hiv Flashcards

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

A

higher

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?

A

no

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
Q

whats the usual process from HIV diagnosis

A

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
Q

Which viral infections are opportunistic for HIV?

A

HSV, CMV, JC virus

27
Q

what are some opportunistic bacterial infections?

A

mycobacteria, tb, mai, pneumococcus,

28
Q

what are some opportunistic fungal infections?

A

pneumocytis carinii, histoplasma, cryptococcus, coccidiodomyces

29
Q

what are some opportunistic protozoal infections?

A

cryptosporidium, toxplasma, isospora

30
Q

what are some opportunistic tumours?

A

kaposi’s sarcoma, b cell lymphoma, primary cerebral lymphoma, invasive ca cervix

31
Q

why dont ccr5 drug inhibitors work forever?

A

over time, the virus stops using the ccr5 receptor and starts using the cxcr4

32
Q

what are some actions of hiv drugs?

A

ccr5 inhibitor (maraviroc), reverse transcriptase inhibitor, integrase inhibitor (raltegravir), protease inhibitors (ritonavir)

33
Q

which combinations are in haart?

A

2 nucleoside reverse transcriptase inhibitor plus..
1 non nucleoside reverse transcriptase inhibitor or..
1 protease inhibitor