, famvir, valacyclovir
- acyclovir the earliest hence most studied
Acyclovir
- acyclic guanosine derivative
- requires 3 phosphorylation steps for activation --> eventually inhibit viral DNA polymerase
- clinical uses
- primary genital herpes - shortens duration by 5 days
- recurrent genital herpes - shortens by 1-2 days
- VZV - needs higher dosage
- generally well tolerated
- minor GIT SE: N/V
- neurotoxic - tremor, deliriumm seizure
- L-valyl ester of acyclovir
- rapidly converted to acyclovir after po
- serum levels 3-5x higher than with aciclovir
Famcyclovir
Penciclovir
Trifulridine
Agents against CMV
Ganciclovir
- affinity against CMV 100x more than aciclovir
- active against CMV, HSV, VZV, EBV, HHV-8
Valganciclovir
- converted into ganciclovir
- for treatment of CMV retinitis for pt with AIDS
Cidofovir
Foscarnet
Fomivirsen
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