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Virology > Lecture 19 - HIV > Flashcards

Lecture 19 - HIV Flashcards

1
Q

Number of people infected with, or dead from HIV in history

A

75.8 million

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2
Q

Where are most deaths due to HIV?


A

Sub-Saharan Africa (a third of deaths)

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3
Q

New trend in HIV in Australia

A

Slowly increasing number of newly diagnosed cases

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4
Q

Major Australian demographic at risk of HIV

A

Male homosexuals

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5
Q

Prevalence of chronic blood-borne viral infections in Australia
1)
2)
3)

A

1) Chronic hep C - 210,000

2) Chronic hep B - 160,000
3) HIV - 17,000

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6
Q

Worldwide most common mode of HIV transmission

A

Heterosexual contact (80-85%)

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7
Q

Size of HIV

A

80-130nm

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8
Q

HIV capsid symmetry

A

Icosahedral

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9
Q

Size of HIV genome

A

9.2kb

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10
Q

Where is the HIV genome replicated?

A

Nucleus

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11
Q

Where is the HIV virion assembled?

A

Cytoplasm

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12
Q

Where did HIV originate?

A

Zoonosis from chimpanzees. Probably from eating bush meat in the Belgian Congo.

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13
Q

Who discovered HIV?


A

Professor Francois Barre-Sinoussi

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14
Q

What did HIV-1 evolve from?

A

SIVcz (chimpanzee)

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15
Q

What did HIV-2 evolve from?

A


SIVsmm (sooty mangabey)

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16
Q

Where does reverse transcription occur?

A

In the cytoplasm, within a loosened viral protein cone.

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17
Q 
Proteins encoded by pol
1)
2)
3)
4)
A

1) Protease
2) RT
3) RNase H
4) Integrase

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18
Q

How is pol expressed?

A

As a polyprotein (gag/pol) before autocleavage.

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19
Q

Error rate of reverse transcription

A

1 in 10,000 bases

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20
Q

Current most important drug target in HIV

A

Reverse transcriptase

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21
Q

What acts as the HIV gene promoter?

A

5’ LTR.

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22
Q

What increases the transcription of HIV genome?


A

Tat protein. Binds to the 5’ LTR.

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23
Q

What occurs to HIV genome transcription after initial replication?

A

Silencing of 5’ LTR promoter, until activation of host T cell (EG: NF-kB)

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24
Q

Function of tat protein

A

Tat (transactivator of HIV translation) binds to TAR (trans-activation response) RNA element.
Binding to TAR promotes transcriptional elongation.

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25
Q

How does Tat binding to TAR promote transcriptional elongation?
1)
2)
3)

A


1) Tat binds to bulge in TAR RNA tertiary structure.

2) Cyclin T is recruited. CDK9 binds cyclin T.
3) RNA polymerase II is phosphorylated, activated.

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26
Q

Rev function.
1)
2)

A

1) Binds to REV response element (RRE

2) This stabilises, transports unspliced (9kb) and partially-spliced (4kb) HIV RNA into the cytoplasm.

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27
Q 
How does HIV regulate early and late gene expression?
1)
2)
3)
4)
A

1) Early gene expression from tat binding to TAR in a low-REV environment.
2) Unspliced RNA is degraded, non-structural genes are translated.
3) REV is translated, increases in concentration in the nucleus.
4) In a high-REV environment, REV binds to REV response element (RRE), prevents degradation of unspliced RNA. Structural genes are translated (gag, gag/pol).

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28
Q

HIV-1 proteins necessary for replication in vivo and in vitro.

A

Tat, rev

29
Q 
HIV-1 proteins not necessary for replication in vitro, but necessary for in vitro pathogenesis
1)
2)
3)
4)
A

1) Vif
2) Vpr
3) Vpu
4) Nef

30
Q

Vif role
1)
2)

A

1) Promotes infectivity of cell-free virus

2) Blocks cell defences targeting ssDNA

31
Q

Vpr role
1)
2)
3)

A

1) cDNA nuclear import
2) Cell growth arrest
3) Weak transcription transactivation

32
Q

Vpu role
1)
2)

A

1) Regulator of particle release, env processing.

2) Promotes degradation of MHC-I, CD4

33
Q

Nef role

A

Downregulates MHC-I and CD4

34
Q

Cell tropism of C5 viruses

A

Macrophages, T cells

35
Q

Cell tropism of X4 viruses

A

T cells

36
Q

HIV type that forms syncitia

A

X4

37
Q

Initial exposure to HIV

A

Exposed to polyclonal HIV. A C5 HIV clone is selected for, as it can most-effectively bind a DC, which takes HIV to a regional lymph node.

38
Q

Untreated HIV progress
1)
2)
3)

A

1) Primary infection
2) Asymptomatic infection

3) AIDS

39
Q

Symptoms of primary HIV infection

A 
Flu-like
Fever
Myalgia
Vomiting, diarrhoea
Lethargy
Rash
Lymphadenopathy
Pharyngitis
Oral thrush
Transient CD4+ cell depletion
40
Q

Number of mucosal CD4+ cells killed by initial HIV infection

A

60% killed within days

41
Q

What leads to initial decline in HIV viral titres?

A

Depletion of permissive cells (all dead)

42
Q

How does HIV infection lead to breakdown of tight junctions between enterocytes?

A

Th cells secrete IL-17, which promotes tight junction formation between enterocytes

43
Q

Incubation period of primary HIV

A

2-4 weeks

44
Q

Duration of primary HIV symptoms

A

1-4 weeks

45
Q

Proportion of cases where ELISA can detect HIV antibodies in early primary infection

A

~50%

46
Q

Time taken for HIV RNA to be detectable after infection

A

1-18 days

47
Q

Will a Western blot show a positive result before or after ELISA will?

A

Before.

48
Q

Three main HIV tests

A

1) vRNA PCR
2) p24 antigen EIA
3) HIV-1/HIV-2 ELISA

49
Q

Initial immune response to HIV infection
1)
2)

A

1) 1-5% of all CTLs are specific to a single immunodominant HIV epitope
2) ~5% of total IgG specific to HIV envelope

50
Q

Problem with anti-HIV antibody response
1)
2)

A

1) Most antibodies aren’t neutralising

2) Virus-bound gp120 oligomers less immunogenic than free gp120 in plasma

51
Q

Why can the virus cause acute disease after asymptomatic phase?

A


During ‘quasi steady state’, virus is mutating.

Immune system is exhausted.

52
Q

Number of HIV virions produced per day

A

10^9

53
Q

Where is HIV mutation rate the greatest?

A

V regions of env, which promote antibody escape

V3 loop involved in co-receptor binding

54
Q 
Causes of CD4+ T cell destruction
1)
2)
3)
4)
A

1) Direct destruction of infected cells
2) Indirect destruction
3) Chronic immune activation, as GIT mucosal barrier integrity is lost, leading to chronic immune activation
4) Interference with migration of thymocytes to thymus

55
Q

Indirect death of infected T cells
1)
2)

A

1) CTL, NK cytolysis

2) Incorporation of healthy cells into syncitia (with X4 virus)

56
Q 
Chronic immune activation from HIV
1)
2)
3)
4)
5)
6)
A

1) Integrity of GIT mucosa is lost
2) Microbes enter blood stream, stimulate PRRs
3) Elevation of pro-inflammatory cytokine levels
4) CD4+ enter cell cycle, die from HIV activation
5) CD8+ trapped in lymph nodes
6) B cells make autoantibodies

57
Q

Effect of HIV infection on neutrophils

A

Reduced killing of bacteria

58
Q 
Effect of HIV on B cells
1)
2)
3)
4)
A

1) General increase in antibodies
2) Generation of autoantibodies
3) Poor response to vaccines
4) Reduced killing of capsulated bacteria

59
Q

Effect of HIV on macrophages
1)
2)
3)

A

1) Reduced phagocytosis
2) Reduced chemotaxis
3) Reduced microbial killing

60
Q

Common first sign of AIDS

A

Pneumocystis jirovecii pneumonia (a fungus)

61
Q

Hairy leukoplakia

A

EBV reactivation during AIDS. Forms plaques in the mouth.

62
Q

What causes Kaposi’s sarcoma?


A

Human herpesvirus (HHV) 8 activation during AIDS

63
Q

Viral factors affecting HIV disease progression
1)
2)
3)

A

1) Attenuated strain (EG: nef deficient)
2) R5 phenotype
3) Co-infection with hepatitis G reduces pathogenicity

64
Q 
Host factors affecting HIV disease progression
1)
2)
3)
4)
5)
6)
7)
A

1) CCR5 delta32 mutation
2) CCR5 promotor mutations
3) CCR2-64 I mutation
4) SDF-1 3’ untranslated region
5) HLA type
6) Ability to mount an immune response
7) Age

65
Q

HLA types that can confer increased resistance to HIV

A

B27, B57

66
Q 
Reservoirs of HIV latency
1)
2)
3)
4)
5)
A

1) Resting CD4+ memory T cells in lymph nodes, blood
2) Accumulation of virions in LN germinal centres, trapped on follicular dendritic cells
3) Lymph node, tissue macrophages
4) In brain microglia and astrocytes
5) Testes, seminal secretions

67
Q

Proportion of resting T cells harbouring HIV genome

A

1/10^5 - 1/10^6

68
Q

Cell type primarily infected with HIV

A

Central memory T cells

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