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HIV Flashcards

1
Q

What is HIV?

A

Human Immunodeficiency Virus

2 species of single stranded RNA lentivirus
over time it damages cells within the immune system increasing the risk of infections

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2
Q

What is AIDS?

A

Acquired immunodeficiency syndrome

To be diagnosed with AIDS person with HIV must have:
An AIDS defining illness (opportunistic infection, cancer)
OR a CD4 count less than 200 cells/mm3

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3
Q

How is HIV transmitted?

A
  1. Unprotected sex
  2. Passed from mother to baby
  3. Sharing injection equipment
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4
Q

How is HIV diagnosed?

A

point of care testing

4th gen ELISA test

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5
Q

What are the 2 markers of HIV progression?

A
  1. CD4 count (no. of CD4+ T cells in 1mm3 of blood)
    this represents how well the immune system is functioning
  2. Viral load (no. of copies of HIV RNA in 1ml of blood
    it is the conc of virus in blood NOT amount
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6
Q

What is the difference between CD4 count and CD4 %?

A

CD4 count is the number of CD4+ T cells in 1mm3 of blood however CD4% is the proportion of CD4+ to other WBCs

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7
Q

How does HIV typically present at the beginning?

A

As an acute infection
Pt has high viral load, unaware of HIV status
Non specific flu like symptoms last between 7-28 days

however some pts are asymptomatic

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8
Q

What is the clinical latency period?

A
  • Declining CD4 count but stable viral load
  • Increases risk of infections or lymphomas
  • May last over 8 years
  • Asymptomatic
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9
Q

What is PCP

A

Pneumocitis Jirovecci Pneumonia
Is a common infection in HIV pts
symptoms = non productive cough and dyspnoea

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10
Q

What is the treatment of PCP

A

Co-trimoxazole

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11
Q

What is the prophylaxis treatment for PCP

A

Co-trimoxazole 480mg OD

in CD4 less than 200 and consider stopping when CD4 is greater than 200 for 3 months

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12
Q

Explain the viral replication cycle

A
  1. Interaction between gp120 on surface of virus and CD4 antigen on host cell membrane
  2. This causes a confirmational change that allows gp120 to bind to either CXRC-4 or CCR5
  3. This causes a further confirmational change that exposes the gp41 fusion peptide
  4. gp41 punctures a hole in the membrane to allow fusion of the 2 membranes
  5. HIV interacts w cell membrane bound proteins to open up a pore which the viral core material can pass into the interior of the cell
  6. RT takes viral RNA and uses its polymerase function to build a complementary viral DNA strand producing a DNA RNA hybrid
  7. RT uses its endonuclease function to cut out RNA
  8. RT uses its polymerase function to build double stranded viral DNA
  9. HIV produces its envelope through a complex process where viral gp41 and 120 are inserted into host cell membrane. Forms the capsid as well
  10. Virion release by budding
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13
Q

What type of antiviral drugs are there?

A
  1. Entry inhibitors
  2. NRTIs
  3. NNRTIs
  4. Integrase inhibitors
  5. Protease inhibitors
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14
Q

What are the different types of entry inhibitors and how do they work?

A
  1. Fusion inhibitors - bind to gp41 which inhibit the fusion of the 2 membranes
  2. Attachment inhibitors - bind to CD4 receptor on host cell membrane so that gp120 cannot bind
  3. CCR5 receptor antagonists - bind to an allosteric site on the CCR5 receptor causing a confirmational change so that gp120 cannot bind
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15
Q

What are the goals of HIV treatment?

A
  1. Clincal - extend life expectancy and improve QoL
  2. Immunological - preserve and restore CD4 cell count
  3. Virological - undetectable viral load within 4-6 months
  4. Epidemiological - prevent transmission
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16
Q

When should treatment be started in primary infection?

A 
When patient is ready to commit to ARVs
However should be started asap if:
- neurological involvement 
- any AIDS defining illness
- CD4 count <350 cells/ul
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17
Q

When should treatment be started in chronic infection?

A

When patient is ready to commit to ARVs (asap)

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18
Q

When should treatment be started in those who present with AIDS or major infection?

A

Start within 2 weeks of antimicrobials

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19
Q

What factors would you consider when starting ARV treatment?

A
  • CD4 cell count
  • Viral load
  • Patients likely adherence
  • Discordant couples where 1 partner has high VL
  • Transmission risk
  • Pregnancy
  • Patient wishes
  • Co morbidities: AIDS related/diagnosis
    Hep B/C infection
    TB
    Neurological involvement
    CVD/ high risk
    Risk of IRIS = Immune reconstitution inflammatory syndrome
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20
Q

What is PEP?

A

Post exposure prophylaxis

28 days treatment within 72 hours after exposure

21
Q

What is PrEP?

A

Pre exposure prophylaxis

Taken daily/PRN by HIV negative individuals at high risk e.g., multiple sexual partners

22
Q

Give examples of NRTI backbone drugs

A

Truvada (TDF + emtricitabine)
Descovy (TAF + emtricitabine)
Kivexa (Abacavir + Lamuvidine)

23
Q

Give examples of protease inhibitors

A

Atazanavir/Ritonavir*
Evotaz (Atazanavir/Cobicistat*)
Darunavir/Ritonavir
Rezolsta (Darunavir/Cobicistat)

*pharmacokinetic boosters

24
Q

Give examples of integrase inhibitors

A

Dolutegravir
Elvitergravir
Raltegravir

25
Give examples of NNRTIs
Efavirenz Nevirapine Rilpivirine
26
Give an example of a CCR5 inhibitor
Maraviroc (rare)
27
What is the first line drugs for HIV?
Usually 2 NRTIs and 1 drug from another class
28
What are the disadvantages of Truvada/TDF
- Effects on renal function so cautioned in stage 3-5 CKD Renal accumulation results from highly efficient uptake from plasma with reduced efflux into urine - Effects bone mineral density
29
What are the advantages and disadvantages of Descovy/TAF
(+) Reduced kidney damage reduced bone demineralisation equivalent efficacy to Truvada and fewer side effects (-) cost
30
What is the alternative treatment for HIV?
Kivexa (abacavir and lamivudine) if viral load is less than 100,000 and HLA-B*5701 negative cautioned in CVD 8% of population is allergic
31
What is the HAART regimen?
2 NNRTIs and 1 NRTI | Truvada and Efavirenz
32
What are the 2 types of reverse transcriptase inhibitors?
Nucleoside RT inhibitors (NRTIs) | Non nucleoside RT inhibitors (NNRTIs)
33
What is the MoA of NRTI
- taken as a pro drug and therefore taken into host cell and phosphorylated before they become active - NRTIs lack a 3' OH group and will have a nucleotide as a base - Due to the missing 3' OH group the NRTI prevents the formation of a 3'-5' phosphodiester bond in growing DNA chains to prevent replication of virus - therefore they are known as obligatory chain terminators
34
What is the MoA of NNRTIs
- binds to the allosteric pocket in the palm domain of the p66 subunit of RT - this pocket is hydrophobic and NNRTIs have a high LogP therefore can bind - this binding results in a confirmational changes which causes movement of the 2 aspartic acid residues in the active site - also misaligns the position of thumb which slows/prevents translocation of the primer/template strand
35
What is the function of protease
Cleaves long non functional polypetides into functional proteins e.g., matrix/capsid/nucleocapsid proteins
36
What is the MoA of protease inhibitors
Inside the active site of protease there are 2 aspartic acid residues that allow protease to add a molecule of water to the amide bond to produce an amine and a carboxylic acid
37
What is the MoA of protease inhibitors
Inside the active site of protease there are 2 aspartic acid residues that allow protease to add a molecule of water to the amide bond to produce an amine and a carboxylic acid (leaving groups) However protease are transition state mimics that bind to the active site of protease and have no OH/a single OH/OH on different carbon therefore amine and carboxylic acid are NOT produced drug stays on the active site irreversibly
38
What is the purpose of integrase
1. 3’ processing | 2. Strand transfer
39
What is the MoA of integrase inhibitors
- LEDGEF binds to the CCD-CCD interface of one diner whilst binding to the NTD of another dimer - Forms a stable tetramer (active form) - 3’ processing in the cytoplasm can occur - which generate sticky ends on the viral DNA - this allows to enter the nucleus - integrase cuts the cellular DNA - inserts viral DNA into cellular DNA = strand transfer - which is permanent infection 72 hrs from exposure before strand transfer is permanent
40
How do integrase inhibitors work?
- The active site in the CCD has 2x Mg2+ which is a strong Lewis acid - phosphates in DNA are strong Lewis base so integrase is attracted to DNA - this allows strand transfer to occur - integrase inhibitors have oxygen instead of phosphate to make it a strong Lewis base - mg2+ ions in the active site of integrase bind to stronger Lewis base (the inhibitor)
41
What are the pros and cons of protease inhibitors?
(+) high efficacy (-) low barrier to resistance so can easily become resistant - drug interactions - many side effects e.g., lipodystrophy
42
What are the pros and cons of integrase inhibitors?
(+) high barrier to resistance so less likely to become resistant (+) few drug interactions (+) few side effects
43
What are the pros and cons of NNRTIs
(+) high efficacy (-) low barrier to resistance so can easily become resistant - drug interactions
44
Why is it important to stress adherence to patients>
Poor adherence is associated with: - treatment failure - disease progression - transmission of resistant virus - increased healthcare costs
45
How does resistance occur?
RT is prone to high no. of errors because it has no proof reading function leading to many drug resistant strains
46
Why are most ARVs taken with food?
1. reduce side effects involving the stomach (Ritonavir) | 2. increased absorption of lipid soluble drugs
47
What interacts with integrase inhibitors?
Calcium (avoid dairy products) Iron supplements Integrase is chelated in the stomach as a result of these polyvalent ions so don't get absorbed
48
what interacts with Atazanavir and Rilpivirine?
PPIs because they change the gastric pH

HIV (1 decks)

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