hiv Flashcards

(33 cards)

1
Q

what three polyproteins are synthesised by retroviruses?

A

gag (group specific antigen), pol (polymerase) and env (envelope glycoprotein)

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2
Q

what is reverse transcription?

A

copying rna template into dna one

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3
Q

what enzyme is used to insert the viral cDNA into the host cell genome?

A

integrase

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4
Q

describe budding

A

virus buds from cell membrane taking parts of the host membrane with it

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5
Q

how long is a retrovirus life cycle under permissive conditions?

A

24 hours

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6
Q

HIV is trophic for ___ expressing cells

A

CD4

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7
Q

name 2 cd4 expressing cells

A

t helper cells, macrophages

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8
Q

name the 2 chemokine receptors that HIV must also bind to to enter cell

A

CCR5 and CXCR4

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9
Q

name the 3 enzymatic activities of reverse transcriptase

A

RNA dependent DNA polymerase
RNAshH (cleaves RNA from RNA/DNA hybrid - degrades viral RNA once transcription has occured)
DNA dependent DNA polymerase - makes double stranded DNA

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10
Q

reverse transcriptase can’t proofread, true or false?

A

true - allows mutations

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11
Q

list 4 modes of HIV-1 sequence diversification

A

copying errors (drift)
recombination (shift)
drift plus shift
post synthesis editing

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12
Q

what is the major target tissue in acute HIV-1 infection?

A

gut associated lymphoid tissue (GALT)

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13
Q

what is the effect of hiv on GALT?

A

in acute infection: virtually all t cells destroyed

immune integrity never recovers

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14
Q

What is the progression of a ‘normal progressor’

A

AIDS in 8 - 10 years

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15
Q

what is the progression of a ‘rapid progressor’

A

AIDS in 1-3 years

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16
Q

what is a long-term non progressor?

A

maintains low levels of viral RNA in blood, but can be AIDS free indefinitely

17
Q

what is an elite controller?

A

<50 copies of viral rna/ml in blood, remain aids free indefinitely, genetic association with MHC haplotype

18
Q

lower viral set point = ____chance of survival

19
Q

which cells control the acute infection?

A

cd8 t cells, kill infected cells

20
Q

do antibodies have any effect on viral load?

21
Q

name two antibodies produced against to HIV

A

non-neutralising anti-env abs

neutralising anti-env abs

22
Q

which antibody is produced in some individuals after some time and can neutralise viruses

A

neutralising anto-env abs

23
Q

how do the viruses directly kill the cells?

A

syncytia, increased cell permeability, apoptosis

24
Q

how else are t cells depleted?

A

immune hyperactivation - t cells get activated which makes them more susceptible to infection
homeostatic strain
diminished regeneration of t cell populations - thymic dysfunction, loss of lymphoid tissue, bone marrow dysfunction

25
whats the usual process from HIV diagnosis
ELISA test for anti-p24 antibodies, repeated with different ELISA or western blot if positive. only works after 3 months (seroconversion) negative p24 should be confirmed with RT PCR to detect HIV genomic RNA in blood - can detect HIV before seroconversion
26
Which viral infections are opportunistic for HIV?
HSV, CMV, JC virus
27
what are some opportunistic bacterial infections?
mycobacteria, tb, mai, pneumococcus,
28
what are some opportunistic fungal infections?
pneumocytis carinii, histoplasma, cryptococcus, coccidiodomyces
29
what are some opportunistic protozoal infections?
cryptosporidium, toxplasma, isospora
30
what are some opportunistic tumours?
kaposi's sarcoma, b cell lymphoma, primary cerebral lymphoma, invasive ca cervix
31
why dont ccr5 drug inhibitors work forever?
over time, the virus stops using the ccr5 receptor and starts using the cxcr4
32
what are some actions of hiv drugs?
ccr5 inhibitor (maraviroc), reverse transcriptase inhibitor, integrase inhibitor (raltegravir), protease inhibitors (ritonavir)
33
which combinations are in haart?
2 nucleoside reverse transcriptase inhibitor plus.. 1 non nucleoside reverse transcriptase inhibitor or.. 1 protease inhibitor