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42 Cards in this Set

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what kind of cells have Rc for HIV virus
macrophages
dendritic cells
t cells
what are the co-receptors for HIV
CCR5
CXCR-4
what are the viral proteins in HIV and what is the name of the complex
gp41
gp120

they form the complex gp 160
how does the HIV virus attach onto the cells
binds to CD4
then binds to CCR5 early in the infection
then binds CXCR-4 later on in the infection
what is viral tropism
the preference for certain types of cells

herpes: nerve cells
t-cell tropic virus CD4+CXCR-4 or CD4+CXCR-4+CCR-5

monocyte tropic virus CDR4 + CCR5 or CD4+CXCR-4+CCR-5
how does HIV manage to fuse onto the virus
requires HR2 and HR1 proteins
gp41 contains HR2 (and HR1) which unfolds to reveal a hydrophobic segment which inserts itself into the cell membrane
what does Reverse transcriptase do
makes a DNA copy out of RNA

HIV's polymerase will then copy the DNA made to form a double stranded DNA
what are the steps in the synthesis of viral HIV proteins
virus enters cell
RTase converts the RNA into DNA
DNA becomes dbl stranded via polmerase
viral DNA inserted into cell DNA via integrase
once cell makes message, viral protease will come and cut out the useful proteins
what are the drug targets of HIV
protease
RTase
inegrase
what is the state of a virus in a G1 cell
latent
what is the state of a virus in a G0 cell
G0 cell does not support infection or allow for the incorporation of viral DNA
what are the classes of inhibitors for RTase
nucleoside inhibitors
non nucleoside inhibitors
what is the MOA of nucleoside inhibitors
bind to RTase by going to the active site and stops the production of viral DNA from RNA
what is the MOA of nonnucleoside inhibitors
NON COMPETITIVE INHIBITORS
DON'T BIND TO THE ACTIVE SITE OF RTase but bind else where inhibit RTase activity by reducing the affinity of RTase for RNA thereby stopping viral DNA production from RNA
what are the properties of the NRTIs, NtRTIs

NUCLEOSIDE INHIBITORS
prodrug (becomes active via cellular kinase)
some drugs accumulate if cell is latent
cause chain termination (due to lack of 3'OH)
less affinity for cellular DNA polymerase but may effect mitochondria DNA polymerase
what is an adverse effect of NRTIs, NtRTIs
bone marrow suppression
what drugs are part of the HAART regiment
NtRTIs
NRTIs
why can't drugs that become active via TK effect HIV virus
because TK is specefic for only herpes
what are the Thymidine analogs (VUDINE) and what phosphorylates them
ziduovudine
stavudine

phosphorylated via TTPs
what are the cytosine analogs
emtricitabine
lamivudine

phosphorylated by cellular kinase
what are the adenosine analogs
didanosine
tenofovir

didanosine is phosphorylated to triphosphate form by cellular kinase

tenofovir already has a phosphate and only gains 2 from the cellular kinase
what are the guanosine analogs
abacavir (carbocyclic purine)
what is the MOA of guanosine analogs of NRTIs
abacavir

potent inhibitor of RTase
MOA: chain termination
what is the side effect of guanosine analogs
hypersensitivity reaction
what are the NNRTIs
nevirapine
delavirdine
efavirenz
etravirine
what is the oral bioavalability, metabolism, and drug interactions of the NNRTIs
good oral bioavailability
hepatic metabolism
lots of drug interactions but less for nevirapine
if you're resistant to nevirapine, or delaviridine, or efavirenze what can you give the pt
etravirine
why are you able to give Etravirine if someone is resistant to Efravirenz
due the etravirine being structurally flexible that even after the mutation it will still have good affinity for RTase

reserved use
what is the most common adverse reaction w/ NNRTI (non nueclosides)
rash
do NNRTI's (nonnucleoside inhibitors) induce cytochroms
yes
what are the properties of the protease inhibitors and what is the MOA
peptidomimetic
prevent the processing of long viral protein
what is the adverse effect of protease inhibitors
lipodystrophy (seen in cusshings)
what are the protease inhibitors
atazanavir
indinavir
nelfinavir
ritonavir
darunavir
lopinavir
tipranavir
saquinavir

end in NAVIR
atazanavir CYP3A4
metabolized
indinavir CYP3A4
inducer
ritonavir CYP3A4
inhibitor
saquinavir CYP3A4
inducer
what drugs are given w/ ritonavir
darunavir
lopinavir
tipranavir

all of these are extensively metabolized by CYP3A4 and one major use of ritonavir is to keep other drugs from being extensively metabolized by CYP3A4
what are the entry inhibitors
Enfuvirtide
Maraviroc
what is the MOA of entry inhibitors
Enfuviritide

block viral absorption and block viral entry into CD4+ lymphocytes

they mimic HR2 region of gp41 to prevent viral fusion to membrane
what are the co-receptor antagonist (entry inhibitor)
maraviroc
how does Maraviroc work
co-Rc antagonist

CCR5 Rc antagonist thereby blocking ability of virus to bind to CCR5 Rc