HIV and AIDS Flashcards

1
Q

What 2 rare, opportunistic infections in previously healthy men first sparked the first reposts of HIV?

A

Pneumocystis Carinii

Kaposi’s Sarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does HAART stand for and what is it?

A

Highly active anti-retro viral therapy = the use of multiple (3) drugs on viral targets for the treatment of HIV

Usually 2 NRTI’s and 1 NNRTI or 1 protease inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When was HAART first introduced?

A

Mid-90’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a retrovirus?

A

It is an RNA virus that inserts a copy of its genome (genetic material) into the host cells DNA after invasion in order to replicate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What 3 groups of polyproteins does the RNA of retroviruses synthesise?

Name some of the enzyme groups within each.

A

1) Gag (group specific antigen) = matrixes, capsid, nucleocapsid
2) Pol (polymerases) = protease, reverse transcriptase, integrase
3) Env (envelope glycoproteins) = surface, transmembrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is seroconversion?

A

The time at when antibodies have been produced to the viral antigen and are detectable in the blood (blood test positive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How long does seroconversion take?

A

Usually within the first 1-3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the name given to the flu like symptoms that occur within the first few weeks of HIV infection?

A

HIV prodrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does reverse transcriptase work?

A

Retrovirus RNA is reverse transcribed into cDNA which then integrates into the host cells genome in order to hijack and replicate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What name is given to a retrovirus after it has undergone reverse transcriptase and integrated into the host cell?

A

The retrovirus is now called a provirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the consequence of integration of retroviruses into host cells?

What effect does this have on retroviral infection?

A

The infected cell can NOT be cured of the retroviral infection, the cell can only be destroyed by the killing of that cell

This means retroviral infections can not be cured and persist for life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which cells does HIV infect? (E.g. which is it ‘tropic’ for)

Why is this?

A

Primarily CD4 T cells, but others too

The virus can only infect cells which have CD4 co-receptor (CD4 T cells, macrophages, monocytes and dendritic cells) as well as co-stimulators molecules such as CCR5/CXCR4, as these are required for membrane fusion and endocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What 2 membrane proteins does HIV entry require?

A

1) CD4 protein

2) chemokine receptor (CCR5/CXCR4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the name of the structure formed when CD4 and the chemokine receptor of the host cell and the HIV retrovirus bind, which allows the membranes to fuse and endocytosis to occur?

A

6-helix bundle formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Does reverse transcriptase have a function to check its accuracy?

A

No, this allows mutations to occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 2 heterodimer polyprotein subunits of the RT enzyme?

A

P66 and P51

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 enzymatic activities of reverse transcriptase?

What does each do?

A

1) RNA-dependant DNA polymerase = synthesises DNA on virus RNA genome
2) RNAsH = cleaves RNA from the able RNA/DNA hybrid
3) DNA-dependant DNA polymerase = synthesises DNA from DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the name of the primer molecule for reverse transcription in HIV infection?

A

tRNAlys3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does HIV lead to aids?

A

CD4 T cells are inexorably depleted by the virus as they inject and hijack the cells

20
Q

What is viral load?

A

The number of viral RNA genomes per ml of blood

21
Q

What areas and cells are the main primary targets of acute HIV infection?

A

CD4 T cells in the mucosa (where majority of CD4 T cells live)

Gut assisted lymphoid tissue (GALT) = T cell nodes eradicated

22
Q

Which host cell protein interferes with HIV entry?

Which virally encoded protein counteracts the activity of this protein?

A

SERINC (serine inclusion into phospholipids)

Counteracted by NEF

23
Q

Which host cell protein inhibits HIV release from the cell surface?

Which virally encoded protein counteracts the activity of this protein?

A

Tetherin

VPU

24
Q

Which host cell protein catalyses C to U to inhibit RT?

Which virally encoded protein counteracts the activity of this protein?

A

APOBEC3

VIF

25
Q

Which host cell protein hydrolysis dNTP’s to inhibit RT?

Which virally encoded protein counteracts the activity of this protein?

A

SAMHD1

VPX

26
Q

What is the main way HIV is transmitted?

A

Via mucosal routes

27
Q

Over what time frame does a normal person (professor) progress to AIDS from HIV infection?

A

8-10 years

28
Q

Over what time frame does a rapid person (professor) progress to AIDS from HIV infection?

A

1-3 years

29
Q

Over what time frame does a long term non-progressor person (professor) progress to AIDS from HIV infection?

A

Remains AIDS free indefinitely

30
Q

Over what time frame does a elite controller progress to AIDS from HIV infection?

A

Aids free indefinitely AND <50 copies RNA/ml of blood

31
Q

What causes the acute drop in viral load just after acute infection?

A

CD8 T cells killing infected CD4 T cells

32
Q

How is HIV diagnosed?

A

ELISA testing for anti-p24 (capsid) antibodies in the serum in those who have seroconverted

33
Q

Does a negative ELISA HIV test mean a person does not have HIV?

A

No, they may have just not seroconverted

34
Q

Which test can confirm HIV and level of viral loads before seroconversion?

A

RT-PCR

35
Q

What causes karposi’s sarcoma?

A

Human herpes virus 8

36
Q

What is pneumocystis carinii?

A

A fungal pneumonia

37
Q

How does maraviroc work?

A

Binds to CCR5 co-receptor to prevent virus interaction with host cell

38
Q

How does enfirvitide (T20) work?

A

Prevents fusion of two membranes between HIV and host cells

39
Q

What are the two types of RT inhibitor drugs and how do each work

A

1) Nucleoside analogue reverse transcriptase inhibitors (NRTI) = act as a nucleoside lacking functional group to allow virus chain to grow, therefore terminate chain short
2) Non-nucleoside reverse transcriptase inhibitors (NNRTI) = bind to RT (away from active site) causing conformational change and block it’s action

40
Q

How does raltegravir work?

A

Is an integrase inhibitor, stopping cDNA from virus integrating with host cell DNA

41
Q

How do protease in inhibitors work?

A

Stop Gag and Pol proteins, meaning new viruses are created but are non-infectious

42
Q

What needs to happen to latent infected cells to cure HIV?

A

We need a drug to shock and kill them, i.e. wake them up, get the, to start transcription of new virus particles and kill them, all while the patient is taking a HAART

43
Q

What is an ‘undetectable’ viral load (which is also the aim of treatment)?

A

<50 cpm (copies per ml)

44
Q

At what CD4 count do most AIDS diagnoses occur?

A

<200 cpm

45
Q

What CD4 count gives a HIV+ person the same survival rate as the general population?

A

CD4 count >500cells/ml for >5 years

46
Q

When should we be targeting people for HIV blood test screening?

What % are we currently screening and what is the % target?

A

On A&E admission

We are currently hovering around 60-70% but are aiming for 85%