Immunology 2 - HIV infection Flashcards

1
Q

HIV-2 vs HIV-1

A

Harder to transmit and less virulent

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2
Q

genetic material of HIV-1

A

RNA, diploid (2 single stranded RNA)

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3
Q

How is HIV RNA incorporated in to human genome?

A

Uses reverse transcriptase to convert RNA to DNA

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4
Q

Cells which can be infected by HIV

A

CD4+ T cells, CD4+ monocytes, CD4+ DCs

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5
Q

What is the receptor for the HIV virus?

A

CD4+ molecules/antigen

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6
Q

HIV co-receptor

A

CCR5/CXCR4

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7
Q

What does effective immunity to HIV require?

A

Antibodies to prevent infection and neutralise virus, and sufficient CD8+ T cells to eliminate latently infected cells

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8
Q

Acquired immunity to HIV

A

Antibodies: anti-gp120 and anti-gp41 (neutralising)

Non-neutralising anti-p24 gag IgG

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9
Q

Where are the CD4+ T cells mainly killed in HIV?

A

In the gut mucosa

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10
Q

Effects on other cells of infected CD4+ T cells being anergised by the virus

A

MO/DC are not activated by CD4+ T cells and cannot prime CD8 + T CELLs
CD8+ T nad B cell responses diminished without CD4+ T cell help
CD4+ T cell memory is lost
Infected MO/DC are killed by CTLs or virus

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11
Q

• Replication of the HIV genome is dependent on TWO steps during which errors can occur

A
  1. Reverse transcriptase (RNA –> DNA)
  2. Transcription of DNA in to RNA virus

Both low fidelity

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12
Q

Does antibody coating of HIV virus stop its infectivity?

A

no

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13
Q

7 main steps of HIV life cycle

A
  1. Attachment and entry
  2. Reverse transcription and DNA synthesis
  3. Integration
  4. Viral transcription
  5. Viral protein synthesis
  6. Assembly and release of virus
  7. Maturation
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14
Q

“gravir” which treatment?

A

integrase inhibitor e.g. raltegravir

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15
Q

“avir” which treatment?

A

protease inhibitor e.g. ritonavir, indinavir

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16
Q

Example of attachemnt inhibitor and its target

A

Maraviroc, CCR5 (RANTES)

17
Q

Median time from HIV infection to AIDS development…

A

8-10 years

18
Q

Rapid progressors time from HIV –> AIDS

A

2-3 years (10%)

19
Q

Long-term non progressors

A

<5%, stable CD4+ counts and no symptoms after 10 years

20
Q

Exposed seronegatives

A

people who are repeatedly exposed to HIV but do not seroconvert

21
Q

Elite controllers

A

Can suppress viral replication

22
Q

Long term non progressors host genetic factor

A

Heterozygosity for 32bp deletion in CCR5

23
Q

LNPs host immune responses factors

A

Effective cTL and antibody response
Secretion of antibodies that block HIV entry co-receptors
CCR5 –> MIP1a MIP1b, RANTES
CXCR4 –> SDF-1

24
Q

Screening test for HIV

A

ELISA

25
Q

Confirmatory test for HIV

A

Western blot

26
Q

How to assess viral load

A

PCR

27
Q

How is the CD4+ T cell count monitored?

A

Flow cytometry

28
Q

Antigens on T cells

A

CD3, CD4, CD8, CD19, CD56

29
Q

2 WAYS to assess HIV ART resistance

A

Phenotypic (viral replications measured in cell cultures iwth increasing conc of ART)
Genotypic (sequence HIV genome)

30
Q

General HAART combination

A

2 NRTIs + NNRTI or PI

31
Q

When to treat

A

Treat all immediately if chronic infection confirmed, treat if symptomatic

32
Q

What is tenofovir an example of?

A

NucleoTIDE reverse transcriptase inhibitor

33
Q

What is zidovudine/AZT an example of?

A

NucleoSIDE reverse transcriptase inhibitor

34
Q

Example of NNRTI

A

Efavirenz

35
Q

Example of a fusion inhibitor

A

Enfuviritide

36
Q

Which HIV drug is a P450 inducer?

A

Efavirenz

37
Q

Which drugs inhibit P450?

A

Protease inhibitors e.g. ritonavir, indinavir

38
Q

Big limitation of HAART

A

Does not eradicate latent HIV-1

39
Q

When =is hIV ELISA/western blot positive?

A

After 10+ weeks infection