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39 Cards in this Set

  • Front
  • Back
Influenza overview
- common viral diesase caused by influenza viruses A and B
- usually self-limiting within 3-4 days of fever, chills, myalgia
- causes 20,000 deaths/yr in USA; elderly and patients with chronic diseases most at risk
Influenza therapy
**First line therapy is immunization -- prevents influenza and decreases severity

rimantidine and oseltamivir
Rimantidine MOA?
blocks uncoating of the viral RNA inside the human cells by interfering with the function of the viral M2 protein which functions as an ion channel

**only active against influenza A
Rimantidine clinical effects?
-- prophylaxis use decreases risk of infection by 50-90%
-- reduces symptoms if tx begun within 48h of onset
-- fewer CNS S/Es so better use in elderly patients and patients w/ renal disease
-- influenza A H3N2 resistance has rendered this drug ineffective for prophylaxis and treatment of the most current flu virus******
Oseltamivir MOA?
-- blocks release of new viral particles from infected cells via inhibition of viral neuraminidase
Oseltamivir therapeutic effects?
-- decrease duration of symptoms by one day; do NOT decrease incidence of complications

-- current strain of avian H5N1 virus appears to still be susceptible to the NA inhibitor
Herpes Simplex viruses
1. HSV-1 = fever blister, keratoconjunctivitis
2. HSV-2 = genital herpes, neonatal herpes
-- incurable STD with periods of exacerbations/remissions
-- incidence has increased 30+% since late 1970s
-- 22 million older than 12 affected
--45 million seropositive for HSV-2
3. Varicella-zoster virus = chicken pox, shingles, encephalitis, pneumonia
4. CMV = retinitis
Name the drugs used to treat HSV and VZV?
MOA of acyclovir, valacyclovir, penciclovir, famciclovir, and valgangcyclovir?
***inhibit viral DNA polymerase, but not effective against non-replicating, latent viruses

--acyclovir is guanosine derivative that must be phosph 3 times to yield active metabolite, acyclovir triphosphate
-- virus-specific thymidine kinase found ONLY in infected cells, produces the monophosphate
-- phosphorylase enzymes of the host cell then produce the di and triphosphates
-- acyclovir triphosphate competes with the dGTP at the viral DNA polymerase and also causes chain termination when incorporated into the viral DNA
Resistance to acyclovir, valacyclovir, penciclovir, famciclovir, and valgangcyclovir?
Most common form is mutation of the viral thymidine kinase which prevents conversion of acyclovir to the monophosphate.

Resistance to one drug leads to cross resistance.
Therapeutic uses of p.o. acyclovir and valacyclovir?
1. fever blister - begin therapy ASAP
2. Primary or recurrent genital herpes
3. Suppressive therapy for recurrent genital herpes - has been used for 10+ years in some patients w/o adverse S/Es
4. Treatment of HSV proctitis
5. Herpes zoster
S/E of acyclovir and valacyclovir?
n/v, diarrhea, and headache
MOA of foscarnet?
given i.v.

-- is an inorganic pyrophosphate which acts directly to inhibit viral DNA and RNA polymerases and HIV reverse transcriptase
-- No activation by viral or host-cell enzymes is required
Therapeutic use of foscarnet?
Treat HSV and VZV which are resistant to acyclovir

Treat CMV which is resistant to ganciclovir
HSV, VZV med dosing and availability?
acyclovir = p.o., i.v., and topical
F(p.o.) = 15-20%

valacyclovir = p.o. (F=48%)
-- is a prodrug converted to acyclovir
-- oral tx w/ valacyclovir results in plasms conc that are 3-5xgreater than those achieved with oral acyclovir
-- decrease dose of acyclovir and valacyclovir in patients with renal failure

famciclovir = p.o. converted to active drug penciclovir

penciclovir = topical
Drugs to treat Herpes keratitis?
Trifluridine MOA?
-- is converted to trifluridine triphosphate by host-cell enzymes
-- the active metabolite inhibits viral DNA synthesis
Drugs to treat CMV?
Foscarnet MOA?
given i.v.

-- is an inorganic pyrophosphate which acts directly to inhibit viral DNA and RNA polymerases and HIV reverse transcriptase
-- no activation via viral or host-cell enzymes is required
Foscarnet therapeutic use?
-- used to treat HSV and VZV which are resistant to acyclovir

-- Used to treat CMV which is resistant to ganciclovir
Fomivirisen MOA?
It is an antisense oligonucleotide which binds to mRNA and prevents viral replication
What is HIV?
It is an RNA retrovirus which invades (CD4+) T cells
Steps in the HIV viral life cycle?
1. Attachment and fusion
2. Uncoating
3. Reverse transcription of viral RNA via reverse transcriptase
4. Integration into human DNA in Tcell nucleus
5. Transcription
6. Translation
7. Processing by viral protease which cuts viral proteins into subunits needed for assembly of viral particles
8. Assembly and release via "budding" at T cell surface
9. Eventually infected T cells die
Why does HIV cause death?
--T cells are killed faster than they can be produces
--The lack of T cells causes immunodeficiency
--this leads to development of tumors and infections
--immune deficiency syndrome (AIDS) reached when CD4+ count <200
What determines the rate of progression of the disease?
The CD4+ count and viral load (number of copies of RNA)
What classes of drugs are used to treat HIV?
fusion inhibitors, nucleoside reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), and protease inhibitors
What is the name of the fusion inhibiting drug?
Enfuvirtide MOA?
It is a synthetic peptide which blocks fusion of the viral and T cell mbrns so HIV can't enter CD4+ cell
Enfuvirtide cross resistance, mode of administration?
Shows no cross resistance with other classes of antiretrovirals!!

Given s.c. with half life of 4h
Name the NRTIs.
-- These nucleosides are converted to "false" nucleotides by intracellular kinases

-- These "false" nucleotides competitively inhibit HIV reverse transcriptase and cause chain termination of the viral DNA

-- NRTIs can also be incorporated into the viral DNA
NRTI cross-resistance?
SOME cross-resistance in this class b/c each of the drugs has a slightly different MOA
Name the NNRTIs.
--they do not require phosphorylation to be active inhibitors
--directly inhibit reverse transcriptase to stop HIV replication
--bind to a site different than that of the NRTIs and thus do not compete with the nucleotides for binding to the reverse transcriptase

--Net effects: blockade of both RNA-dep-DNA-pol and DNA-dep-DNA-pol
NNRTI resistance?
--resistance develops quickly with monotherapy because all of these drugs have the same MOA

--resistance to one means resistance to all NNRTIs

--used with NRTIs b/c they have a different MOA
NNRTI interactions?
many CYP450 interactions
Name the protease inhibitors.
Protease inhibitor MOA?
--block viral protease to prevent the cleavage of viral polyproteins into the functional subunits needed for the assembly of the new virus particles
What's special about ritonavir?
-- it is used as a "pharmacokinetic enhancer
-- inhibits the CYP450 which metabolizes saquinavir to decrease the daily dose of saquinavir needed to maintain an effective plasma concentration of saquinavir
-- effectively decreases hepatic clearance so daily maintentance dose of saquinavir can be reduced