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Infectious diseases > HIV > Flashcards

HIV Flashcards

1
Q

Give an example of integrase inhibitor that is effective against both HIV-1 and 2.

A

Raltegravir

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2
Q

What gene is integrase enzyme coded by? What does the same gene also code for?

A

Pol

  • RT and protease
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3
Q

What are the side effects of NRTis?

A
  • hypersensitivity- abacavir
  • nausea/vomiting
  • rashes
  • Mitochondrial toxicity: myopathy, lactic acidosis, pancreatitis
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4
Q

What is the MoA of NRTIs?

What are some analogs?

A
  • Competitive inhibitors
  • Zidovudine (AZT): Thymidine (T) analog
  • Didanosine: Adenosine (A) analog
  • Lamivudine: Cytidine (C) analog
  • Abacavir: Guanosine (G) analog

All competitive inhibitors of HIV-1 RT (most also active against HIV-2)

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5
Q

When is HAART stopped and changed?

A
  • Progression of clinical disease to AIDS
  • Virological failure – inadequate suppression of viral load>10,000 copies ml
  • CD4 count falls or persistently below 100
  • Relieving drug side effects/toxicities

​

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6
Q
A
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7
Q

What is a protease inhibitor that can be use as boosting agent?

What is the name of the combination drug? What is it combined with?

A
  • Ritonavir
  • suppresses hepatic metabolism
  • Kaletra (lopinavir 100mg, ritonavir 25mg)
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8
Q

What is an immune reconstituation inflammatory syndrome?

A
  • an inert immune system will not fight infection
  • HAART may permit restoration of immunity
  • perverse restoration of disease symptoms with recovery
  • Tb, CMV, MAC
  • May require polypharmacy
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9
Q

What are the three types of RT inhibitors?

A

–Nucleoside analog reverse transcriptase inhibitors (NRTIs)

– Nucleotide analog reverse transcriptase inhibitors (NtRTIs)

– Non-Nucleotide/nucleoside reverse transcriptase inhibitors (NNRTIs)

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10
Q

What are examples of protease inhibitors?

A

Atazanavir, darunavir, fosamprenavir (a pro-drug of amprenavir), lopinavir, ritonavir, saquinavir, and tipranavir

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11
Q
A
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12
Q

Why are 3 drugs needed for the treatment of HIV?

A
  • Mutability of virus
  • evading single/dual agents
  • different MoA
  • Class resistance
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13
Q

What is the MoA of maturation inhibitors?

A

•Bind the gag protein, not the protease. Causes immature virus particles.

(GAG: capsid, matrix, nucleocapsid)

  • Berivimat first studied (clinical testing in 2009)
  • Effectiveness impaired by polymorphisms, drug effective in about 50% patients trialled.

​

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14
Q

What are examples of NNRTIs? MoA?

-

A
  • Efavirenz…associated with psychiatric symptoms
  • Etravrine
  • Nevirapine
  • Rilpirvine

These are all non-comopetitive inhibitors of HIV-1 RT, but have less effect on HIV-2

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15
Q

What is the MoA of Non-nucleoside.nucleotide RT inhibitors?

-

A
  • binds directly to the RT enzymes
  • non-competitive inhibitors of HIV-1 RT
  • Physically block or cause confirmation change in RT active site.
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16
Q

How does Maraviroc work? What form is it in?

A
  • A type of GP120/CCR5 association inhibitor
  • physically blocks GP120 binding
  • without GP120/CCR5, GP41 mediated membrane penetration is inhibited
17
Q

What are the side effects of NNRTIs?

A
  • Inactive against HIV2
  • Nausea, dizziness
  • Rash/ Stevens-Johnson
  • Hypersensitivity

•Neuro-psychiatric disease

•Lipid abnormalities

Pancreatitis

18
Q

What are the potential targets of entry inhibitors?

A
  • GP210/CD4 association
  • GP210/CCR5 association
  • Gp41/Plasma membrane fusion
19
Q

What are the fixed-dose combinations?

A
  • Eviplera (Complera in US)

…emtricitabine 200 mg, rilpivirine 25 mg, tenofovir 245 mg

  • Atripla

….efavirenz 600 mg, emtricitabine 200 mg, tenofovir 245 mg

  • Truvada

…tenofovir 245 mg, emtricitabine 200 mg

20
Q

What are the treatments of HIV according to BNF?

A
  • 2 x nucleoside RT inhibitors
  • and either non-nucleoside RT inhibitor
  • or a boosted protease inhibitor
  • or an integrase inhibitor
21
Q

What is the MoA of enfuvirtide? How is it taken into the body? How often?

A
  • Physically blocks the GP41 membrane pore through which virion enters cell
  • Twice daily sub-cutaneous injection
22
Q

What does ENV, GAG ad POL encode for?

A
  • Env- gp160 -> gp41, gp120
  • Gag-Pol precursor polyprotein
  • Gag: p24 (capsid), p17 (matrix), p7 (nucleocapsid)
  • Pol: protease, reverse transcriptase, integrase
23
Q

What are the 5 types of HIV Therapeutic targets and what are the MoA in each?

A
  1. Viral entry… Fusion inhibitors
  2. Reverse transcriptase… RT inhibitors
  3. DNA integration… INtergrase inhibitors
  4. Virion production that is for protease cleavage… Protease inhibitors
  5. Virion production that is for maturation… Maturation inhibitors
24
Q

When to start HAART?

A

•WHO 2010 – recommend starting HAART when CD4 count is around 350cells/mm3

25
Q

What are the limitations of entry inhibitors?

A
  • high mutation rate in all viral proteins as don’t have proofreading
  • Most Entry inhibitors also act as antagonists…which can prevent physiological function of the bound cells, effectively suppressing immune responses
26
Q

What are the drugs that HAART drugs can possibly interact with?

A
  • Drugs may inhibit or induce liver enzymes
  • Reduce or increase bioavailability
  • Fluconazole
  • Rifampicin
  • Warfarin
27
Q

Side effects of PIs?

A
  • GI upset
  • Fat redistribution (lipodystrophy)
  • Hepatic enzyme suppression
  • Insulin resistance/ hyperglycaemia
  • Osteonecrosis

Infectious diseases (5 decks)

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