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IMMUNO - Abbie > Immunology 4 - HIV infection > Flashcards

Immunology 4 - HIV infection Flashcards

1
Q

Using which enzyme does HIV replicate inside cells?

A

Reverse Transcriptase

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2
Q

How many genes are inside the HIV genome?

A

9

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3
Q

What is the role of reverse transcriptase in HIV?

A

Converts RNA into DNA which can be incorporated into host cells’ genes

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4
Q

What are the two key glycoproteins encoded by the HIV virus?

A

gp120
gp41

**both of these are envelope proteins

They are used to enter cells

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5
Q

Which cell of the immune system are affected by HIV?

A
  • CD4+ T cells
  • Other cells of monocytic lineage that express CD4
    • monocytes
    • macrophages
  • Also dendritic cells - especially follicular dendritic cells
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6
Q

Recall the receptor and co-receptors for HIV on CD4+ T cells

A

CD4 receptors
CCR5 CXCR4 coreceptors

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7
Q

In people who have natural immunity to HIV, what antibodies may be present in serum?

A

Anti-gp120 and anti-gp41 (Nt) antibodies

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8
Q

How does HIV infection affect CD8+ T cells?

A

Interferes with activation, as CD4+ T cell and antigen-presenting cell help are not present due to the virus

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9
Q

How does HIV infection affect monocytes and dendritic cells?

A

Not activated by CD4+ T cells and so cannot prime naive CD8+ T cells

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10
Q

How does HIV affect immunological memory?

A

CD4+ T cell memory is lost

CD8 memory cell not activated by antigen-presenting cell

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11
Q

Why does HIV have high mutation rate?

A
  1. reverse transcriptase conversion of RNA –> DNA - enzyme lacks proofreading mechanisms
  2. High error rate in transcription of integrated viral DNA –> RNA
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12
Q

Why is HIV mutation within the host problematic?

A

Escape from neutralising antibodies.

Escape from HIV-1-specific T cells.

Resistance and escape from antiretroviral drugs.

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13
Q

Recall the 7 steps of the HIV life cycle

A
  1. Attachment/Entry
  2. Reverse Transcription and DNA Synthesis
  3. Integration
  4. Viral Transcription
  5. Viral Protein Synthesis
  6. Assembly of Virus and Release of Virus
  7. Maturation
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14
Q

Which drugs are capable of inhibiting the action of reverse transcriptase in HIV infection?

A
  1. Nucleoside analogues
  2. Non-nucleotide reverse transcriptases
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15
Q

Which class of HIV drugs can prevent integration of viral DNA?

A

Integrase inhibitors

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16
Q

Which HIV drugs can prevent modification of translated viral proteins?

A

Protease inhibitors

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17
Q

What is the median time of infection with HIV to AIDS development?

A

8-10 years

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18
Q

What does it mean if someone is an HIV exposed seronegative individual?

A

Partner of individual with HIV who remains uninfected

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19
Q

What are the 3 major markers used to monitor HIV?

A

CD8 - initially they rise in response to infection then fall as CD4 cell count falls
CD4 - eventually falls
Plasma viral load

20
Q

What is long-term nonprogression of HIV?

A

Individual who is asymptomatic 10 years after infection

21
Q

How can HIV be detected?

A

1) screening

anti-HIV antibodies (ELISA) - need to do 3 assays to avoid false positives

2) confirmatory test of infection

Western Blot = Confirmatory test

3) most sensitive test

Viral PCR (detects HIV RNA)

4) monitoring course of HIV
- flow cytometry- detects CD4 cell count

22
Q

How are CD4+ T cell levels measured in HIV infection?

A

Flow cytometry

23
Q

What are the two methods of testing for ARV resistance?

A
  • *Phenotypic** - viral replication is measured in cell cultures exposed to HAART and compared to wild type
  • *Genotypic** (involves directly sequencing the amplified genome)
24
Q

Which drugs make up a HAART regimen?

A

Three or more drugs from 2 different classes + one or more binding agents

Two possibilities:

1) 2 NRTIs + 1 NNRTI
2) 2 NRTIs + 1 protease inhibitor

25
Q

When should HAART treatment be initiated?

A

Immediately

26
Q

Give 2 examples of NRTI HIV drugs

A

Zidovudine
Lamivudine

27
Q

Recall 2 examples of protease inhibitor HIV drugs

A

Tenofovir
Truvada

28
Q

What class of drug is raltegravir?

A

Integrase inhibitor

29
Q

Which drugs make up the HAART regimen initially?

A

2 NRTIs + PI

30
Q

What CD4 count defines AIDS?

A

<200 cells/ nanolitre

31
Q

Which drugs make up the atripla pill?

A

Emtricitabine + tenofavir + efavirenz

32
Q

Which ARV is best to use in pregnancy?

A

Zidovudine

33
Q

How can CD8+ T cells provide HIV entry into cells?

A

Producing chemokines MIP-1A, MIP-1b and RANTES

34
Q

Which infectious disease causes the most deaths?

A

HIV

35
Q

What type of virus is HIV?

A

Retrovirus

It has an RNA genome

That is converted to DNA using reverse transcriptase enzyme once inside the human cell

36
Q

How is the HIV genome organised?

A
  • contains 2 RNA molecules
  • each of the 2 RNA moelcules contains HIV genome and reverse transcirptase enzyme
  • each of the RNA moelcules is encapuslated by capsid gag p24
  • p17 matrix closely attached to the envelope in virus membrane
  • virus membrane is derived from the host cell and contains protease enzyme
37
Q

How does HIV enter T cells? What happens to the T cells when infected by HIV?

A
  • gp120 on HIV binds to CXCR4 on T cells
  • This then exposes GP41 on HIV membrane
  • binding of gp41 to T cell stabilises the binding

Once HIV enters T cells, it injects its RNA which integrates into host DNA–> kills off the T cell

38
Q

How does HIV infect macrophages and what happens to macrophages afted they’re infected?

A

HIV binds to macrophages via CCR5 receptor

Macrophages don’t die, but contain a reservoir of HIV

macrophages can then infect the CNS as they are able to cross the blood brain barrier

39
Q

What is the innae immune response to HIV?

A
  • non specific activation of macrophages
  • activation of NK cells
  • non specific activation of complement
  • release of cytokines and chemokines
  • stimulation of plasmacytoid dendritic cells via TLR
40
Q

Is our antibody response to HIV effective and why?

A
  • takes a while to produce these neurtaolising antibodies (3-6 months)
  • by then it’s too late to neutralise the virus
  • also just because the antibodies coat the virus doesn’t affect the virus as it can still infect cells via Fc receptor
41
Q

How long from HIV–> AIDS?

A

8-10 years (usually)

42
Q

2 examples of integrase inhibitors

A

Raltegravir

Elvitagravir

43
Q

2 examples of entry inhibitors

A

Maraviroc

44
Q

Example of fusion inhibitor

A

Enfuvirtide

45
Q

Mechanisms of action of HAART

Why is it problematic?

A
  • reduces viral replication
  • causes 2 rises in CD4 count because a) redistributes memory T cells from lymphoid tissues to blood and b) preserves thymus so it’s able to pump out naive T cells

–> improvement in immune defenses

Problematic because:

1) does not elminate the virus
2) fails to restore HIV specific T cell responses

IMMUNO - Abbie (11 decks)

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