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FMS > FMS Week 10: HIV > Flashcards

FMS Week 10: HIV Flashcards

1
Q

HIV is what type of virus

A

Retrovirus

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2
Q

Gag genes

A

Viral structural proteins

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3
Q

Pol genes encode

A

Viral Enzymes

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4
Q

Env genes encode

A

Surface glycoproteins

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5
Q

HIV regulatory proteins

A
  • tat
  • rev
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6
Q

HIV accessory proteins

4 Listed

A
  • vif
  • vpr
  • vpu
  • nef
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7
Q

HIV Virion Structure

  • viral glycoproteins
  • Viral Matrix
  • 2 copies of viral single stranded (+) sense RNA Genome
  • assoicated nucleocapsid protein
  • Viral enzymes (protease, integrase, reverse transcriptase, accessory proteins)
A
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8
Q

The HIV Life Cycle

6 Listed

A
  1. Binding and Fusion
  2. Reverse transcription
  3. Integration
  4. Transcription and Translation
  5. Assembly
  6. Budding
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9
Q

The HIV Life Cycle: Binding and Fusion

A

The virus binds to CD4 receptor and a coreceptor (CCR5 and CXCR4) and initiated fusion with the cellular membrane

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10
Q

HIV Tropism is largely defined by?

A

Receptor expression

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11
Q

CD4 is expressed on?

6 Listed

A
  • T helper cells
  • macrophages
  • monocytes
  • DCs
  • Eosinophils
  • microglial cells
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12
Q

CCR5 is ____________ tropic

A

Macrophage R5-tropic

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13
Q

CCR5 is expressed on

3 listed

A
  • many immune cells

in particular

  • Memory T cells and Macrophages
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14
Q

50% of HIV infected individuals only have …

A

R5-Tropic HIV

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15
Q

CCR5Δ32 mutation

A

confers resistance to HIV infection

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16
Q

HIV type that predominates early after transmission

A

R5-tropic HIV

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17
Q

CXCR4 HIV AKA

A

T-cell (X4)-tropic HIV

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18
Q

CXCR4 is expressed on

A

Naive T cells and DCs

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19
Q

X4-tropic HIV is associated with

A

immunodeficiency

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20
Q

X4-isolates are typically highly?

A

Cytotoxic

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21
Q

The HIV Life Cycle: Reverse Transcription

A

The viral enzyme reverse transcriptase converts the viral RNA genome into dsDNA

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22
Q

HIV Reverse Transcriptase proofreading activity Consequences

2 Listed

A
  • Replication of the viral genome is an error-prone process
  • ~1 base/genome is mutated per replication cycle
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23
Q

The HIV Life Cycle: Integration

A

The viral enzyme integrase transports the viral DNA into the nucleus and inserts the viral genome into the host chromosomal DNA (this is referred to as proviral DNA)

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24
Q

Proviral DNA AKA

A

when the viral genome is inserted into the host chromosomal DNA

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25
Q

Integration into the host genome allows the virus to establish a…

A

Latent State

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26
Q

The HIV Life Cycle: Transcription and Translation

3 Listed

A
  • Viral mRNA is transcribed and translated using host cell machinery
  • Viral proteins are synthesized as polyproteins
  • Viral transcription only occurs in actively replicating cells
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27
Q

The HIV Life Cycle: Assembly

2 Listed

A
  • Polyproteins are cleaved by the viral enzyme protease
  • Viral RNA and enzymes are encapsidated by gag proteins (CA and NC)
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28
Q

The HIV Life Cycle: Budding

2 Listed

A
  • The viral glycoprotein is expressed on the membrane of the host cell
  • Immature viral capsid structures traffic to the cell membrane and bud from this surface
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29
Q

The HIV Life Cycle Figures

A
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30
Q

Anti-retroviral drug classes that interfere with essential steps in the viral life cycle

4 Listed

A
  1. Entry inhbitors
  2. RT inhibitors
  3. Integrase inhibitors
  4. Protease Inhibitors
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31
Q

Anti-retroviral drugs: Entry Inhibitors Drug Name and Target

2 Listed

A
  • Maraviroc (CCR5)
  • Enfuvirtide (viral gp41)
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32
Q

Anti-retroviral drugs: RT Inhibitors Drug Name and Target

2 Listed

A
  • Nucleotide/nucleoside analogs
  • Non-nucleotide inhibitors
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33
Q

Anti-retroviral drugs: Integrase inhibitors Drug Name and Target

1 Listed

A
  • Raltegravir (Isentress)
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34
Q

Anti-retroviral drugs: Protease Inhibitors Drug Name and Target

A

~10 clinically approved

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35
Q

Clinical Course Stages of HIV Infection

3 Listed

A
  1. Acute Phase
  2. Clinical Latency
  3. AIDS
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36
Q

Clinical Course of HIV Infection: Acute Phase Description

3 Listed

A
  • Marked by a mild acute flu-like illness and an acute viremia
  • These high viral loads then rapidly decrease
  • Wide dissemination of the virus throughout lymphoid tissues
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37
Q

Clinical Course of HIV Infection: Clinical Latency Phase Description

5 Listed

A
  • Typically absent clinical symptoms
  • Low viral loads, strong debatable immunity
  • Massive viral replication and turnover of infected T cells
  • Disruption of lymphoid architecture
  • A slow decline in CD4+ T cell numbers
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38
Q

Clinical Course of HIV Infection: AIDS Phase Description

3 Listed

A
  • CD4+ T cell count <200
  • Dramatic Increase in plasma viral loads
  • Increased susceptibility to opportunistic infection due to compromised B and T cell function
39
Q

Routes of Transmission for HIV

3 Listed

A
40
Q

HIV Trojan Horse

4 Listed

A
41
Q

Productive HIV Viral infection is dependent on

A

Cellular Activation

42
Q

HIV can only establish a productive infection in?

A

Activated T cells

43
Q

HIV can infect

A

Activated and memory T cells by can only establish a productive infection in activated T cells

44
Q

How do T cells become activated for HIV to establish a productive infection

A

The initial immune response to HIV infection provides a source of activated T cells allowing enhanced infection

45
Q

HIV can infect activated and memory T cells that are positive for?

A

CCR5-positive cells

46
Q

Infection of activated cells produces virions and causes…

A

More T cell activation

47
Q

HIV can remain in a latent form in

A

long-lived memory T cells

48
Q

Memory T cells found at high levels in

A

lymphoid tissues (especially the mucosal lymphoid tissues)

49
Q

Mucosal T cells are typically…

A

activated and owing their stimulation to gut flora

50
Q

CCR5-positive cells CD4+ location percentiles

A
  • 20% of peripheral blood CD4+ T cells
  • 80% of gut CD4+ T cells
  • 10% of LN CD4+ T cells
51
Q

________ Lymphoid tissue is a site of HIV Replicaiton early in infection

A
52
Q

Summary of early events upon HIV infection

3 Listed

A
  • Depletion of T cells in gut-associated lymphoid tissue
  • Immune responses against HIV may provide a source of target cells
  • Nevertheless, viral replication is eventually controlled by host immune responses
53
Q

Immune Responses against HIV

2 Listed

A
54
Q

Virus specific Ab effective against

A
  • Viral particles
55
Q

Viral Specific Ab poor effectiveness against

A

Virally infected cells

56
Q

Virus specific Ab not effective against

A

latently infected cells

57
Q

Virus-Specific CTL Effective against

A
  • Virus Infected cell
58
Q

Virus-Specific CTL Not Effective against

2 Listed

A
  • Latently infected cells
  • Virus Particles
59
Q

Clinical latency coincides with the?

A

Induction of anti-HIV antibody and CTL responses

60
Q

Set point viral load is correlated with time to _______.

A

AIDS

61
Q

Characteristics of Chronic HIV Infection

4 Listed

A
62
Q

Viral Variation explanation

2 Listed

A
  • Gradual loss of immune control
  • Gradual increase in viral cytopathicity
63
Q

Clinical Latency is not?

A
64
Q

Humoral Immune Responses against HIV

5 Listed

A
65
Q

Neutralizing antibodies in HIV

A
66
Q

Clinical Latency is not?

A
67
Q

Antibodies lose the ability to?

A

Neutralize Virus

68
Q

Why is it so difficult to elicit broadly neutralizing antibodies against HIV?

A

HIV has evolved several strategies to escape humoral immune responses

69
Q

Vaccines against HIV are based on?

A

Neutralizing Antibodies

70
Q

Neutralizing Antibodies are likely ineffective at controlling HIV infection but…

A

There is still great interest in developing prophylactic vaccines based on neutralizing antibody activity

71
Q

Major probles to HIV Vaccines

A
  • Viral evolution
  • HIV Variability
72
Q

Summary of Humoral immunity and HIV

5 Listed

A
73
Q

Cell mediated immune responses against HIV

2 Listed

A
74
Q

In HIV patients _____% of all CD8 cells are HIV specific.

A

2-10%

75
Q

CTL responses target?

A

Multiple Viral Proteins

76
Q

Immune responses thought to be the most important for controlling viral replication.

A

CTL Responses

77
Q

CTL Responses in HIV Properties

5 Listed

A
78
Q

Why do CTL responses ultimately fail?

3 Listed

A
  • Viral escape from CTL through mutation
  • Viral gene product nef may downregulate MHC Class I
  • Chronic stimulation CD8+ T cells can lead to loss of effector functions
79
Q

Role of immunodominance in CTL escape

3 Listed

A
80
Q

Immunodominance places individuals at risk for? And reason?

2 Listed

A
  • Immune escape by epitope variation
  • Epitope variation prompts a switch such that CTL response is directed against subdominant viral epitope which must be less efficient in stimulating T cells
81
Q
A
82
Q

CTL escape in early, intermediate, and late

A
83
Q

HLA Types can be related to

A

more rapid or slower disease progression

84
Q

CTL responses bad, good and ideal

A

ideal - no escape from CTL and is lethal to the virus (invariant region, virus isn’t able to mutate or escape)

Good - the virus can escape however virus suffers a loss of fitness

Bad - virus can escape and at no fitness cost

85
Q

Which epitopes do you target for CTL inducing Vaccines for HIV?

A

Could depend on HLA type

86
Q

How do you get protection against multiple strains/viral variants?

2 Listed

A
  • 9 Major HIV subtypes, with up to 30% sequence variation in env
  • every amino acid could change everyday
87
Q

HIV Vaccines designed to induce CTL responses Considerations

A
88
Q

The initial immune response to HIV reduces the virus levels by?

A

About 100 fold but no further

89
Q

HIV infection summary

3 Listed

A
90
Q

Why does HIV infection lead to CD4+ T cell depletion?

Virus Mediated

2 Listed

A
91
Q

Why does HIV infection lead to CD4+ T cell depletion?

Immune System Mediated

2 Listed

A
92
Q

HIV doesn’t cause disease, the __________ does.

A

Immune system does

93
Q

The reason why HIv gets people sick is because

A

the adaptive immune responses against the virus

in absence of an adaptive immune response against the virus the virus causes no sickness

94
Q

Gut barrier function followed by microbial translocation

A
  • during HIV infection the gut is leaky
  • immunostimulatory molecules can leak in an exacerbate the chronic inflammation in HIV

FMS (34 decks)

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