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MIIM2002 - 2 > HIV > Flashcards

HIV Flashcards

1
Q

First cases of HIV

A

~1950

Zaire, Cameroon

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2
Q

Is HIV enveloped?

A

yes

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3
Q

Estimated number of people living with HIV/AIDS in 2012

A

35.3 million

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4
Q

Estimated number of AIDS deaths in 2012

A

1.6 million

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5
Q

Proteins making up membrane spike

A

gp41 (membrane spike), gp120 (trimer)

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6
Q

HIV matrix protein

A

p17

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7
Q

HIV capsid protein

A

p24

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8
Q

HIV nucleocapsid protein

A

p7

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9
Q

HIV reverse transcriptase protein

A

p66/51

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10
Q

HIV integrase protein

A

p32

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11
Q

HIV protease protein

A

p11

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12
Q

HIV structural proteins of the matrix, capsid, core, nucleocapsid

A

gag

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13
Q

HIV viral enzymes

A

pol

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14
Q

HIV viral envelope proteins

A

env

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15
Q

Contents of gag

A

HIV structural proteins

Capsid, nucleocapsid, core, matrix

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16
Q

Contents of pol

A

Viral enzymes

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17
Q

Contents of env

A

HIV viral envelope proteins

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18
Q

How are gag and pol expressed?

A

As a polyprotein, before autocleavage

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19
Q

HIV genome

A

2 identical copies of + sense RNA

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20
Q

Mistake rate of HIV reverse transcriptase

A

~1 mistake per 10,000 bases

Roughly one mistake per copy of genome

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21
Q 
HIV replication cycle
1)
2)
3)
4)
5)
6)
7)
8)
A

1) gp120 binds CD4
2) Fusion of envelope with host cell membrane
3) Reverse transcriptase makes DNA copy of genome
4) DNA separated into two linear strands
5) Integrase integrates viral genome into host genome
6) mRNA of viral genes produced
7) Assembly
8) Budding

22
Q

Phases of HIV infection
1)
2)
3)

A

1) Primary infection - massive loss of CD4+ cells, high viral load
2) Clinical latency - Viral replication, slightly contained by immune system. Gradual decline in immune system function
3) AIDS

23
Q

CCR5

A

Coreceptor of CD4 for HIV gp120

24
Q

[CD4+] threshold for opportunistic infection

A

200 CD4+/mL

25
Q

Extent of HIV killing of immune cells in gut

A

Kills ~60% of GALT within days of infection

26
Q

Effect of HIV infection on gut

A

Loss of tight junctions
Enterocyte apoptosis
This leads to microbial invasion (LPS)
Intestinal fatty acid binding protein (I-FABP)

27
Q

Undetectable viral load

A

<50 viral copies/mL

28
Q

How does HIV evade the immune system?

A

1) Extremely high mutation rate
2) Deletion of HIV-specific CD4 clones
3) Faliure of HIV-specific Ab, CTL

29
Q

Effects of HIV infection on immune function

A

Decrease in Th function
Decrease in neutrophil killing
Decrease in NK killing
Th can’t activate B cells, macrophages
Macrophages decrease chemotaxis, phagocytosis, killing
B cells produce more antibodies, autoantibodies, respond poorly to vaccines, reduce killing of encapsulated bacteria

30
Q 
Targets for anti-HIV therapy
1)
2)
3)
4)
A

1) Fusion, entry inhibitors
2) Reverse transcriptase inhibitors
3) Integrase inhibitors
4) Protease inhibitors

31
Q

HAART

A

Highly active antiretroviral therapy

Use a combination of antiretroviral drugs

32
Q

Advantages of HAART

A

Minimise chance of resistance development

33
Q

Shortened life expectancy of HAART patients

A

About 10 years less than healthy controls

34
Q 
Difficulties in making an HIV vaccine
1)
2)
3)
4)
5)
A

1) Natural immune response fails to control the virus
2) Mechanisms of immune control of HIV incompletely understood
3) Very high HIV sequence diversity
4) HIV can evade antibodies, CTL, NK
5) HIV latency and genome integration

35
Q

Immune responses desired for an HIV vaccine
1)
2)

A

1) CD8+ - Kill HIV infected cells
Could silence HIV for a functional cure

2) Antibodies - Prevent transmission
Evaded by sequence variation in the viral envelope

36
Q

Difference in binding location between neutralising and non-neutralising antibodies against HIV

A

Neutralising antibodies bind to structured p120 trimers

Non-neutralising antibodies bind highly immunogenic inner face of gp120 monomers

37
Q

Qualities of broad-neutralising antibodies

A

Long CDRH domain

Highly mutated

38
Q

Issues with dead protein HIV vaccines

A

Efficacy

39
Q

Issues with live attenuated HIV vaccines

A

Safety

40
Q

Issues with genetically engineered live vector HIV vacciens

A

Require new technology

41
Q

Phase I clinical trials

A

10-30 volunteers

8-12 months

42
Q

Phase II clinical trials

A

50-500 volunteers

18-24 months

43
Q

Phase III clinical trials

A

Thousands of volunteers

3 years or more

44
Q

Outsome of B-clade vaccine in Sydney, 2003-2005

A

Poor CD8, CD4 response

45
Q

Merck STEP trial

A

rAd5 expressing HIV B clade gag, Pol, Nef.
Strong CD4, CD8 response
Expected to reduce viral load, have no effect on transmission

46
Q

rAd5

A

Recombinant adenovirus type 5

Expressing HIV gag, pol, nef

47
Q

Outcome of STEP trial

A

Vaccine enhanced rate of HIV infection

48
Q

RV-144 vaccine efficacy

A

~31%

49
Q

RV-144 vaccine effects

A

No obvious impact on viral load
No obvious correlates with immunity
Limited CD8 immunity
Limited primary neutralising antibodies

50
Q

Vaccine trials against HIV

A

1) STEP
2) B-clade in Sydney
3) RV-144

51
Q

Animal that naturally produces broad neutralising antibodies

A

Macaques

Against chimeric simian-human immunodeficiency viruses

52
Q

Reason for few broad-neutralising antibodies being produced naturally in body

A

Most are autoreactive, or have many mutations - eliminated by tolerance mechanisms

HIV envelope is similar to host antigens

MIIM2002 - 2 (12 decks)

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