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Virology > 3 HIV > Flashcards

3 HIV Flashcards

1
Q

what family does HIV belong to

A

Retroviridae family

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2
Q

how is cDNA replication intermediate made

A

RNA viruses which use RNA-dependent DNA polymerase (reverse transcriptase) to make a cDNA replication intermediate

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3
Q

what are the 4 HIV-1 groups

A

M
N
O
P

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4
Q

what is group M HIV-1

A

majority

cause of the global HIV-1 epidemic; many strains

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5
Q

what is group N HIV-1

A

non-O/non-M

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6
Q

what is group O HIV-1

A

outlier

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7
Q

what does HIV-2 cause

A

Non-pandemic

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8
Q

where is HIV-2 found

A

largely restricted to West Africa

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9
Q

why is HIV-2 restricted to West Africa

A

HIV-2 may less efficiently transmitted than HIV-1

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10
Q

which is most pathogenic

A

HIV-1

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11
Q

effect of HIV-2 infection - symptoms

A

HIV-2 infected persons seem to remain symptom-free longer than persons infected with HIV-1

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12
Q

what may protect against HIV-1

A

prior HIV-2 infection

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13
Q

what does HIV-1 give rise to

A

HIV-1 gives rise to Group M, which leads to HIV pandemic

HIV-1 gives rise to Group P, O and N

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14
Q

gene structure of HIV

A

Two copies of +sense RNA
Diploid genome – two copies of RNA, genomes can recombine = generate diversity
Surface of lipid membrane have spikes that allow it to attach to membrane
Long terminal repeats on ends

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15
Q

what are genes are present in all HIV

A

All have Gag, Pol and Env gene

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16
Q

what additional genes for HIV are there

A

HIV has additional genes that are involved in replication and that allow it to escape from normal protective mechanisms

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17
Q

HIV replication - replication and antiretrovirals

A

Virus bind to CD4
Virus enters where reverse transcription occurs
DNA made, integrated into host chromosome
- can stay dormant (rare)
or
- immediately start making new viruses – translation
Assembly of virus, viral budding – released from cell

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18
Q

how is variability formed

A

point mutations as reverse transcriptase has no proof reading capability

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19
Q

HIV against immune system

A

immune escape by changing/masking antigenic determinants

- CTLs and Abs

20
Q

what causes resistance to anti-retroviral drugs

A
  • Point mutations in enzymatic proteins
21
Q

effect of point mutations in enzymatic proteins

A

> RT - resistance to nucleoside and non-nucleoside analogues

> Protease - resistance to protease inhibitors

22
Q

what causes altered cytopathogenicity

A

Env mutations alter co-receptor usage

23
Q

effect of Env mutations alter co-receptor usage

A

> Different cell tropism, eg. Macrophages, T-cells,

> Different tissue tropisms, e.g. brain

24
Q

Transmission

A

Transcutaneous
Sexual
Vertical

25
Q

Transcutaneous transmission

A
  • IVDA
  • Needle-stick injury
  • Contaminated blood and blood products
26
Q

sexual transmission

A

homosexual

heterosexul

27
Q

vertical transmission

A

(mother-infant) (if child has HIV, will get AIDs very quickly)

28
Q

Clinical Features of HIV Infection (progression)

A
  1. Acute Primary Infection Syndrome
  2. Asymptomatic Infection
  3. Symptomatic HIV Infection and AIDS
29
Q

Acute Primary Infection Syndrome

A

Flu-like illness, with high levels of virus replication until the infection is brought under immune control

30
Q

Asymptomatic Infection

A

No outward sign of disease, although there is a slow decline in the CD4 count, and very active viral replication. This stage can persist for 10+ years

31
Q

Symptomatic HIV Infection and AIDS

A

The immune system ceases to function and disease progresses, resulting in death

32
Q

Acute Phase HIV-1 antibody type

A

antibody negative

33
Q

Acute Phase HIV-1 RNA antigen type

A

antigen positive

34
Q

Acute Phase virus co-receptor

A

Virus usually uses CCR5 co-receptor

35
Q

effect of HIV on cell count

A

HIV causes CD4 cell count to become low = 200/ul blood or less = clinical AIDS

36
Q

effect of seroconversion - acute phase

A
  • HIV-1 antibody positive

- Decreased viraemia (RNA , Antigen )

37
Q

Asymptomatic Phase

A

Active replication within lymph tissue

38
Q

Symptomatic Phase

General dissemination of virus

A

CNS, other non-lymph tissue

39
Q

Symptomatic Phase

Opportunistic infections/tumours

A

TB, Kaposis sarcoma

40
Q

what has an Inexorable battle between

A

the virus and the host

41
Q

viral phenotypes

A

Transmission and Asymptomatic – virus that exists use CCR5

42
Q

resistance to HIV infection

A

Homozygote 32/ 32 - CCR5

43
Q

HIV-1-Exposed Seronegative Sex-Workers protection

A

Protection associated with rare HLA types

- Targeting highly conserved T-cell epitopes

44
Q

how do viruses escape the immune system

A

Point mutations in key epitopes bound to HLA molecules (which are recognised by cytotoxic T-cells)
Some mutations neutral, but some induce fitness cost

45
Q

what causes a large cost to virus to escape immune system

A

mutating epitopes recognised by the ‘protective’ HLA types results in large fitness cost to virus

Virology (15 decks)

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