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IHO Week 6 > Regal and Skildum- HIV Learning Exercises > Flashcards

Regal and Skildum- HIV Learning Exercises Flashcards

1
Q

Describe the natural life cycle of HIV in a T cell.

A
  1. Gp120 binds CD4
  2. Gp41 binds CCR5/CXC4
  3. Virus enters cell and uncoats
  4. ssRNA is dumpted into cell w/ RT, integrase and protease
  5. RT copies genome into dsDNA (
  6. Integrase inserts genome into host genome (provirus)
  7. Expression of viral oncogenes and creation of spliced and unspliced RNA.
  8. Spliced RNA–>Rev, Taf, Nef (TF that promote un-spliced genes)
  9. Unspliced RNA–> env, gag, pol (new genome and particle proteins)
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2
Q

Does HIV do the same thing in a macrophage? Why?

A

Yes because Monocytes and macrophages also have a CD4 marker so HIV can bind to it.

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3
Q

What drugs are protease inhibitors? MOA?

A

Atazanavir
Rionavir
Darunavir

Prevent processing of viral proteins into functional conformations.

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4
Q

What drug is a fusion inhibitor?

A

Enfuvirtide

Blocks HIV entry into cell by binding to gp41 preventing the viral transformation necessary for fusion of viral and cellular membranes.

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5
Q

What drugs are NTRIs? MOA?

A 
AZT
Lamivudine
Abacavir
Emtricitabine
Tenofovir

Competitively inhibit HIV-1 RT
Incorporation into viral DNA chain causes premature chain temrmination d/t binding w/ an incoming nucleotide

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6
Q

What drugs are NNTRIs? MOA?

A

Etravirine
Efavirenz

Bind directly to HIV-1RT and directly inhibit

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7
Q

What drug is a chemokine receptor antagonist?

A

Maraviroc

Binds to host protein CCR5

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8
Q

What drug is a integrase inhibitor?

A

Raltegravir

Binds integrase and inhibits strand transfer and the integration of reverse transcribed HIV DNA into chromosomes of host cells.

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9
Q

Which of the antiretroviral host drugs targets a host protein?

A

Maraviroc–targets CCR5

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10
Q

Would you expect any of these drugs to be affective against latent virus?

A

NO

All of the drugs work in virus entry, replication and packaging, which will no longer be necessary when HIV incorporates into the genome

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11
Q

Is the HIV-1 virus genome bigger or smaller than HepB? EBV?

A

HepB< HIV < EBV

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12
Q

What are the implications of genome size on antiviral therapy?

A

Large genome has more unique viral drug targets

A small genome relies more on host machinery , so drugs may target host product

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13
Q

What proportion of potential drug targets are encoded by the virus vs the host?

A

Large- greater proportion of drug targets are viral

Small- greater proportion of drug targets are host

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14
Q

Is it easier to envision development of selectively toxic drugs w/ a bigger or smaller viral genome?

A

LARGER- produce more viral targets

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15
Q

What is a provirus? Where are the sites of integration?

A

A viral genome that is integrated into a host genome. LTRs are the sites of integration of the viral genome and they serve as strong promoters and bind TFs.

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16
Q

If ritonavir is given in combination with darunavir, would you expect an increase, decrease, or no change in serum concentration of darunavir compared to monotherapy with darunavir?

A

Darunavir is extensively metabolized by CYP3A

Ritonavir is an inhibitor of CYP3A.

Using these two drugs together–> decreased metabolism and increased plasma concentration of darunavir.

17
Q

What is the MOA of trimethoprim/sulfamethoxazole?

A

Sulfamethoxazole is a structural analogue of PABA. Interferes with the conversion of PABA into folic acid which is essential for bacterial development.

Trimethoprim binds and irreversibly inhibits DHFR–> bacteria can’t synthesize thymidine–> interferes w/ bacterial nucleic acid and protein formation.

18
Q

Why is it selectively toxic to penumocystis compared to the host?

A

Humans don’t synthesize folic acid through PAPA ( it is a dietary requirement). Also have different DHFR than bacteria.

19
Q

Why do you use a drug combination for treatment of HIV?

A

Minimum of 3 retrovirals necessary to guarantee effective long term suppression of HIV replication w/out resistance.

Includes at least 2 drugs w/ different MOA.

If pt is treated w/ only one drug, a drug resistant virus will inevitably emerge.

20
Q

What is an indirect ELISA?

A

Ag on plate>
detect Abs in serum (amt of colored product is proportional to Ab conc in serum)

Detect anti-p24 Abs, anti-env Abs

21
Q

What is a sandwich ELISA?

A

Ab on plate>
detect viral proteins in serum>
detect specific HIV ags like p24 or viral RNA

22
Q

What is the quickest test for HIV infection?

A

direct ELISA

23
Q

What is the gold standard for confirmation of a HIV infection?

A

Western blot

Detects/confirms specificity of Abs to a variety of epitopes.

At least 3 bands directed against the following Ags must be present (p24, gp41, or gp120/160)

24
Q

What is a tropism test and when is it helpful?

A

Helpful in deciding whether a CCR5 blocker will be useful in controlling a pt.s HIV. Required before beginning treatment w/ maraviroc.

25
Q

What is the best indicator of the immediate state of immunologic competence of the pt?

A

CD4 T cell enumeration

Lets you follow the CD4 count of a pt

26
Q

What is resistance testing?

A

can be done through genotypic or phenotypic testing

genotypic- genomes from pt are compared w/ known antiretroviral resistance profiles

phenotypic- viral isolates form the pt are compared to growth of reference strains of virus in the presence or absence of different antiretroviral drugs.

27
Q

A 35 y/o F who tested for HIV1 has been on efavirenz/tenofovir/emtricitabine for 2 years and maintaining CD4 coutns of 1000. She returns to your office and her CD4 levels are now 400. What are possible explanations for this?

A
  1. emergence of antiretroviral drug resistance from virus
  2. non-compliance
  3. new medication that alters affect of antiretroviral
  4. New infection–> T cell proliferation
28
Q

You are considering including maraviroc in your drug regimen to treat an HIV-1 pt. What would you need to determine prior to initiating therapy w/ a drug?

A

The trophism of the virus. Maraviroc is approvide for adults w/ CCR5 tropic HIV infections.

29
Q

A 43 yo M has a 20 yr hx of alcoholism. His alanine aminotransferase and aspartate amino transferase are severely elevated. HOw does this alter your approach to drug tx of his HIV?

A

Important to avoid or adjust dosage of drugs that are metabolized or activated by the liver.

30
Q

What HIV drug is most important to avoid with reduced renal function?

A

Tenofovir

IHO Week 6 (14 decks)

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