Anti virals Flashcards
interferon alpha
IFN: made and released by host cells in resp. to pathogenic (ie viral) infection
- inhibits TRANSLATION (protein synthesis)
- IFN alpha made by LEUKOCYTES
- treatment w/ exogenous IFN alpha can induce antiviral response! though has sig SEs
- Indic: hepatitis B chronic inf, hepatitis C chronin inf, HPV genital warts, neoplastic diseass
- Tox: flu-like illness, BM tox, neurotoxicity (inhibits translation!)
amantadine
- Indic: influenza A only
- MOA: inhibit the viral *M2 ion channel protein*, preventing acidification of the endosome, thus blocking the fusion of the HA protein and the release of the viral nucleocapsid from the endosome into the cell
- Tox: transient CNS SEs: ataxia, n, irritability, etc. Contraindicated in pregnancy
oseltamivir
- MOA: neuraminidase inhibitor. NA cleaves sialic acid residues at the cell surface, releasing the nascent virion from the cell. NA inhibitors thus prevent virus release and spread
- Indic: influenza A and B
- Pharm: tablet
- Tox: mild GI complaints
acyclovir
- MOA: guanine analog: inhibit viral DNA or RNA synthesis. parent drug is inactive. it is activated by HSV-encoded thymidine kinase (TK) (inhibits VIRAL DNA repl specifically!). activated ACV acts both as an INHIBITOR and as a FAULTY SUBSTRATE for viral DNA pol
- Indic: HSV-1, HSV-2, VZV (varicella zoster)
Note: VZV TK is much less active than HSV TK: requires HIGHER doses of acyclovir, but NO inc toxicity - No activity against CMV or EBV (do not encode TK)
- oral, genital, ocular HSV; shingles, chicken pox
ganciclovir
- MOA: guanine analog: inhibit viral DNA or RNA synthesis. does NOT DEPENDENT ON VIRAL TK for activation, and is thus MORE TOXIC to host than acyclovir. still acts both as an INHIBITOR and as a FAULTY SUBSTRATE for viral DNA pol
- Indic: equally as effective against HSV and VZV as acyclovir, but way more effective against CMV!
- Clinical use: CMV infections
- Tox: greater tox than acyclovir: BM suppression (affects rapidly dividing cells)
valganciclovir
L-valyl ester form of ganciclovir
- pro-prodrug form: greater bioavailability, allowing less frequent dosing!
ribavirin
- MOA: guanosine analog - inhibits reverse transcriptase activity. in vitro activity against DNA and RNA polymerases
- Clincial use: Hpeatitis C and severe Respiratory Syncytial Virus (RSV)
- Tox: since active against DNA and RNA pol, very narrow therapeutic window! Can cause HEMOLYTIC ANEMIA, BM suppression, birth defects
zidovudine (AZT)
nucleoside reverse transcriptase inhibitor (NRTI) - thymidine analog
- inhibits viral DNA elongation by chain termination
lamivudine (3TC)
nucleoside reverse transcriptase inhibitor (NRTI)
- inhibits viral DNA elongation by chain termination
efavirenz
non-nucleoside reverse transcriptase inhibitor (NNRTI)
- inhibits viral DNA elongation by blocking the enzyme active site of RTase
tenofovir
nucleoTide RTI
- inhibits viral DNA elongation by chain termination
ritonavir
protease inhibitor (PI): prevents cleavage of gag and gag-pol polyprotein precursors, preventing maturation of viral particles - immature viral particles are NON infectious! no effect on cells already infected \*\*\* ritonavir inhibits clearance of other protease inhibitors. use in combo w/ other PIs --\> RITONAVIR BOOSTING, less frequent dosing
lopinavir (/ritonavir - Kaletra)
protease inhibitor (PI): prevents cleavage of gag and gag-pol polyprotein precursors, preventing maturation of viral particles - immature viral particles are NON infectious! no effect on cells already infected
atazanavir
protease inhibitor (PI): prevents cleavage of gag and gag-pol polyprotein precursors, preventing maturation of viral particles - immature viral particles are NON infectious! no effect on cells already infected
co-receptor inhibitors
blocks binding of gp120 to CCR5 receptor (main chemokine receptor used during infection)
