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25 Cards in this Set

  • Front
  • Back
What do amantadine and rimantidine block?
Uncoating (as in Influenza A)
What is blocked by fomivirsen?
early protein synthesis
What i the MOA of Acyclovir?
-guanosine analogue; can bind -irreversibly to viral polymerase
-requires phosphorylation to triphosphate form for activity (via viral thymidine kinase)
What is the major drug for infections due to HSV or VZV?
acyclovir
What is the oral prodrug of acyclovir?
valacyclovir
what is the prodrug of penciclovir?
famciclovir
Ganciclovir/Cytovene
-available as prodrug valganciclovir
-effective again CMV
-good CSF penetration
-renal excretion
-significant toxicity, hematologic myelosupression (additive with zidovudine)
Cidofovir/Vistide
MOA: nucleotide analogue, inhibits DNA polymerase, phosphorylated to active form via cell enzymes
-1/2 life 3 hrs except intracellular half life which allows long dosing intervals
-CMV disease IV only
-Renal toxicity, neutropenia
Foscarnet/Foscavir
MOA: pyrophosphate analogue, acts against viral DNA polymerase, reverse tgranscriptase, and RNA polymerase in vitro, blocks PPi binding site of viral DNA poly
-renal excretion
-Use: acyclovir resistant HSV or VZV, CVM retinitis & other CMV unresonsive to ganciclovir
-Renal toxicity, anemia
Fomivirsen sodium/Vitravene
MOA: antisense oligonucleotide complementary to immediate early region of CMV nucleic acid (inhibits viral replication)
-**only for injection into eye
-CMV retinitis in AIDs
-toxicity: uveitis
T/F: all respiratory viruses are RNA viruses
False, adenovirus is not
T/F: respiratory viruses require DNA intermediate
false
What two protuberances do influenza viruses have?
Hemagglutinin (H) and neuraminidase (N)
Ribavirin/Virazole, Rebetrol
MOA: competitive enzyme inhibitor of DNA and RNA synthesis
-administration by aerosol
-Use in pneumonitis due to RSV in combination with interferon for hepB and C
-toxicity is minimal
Amantadine/Rimantadine
MOA: prevents uncoating of the virus, interferes with release of viral RNA genome in cell
-Use: prophylaxis or treatment of Influenza A, parkinson's disease, resistance develops quickly
-toxicity: reversble CNS effects, fewer CNS effects favor rimantadine over amantadine
Zanamavir and Oseltamavir
MOA: neuraminidase inhibitors, active against influenza A&B
-Use: prophylactic treatment of INfluenza A or B
HIV has a _____(high/low) rate of division, ____ multiplicity of infection, and ___ rate of error of viral reverse transcriptase
high X 3
Nucleoside Reverse Transcriptase Inhibitors MOA
competitive inhibition of reverse transcriptase and chain termination
Zidovudine, Azidothymidine=AZT, Retrovir (NRTI)
MOA: thymidine analogue-historically first line agent again HIV
Non-nucleoside Reverse Transcriptase Inhibitors MOA
non competitive; direct binding to reverse transcriptase at an allosteric site that is different from the NRTIs
Protease inhibitors
MOA: inhibit HIV aspartic protease (makes functional core proteins and viral enzymes needed by virus); results in production of non-infectious virus
-toxicity causes syndrome of altered fat distribution called lypodystrophy
highly aggressive anti-retroviral therapy (HAART)
necessary because of rapid development of resistance in HIV;
-1 NNRTI + 2 NRTIs
-1PI + 2 NRTIs
-NRTIs
Immunomodulators
alter immune response via direct or indirect interactions with T cells, B cells, or APCs
Interferons
produced by cells in response to viral infection
Interferon alpha
MOA: blocking viral transcription and translation
Use: salvage therapy of hep B and C, papillomavirus infections
Toxicity: flu like symptoms, cns disorders, hematologic toxicities