3 HIV Flashcards

(45 cards)

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
Transcutaneous transmission
- IVDA - Needle-stick injury - Contaminated blood and blood products
26
sexual transmission
homosexual | heterosexul
27
vertical transmission
(mother-infant) (if child has HIV, will get AIDs very quickly)
28
Clinical Features of HIV Infection (progression)
1. Acute Primary Infection Syndrome 2. Asymptomatic Infection 3. Symptomatic HIV Infection and AIDS
29
Acute Primary Infection Syndrome
Flu-like illness, with high levels of virus replication until the infection is brought under immune control
30
Asymptomatic Infection
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
Symptomatic HIV Infection and AIDS
The immune system ceases to function and disease progresses, resulting in death
32
Acute Phase HIV-1 antibody type
antibody negative
33
Acute Phase HIV-1 RNA antigen type
antigen positive
34
Acute Phase virus co-receptor
Virus usually uses CCR5 co-receptor
35
effect of HIV on cell count
HIV causes CD4 cell count to become low = 200/ul blood or less = clinical AIDS
36
effect of seroconversion - acute phase
- HIV-1 antibody positive | - Decreased viraemia (RNA , Antigen )
37
Asymptomatic Phase
Active replication within lymph tissue
38
Symptomatic Phase | General dissemination of virus
CNS, other non-lymph tissue
39
Symptomatic Phase | Opportunistic infections/tumours
TB, Kaposis sarcoma
40
what has an Inexorable battle between
the virus and the host
41
viral phenotypes
Transmission and Asymptomatic – virus that exists use CCR5
42
resistance to HIV infection
Homozygote 32/ 32 - CCR5
43
HIV-1-Exposed Seronegative Sex-Workers protection
Protection associated with rare HLA types | - Targeting highly conserved T-cell epitopes
44
how do viruses escape the immune system
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
what causes a large cost to virus to escape immune system
mutating epitopes recognised by the ‘protective’ HLA types results in large fitness cost to virus