HIV therapy Flashcards
when is it widely indicated to start ART
CD
3 possible rationale for starting earlier
- cohort studies that suggest MandM benefit
- reduce HIV inflammation
- decreasing transmission
5 absolute indications to start
- opp. infeciton
- pregnancy
- HBV coinfection
- HIV assoc. nephropathy
- HIV assoc. thrombocytopenia
what is effect of drug pressure on virus
causes resistant bugs to survive
5 goals of ART
- supress viral rep
- restore CD4
- reduce MandM
- improve QOL
- prevent onward transmission
5 main classes of ART and the replication points that they hit
- Entry inhibs - CD4 binding
- NRTIs -reverse transcriptase
- NNRTIs - reverse transcriptase
- integrase inhibs. - viral DNA integration
- protease inhib. - assembly
MOA of NRTIs
nucleoside reverse transcripase inhibs - fake nucleosides
**4 main NRTIs and their 2 combos
- lamivudine (3TC)
- abacavir (ABC)
- tenefovir (TDF)
- Emtricitabine (FTC)
TDF/FTC - most common
ABC/3TC
MOA of NNRTIs
bind at pocket distant from active site and block RT
** NNRTI to know and the combo
efavirenz (EFV)
TDF/FTC/EFV
MOA of protease inhibitors
stops enzymes from cleaving parts to make structure
major problem with NNTRIs
common drug interactions
** 3 protease inhibs
- ritonavir (RTV)- mostly booster
- atazanavir (ATV)
- darunavir (DRV)
how does booster work
CYP450 inhibitor so get more of other drugs in the system
what is MOA of entry inhibitors
blocks binding to CCR5 coreceptor or fusion once they are bound
