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25 Cards in this Set
- Front
- Back
What do amantadine and rimantidine block?
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Uncoating (as in Influenza A)
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What is blocked by fomivirsen?
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early protein synthesis
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What i the MOA of Acyclovir?
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-guanosine analogue; can bind -irreversibly to viral polymerase
-requires phosphorylation to triphosphate form for activity (via viral thymidine kinase) |
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What is the major drug for infections due to HSV or VZV?
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acyclovir
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What is the oral prodrug of acyclovir?
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valacyclovir
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what is the prodrug of penciclovir?
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famciclovir
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Ganciclovir/Cytovene
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-available as prodrug valganciclovir
-effective again CMV -good CSF penetration -renal excretion -significant toxicity, hematologic myelosupression (additive with zidovudine) |
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Cidofovir/Vistide
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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 |
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Foscarnet/Foscavir
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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 |
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Fomivirsen sodium/Vitravene
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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 |
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T/F: all respiratory viruses are RNA viruses
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False, adenovirus is not
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T/F: respiratory viruses require DNA intermediate
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false
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What two protuberances do influenza viruses have?
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Hemagglutinin (H) and neuraminidase (N)
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Ribavirin/Virazole, Rebetrol
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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 |
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Amantadine/Rimantadine
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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 |
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Zanamavir and Oseltamavir
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MOA: neuraminidase inhibitors, active against influenza A&B
-Use: prophylactic treatment of INfluenza A or B |
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HIV has a _____(high/low) rate of division, ____ multiplicity of infection, and ___ rate of error of viral reverse transcriptase
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high X 3
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Nucleoside Reverse Transcriptase Inhibitors MOA
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competitive inhibition of reverse transcriptase and chain termination
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Zidovudine, Azidothymidine=AZT, Retrovir (NRTI)
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MOA: thymidine analogue-historically first line agent again HIV
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Non-nucleoside Reverse Transcriptase Inhibitors MOA
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non competitive; direct binding to reverse transcriptase at an allosteric site that is different from the NRTIs
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Protease inhibitors
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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 |
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highly aggressive anti-retroviral therapy (HAART)
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necessary because of rapid development of resistance in HIV;
-1 NNRTI + 2 NRTIs -1PI + 2 NRTIs -NRTIs |
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Immunomodulators
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alter immune response via direct or indirect interactions with T cells, B cells, or APCs
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Interferons
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produced by cells in response to viral infection
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Interferon alpha
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MOA: blocking viral transcription and translation
Use: salvage therapy of hep B and C, papillomavirus infections Toxicity: flu like symptoms, cns disorders, hematologic toxicities |