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3 IIH > 3.3 HIV and its mutations > Flashcards

3.3 HIV and its mutations Flashcards

1
Q

Why isn’t antigenic shift seen in RNA viruses other than influenza, such as measles, mumps, or rubella?

A

their genomes are non-segmented, so don’t undergo rearrangement like flu

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2
Q

Which of Flu and measles has non - human hosts?

A

flu, these non-human hosts act as reservoirs

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3
Q

What is super infection?

A

when multiple viruses infect the same cell, this facilitates genetic shift

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4
Q

What is significant about measles serotypes?

A

it only has 1

the 1 immunodominant epitope which overlaps with the virus binding domain for the receptor CD150

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5
Q

Which of + or - sense viruses are more diverse?

Why is this significant?

A
  • tend to be more diverse
    they also have larger genomes

this makes genome segmentation more common

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6
Q

What is the structure of HIV?

A

enveloped + sense ssRNA virus
has 2 + ssRNA per particle
a Lentivirus
2 subtypes, 1 and 2

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7
Q

How does HIV attach and fuse to T cells?

A

gp120 segment of glycoprotein binds to CD4

conformational change allowing gp120 to bind to CCR4 coreceptor

conformational change moves gp120 out of the way so the fusion peptides of GP41 penetrate the plasma cell membrane

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8
Q

What happens to viral RNA once inside the cell?

A

used to synthesise dsDNA by reverse transcriptase and enters nucleus to be integrated into the hosts’ genome

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9
Q

What are the steps of the productive cycle in HIV?

A

pro virus DNA transcribed into mRNA by host RNA polymerase and exported from nucleus
mRNA translated into proteins
viral proteins assembled into virion
new progeny virus released by budding
virus particle matures and becomes infecitous

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10
Q

Which stages of the HIV life cycle can be targeted?

A 
binding
fusion
reverse transcription
integration
maturation
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11
Q

What are the 6 classifications of drugs used to knock out HIV?

A 
NRTIs
NNRTIs
PIs
FIs
CCR5 antagonists
IIs
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12
Q

What are NRTIs?

A

nucleoside reverse transcriptase inhibitors

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13
Q

What are NNRTIs?

A

non-nucleoside reverse transcriptase inhibitors

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14
Q

What are PIs?

A

protease inhibitors

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15
Q

What are IIs?

A

integrase inhibitors

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16
Q

What is HAART and why do we use it?

A

highly active anti-retroviral therapy
single drug therapy kinda flopped

usually use
2 NRTIs + 1 NNRTI
2 NRTIs + 1 PI

17
Q

What are the advantages of HAART?

A

highly specific - safe
defined specificity
relatively rapid to develop

18
Q

What are the disadvantages of HAART?

A

highly specific - limited utility for diverse virus
defined specificity - resistance mutation occurs rapidly
costly to manufacture

19
Q

What is the MOA of NRTIs?

A

incorporated into virus DNA, competing with natural nucleosides, terminating the chain

has no effect on already infected cells though

20
Q

How does Zidovudine work?

A

NRTI

nucleoside analogue azido (N3) takes place of 3’ -OH terminating incorporation of nucleosides

21
Q

What is the MOA of NNRTIs?

A

bind to reverse transcriptase, non competitive antagonist, preventing RT enzyme from converting RNA into DNA

22
Q

What is the function of HIV protease?

A

cleaves HIV polyproteins into structural proteins and enzymes required for assembly of new infectious virions

23
Q

What do PIs do?

A

bind to protease and inhibit correct cleavage of viral proteins

24
Q

What is the course of primary HIV infection?

A

virus infects immune cells
delivered to lymph nodes
active virus replication
high levels of virinaemia and dissemination
down regulatio ofvirus replication by immune system
virus set point reaches after about 6 months

25
Q

What is the incubation period of HIV?

A

2-4 weeks

26
Q

What are the markers of acute HIV infection?

A

CD4+ T cells decline temporarily
CD8+ cells increase temporarily
Anti-HIV-1 antibodies appear

27
Q

What are the markers of chronic HIV infection?

A

CD4+ cells decline gradually
CD8+ cells largely unaffected
CTL responses evolve, antibodies evolve

28
Q

When does HIV form AIDS?

A

CD4 T cell count drops below 200 cells/ml

29
Q

What are the markers of AIDS?

A 
CD4+ T cell depletion
Loss of helper function
HIV specific CD4+ / CD8+ T cell exhaustion
B cells dysregulated
NK cell impairment
30
Q

What are the defining opportunistic diseases associated with AIDS?

A 
cryptococcal meningitis
toxoplasmosis
pneumocystic pneumonia
oesophageal cadidiasis
certain cancers (Kaposi's sarcoma)
31
Q

What is the principle of cross resistance?

A

muations to resistance to one drug often leads to resistance to many members of the ssame drug family

often occurs with PIs around codon 82

32
Q

How many drugs in combination are required to block viral replication / evolution?

A

at least 3

33
Q

How might HIV become resistant to NNRTI?

A

mutations reduce interactions between RT and the bound drug, steric hinderence

34
Q

How might HIV become mutated to NRTI?

A

altered interactions with the 3’OH of the incoming dNTP

35
Q

How might HIV become resistant to Zidovudine (AZT)?

A

excision involves pyrophosphorolysis
AZT-resistant RT’s preferentially excise AZT-MP
AZT-resistance mutations enhance the ability of RT to bind to ATP (phosphate donor)

36
Q

What 3 reasons make it difficult to make a vaccine against HIV?

A

enormous genetic variability

glycan shielding of the envelope glycoprotein

immune escape

37
Q

How does glycan shielding make it difficult to make an HIV vaccine?

A

Glycans restrict the ability of antibodies ot get to the envelope, where the GP receptros are

38
Q

What is immune escape?

A

HIV mutates to antibodies, original B cell clones mutate in response and neutralise virus

this cycle continues

said to occur in 3 phases

39
Q

What 4 things do we need for a successful vaccine?

A

broadly neutralising antibodies
inhibit all HIV strains
overcome glycan shield
inhibit intial infection

3 IIH (23 decks)

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