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Medical Microbiology > 9 Anti-retroviral agents > Flashcards

9 Anti-retroviral agents Flashcards

1
Q

what is a retrovirus

A

RNA that went to DNA (carries reverse transcriptase)

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2
Q

what is critical for DNA synthesis

A

Oxygen atom

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3
Q

what is Azidothymidine

A

a Nucleoside analogue Reverse Transcriptase Inhibitor (NRTI)

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4
Q

what phosphorylates Azidothymidine:

A

All three phosphate groups are added dependent on the HOST cells

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5
Q

what is the effect of Azidothymidine

A

AZT-triphosphate acts as DNA chain terminator and will stick the reverse transcriptase = inhibit it
No oxygen atom so causes chain termination

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6
Q

does Azidothymidine work

A

AZT increase life from studies - 19 deaths, 18 in placebo arm

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7
Q

effect of treating patients with AZT before getting AIDs

A

no prolonged survival – the period of time that improve doesn’t last
Useful therapeutic life of about 6 months after this = no effect

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8
Q

what were the next NRTIs

A

ddC and ddI

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9
Q

what are ddC and ddI

A

2’3’dideoxy NAs developed

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10
Q

what is the toxicity of ddC and ddI

A

infect other organs (peripheral neuropathy, pancreatitis)

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11
Q

what led to the more sustained CD4 response

A

AZT + ddC or ddI

Give both drugs instead of just AZT = may improve life length

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12
Q

why is it better response giving AZT and ddC/ddI

A

Asking virus to acquire 9 mutations to become resistant to both as opposed to 5 to become resistant to AZT- take virus longer

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13
Q

what are NRTIs

A

Nucleoside and nucleotide reverse transcriptase inhibitors

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14
Q

what are NTRIs like

A

analogues of native nucleotides sharing the common motif of a lack of ‘3-OH group on their ribose ring

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15
Q

what do NTRIs require

A

Must be phosphorylated by cellular kinases before they can effectively exert their actions
NRTIs and native nucleosides

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16
Q

what are NNRTIs

A

Non-Nucleoside analogue Reverse transcriptase Inhibitors

17
Q

what do NNRTIs do

A

Non-competitive RT inhibitors, induce conformational changes within reverse transcriptase

18
Q

what can be given in combination therapy

A

Combination therapy (NRTI + NNRTI) achieves greater loss of viral load, sustained for longer

19
Q

what do protease inhibitors do

A

bind to and inhibit HIV protease-mediated cleavage of HIV polyprotein precursors

20
Q

effect of protein inhibitors on viruses

A

Virus particles can still be made but they are rendered non-infectious

21
Q

what boosts protein inhibitors

A

Metabolised by CYP enzymes (use of ritonavir as CYP inhibitor to boost PIs)

22
Q

what does HIV aspartyl protease do

A

cleaves gag and gag-pol polyproteins into their essential structural and enzymatic (RT and IN) components

23
Q

HIV protease - Mechanism of resistance

A

mutations (a.a changes) modify the number and nature of points of contact between the PI and the protease molecule

24
Q

what is the problem with protease inhibitors

A

a lot of these mutations are the same

If virus become resistant to one – likely will be resistant to the others

25
Q

examples of available protease inhibitors

A
  • Lopinavir (+ ritonavir) = Kaletra

- Atazanavir

26
Q

what is ritonavir

A

booster for protease inhibitors

27
Q

what does ritonavir do

A

Use a very small dose of ritonavir have no anti-HIV affect, but inhibits the degradation of the other protease inhibitors you’re going to give

28
Q

NRTIs: adverse effects

A

block “RT”; They may inhibit the activity of normal cellular DNA polymerases

29
Q

Viral entry

A

2 glycoproteins coming out from envelope – GP120 sticking out binds to CD4 – primary receptor molecule
Brings virus closer and binds to secondary receptor
gp41 bends so viral membrane brought into contact with cell membrane – fusion and virus enter cell

30
Q

New antiretrovirals - HIV-1 Entry inhibitors

A

Enfuvirtide binds to half of gp41 and prevents the hinge activity
Enfuvirtide is a hinge inhibitor

31
Q

Current anti-HIV therapy aim

A

put an absolute brake on ALL viral replication

– if virus is not replicating, then resistance cannot happen

32
Q

HIV Drug resistance - cART effect

A

blocks the selection of mutants

33
Q

how does cART block mutants

A

Multiple mechanisms are required for resistance to occur to all drugs in the regimen

34
Q

how is the current anti-HIV therapy given

A

MUST be combination – Highly Active (HAART) or combination (cART) Antiretroviral Therapy

Medical Microbiology (13 decks)

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