Antivirals Flashcards
Reverse Transcriptase Inhibitor
NRTI (Nucleoside Reverse Transcriptase Inhibitor) e.g AZT mimicing thymidine
Chain terminator: Mimicing amino acids, binding to polypeptide chain, phosphorylated by host cell membrane to produce 5’ triphosphate, which can’t be processed by RT.
NNRTI (Non-nucleoside Reverse Transcriptase Inhibitor)
Binding to RT directly, denature/conformational change to inhibit catalytic activity
Nucleoside inhibitor
Ribavirin
Prodrug, require intracellular phosphorylation by viral/host kinases.
Compete with natural substrate in polymerisation. (dNTP-DNA; NTP-RNA). Not offering 3’ hydroxyl group after binding, which is essential for attachment new nucleotides.
Protease Inhibitors
Host: mRNA — functional proteins
HIV: mRNA — Chemically inert proteins — viral functional proteins via protease during assembly stage
Intergrase Inhibitor
Intergrase as selective target as it processes viral DNA and join them into host DNA to produce functionally intergrated provirus
Entry Inhibitor
Entry of HIV into host cell requires CD4 receptor and CCR5 coreceptors interacting glycoprotein 41, 120.
CCR5 Antagonist. Maraviroc
Maraviroc binds to CCR5, prevent any CCR5 coreceptor-glycoprotein interaction.
Fusion Inhibitor. Enfuvirtide/Fuzeon
Binds to glycoprotein 41, inhibiting its ability to approximate/mediate entry of HIV
Uncoating Inhibitor
Amantidine. Rimantidine
Blocking ion channle M2, prevent fusion of viral membrane and endosome, hence prevent uncoating of virus up entry.
ONLY works before infection. Used for vulnerable contacts
NA inhibitor (Neuraminidase)/Virus release inhibitor
Tamiflu
NA cleaving sialic acid from cell surfaces so that newly synthesised viruses can spread to uninfected cells
NA inhibitor mimics sialic acid as a competitive substrate.
Given early infection used to control extend of secondarily infected cells.
Treatment for Hep C
Ribavirin (Nucleoside Inhibitor) + Peg IFNa + Protease inhibitor (Telaprevir, Boceprevir) with various durations
