Exam 4 - Stahelin NRTIs (study) Flashcards
What is meant by genetic barrier to resistance?
nucleoside reverse transcriptase inhibitors (NRTI)
-human or viral target:
-reason drug is selective for virus or virus-infected cell:
-step in viral life cycle:
-MOA:
-human or viral target:
-reason drug is selective for virus or virus-infected cell:
-step in viral life cycle:
-MOA:
non-nucleotide reverse transcriptase inhibitors (nNRTI)
-human or viral target:
-reason drug is selective for virus or virus-infected cell:
-step in viral life cycle:
-MOA:
-human or viral target:
-reason drug is selective for virus or virus-infected cell:
-step in viral life cycle:
-MOA:
integrase inhibtors (INI)
-human or viral target:
-reason drug is selective for virus or virus-infected cell:
-step in viral life cycle:
-MOA:
-human or viral target:
-reason drug is selective for virus or virus-infected cell:
-step in viral life cycle:
-MOA:
protease inhibitors (PI)
-human or viral target:
-reason drug is selective for virus or virus-infected cell:
-step in viral life cycle:
-MOA:
-human or viral target:
-reason drug is selective for virus or virus-infected cell:
-step in viral life cycle:
-MOA:
abacavir metabolically activated by:
emtricitabine metabolically activated by:
tenofovir alafenamide metabolically activated by:
lamivudine metabolically activated by:
NRTIs
abacavir
emtricitabine
tenofovir alafenamide
lamivudine
Describe how a nucleoside analog is different in structure from a normal nucleoside used by reverse transcriptase.
look at structures of
abacavir
emtricitabine
tenofovir alafenamide
lamivudine
how is tenofovir different in structure and activation than other NRTIs? How does this increase its half life?
tenofovir SE?
abacavir hypersensitivity rxn?
-how does HLA-B*5701 play into this?
Abacavir has black box warning for hypersensitivity reactions that occurs in 4-8% of pts. This can be fatal and presents as dizziness and headache and GI disturbances. It is highly associated with the HLA-B*5701 allele and testing for this allele is needed before treatment initiation.
how can HIV become resistant to RT inhibitors? does cross resistance to all drugs in this class occur? Can you use combos of drugs in this class to manage resistance?