HIV Flashcards

1
Q

what family?

A

retroviradae

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2
Q

type of nucleiec acid?

A

ss RNA

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3
Q

where is replication?

A

nucleus

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4
Q

where is assembly?

A

cytoplasm

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5
Q

what receptor does it bind to on entry?

A

CD4

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6
Q

is latency possible? if so where?

A

yes - memory T cells (central and transitional)

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7
Q

2 proteins he didnt shut up about? what are they involved in

A

TAT and REV. TAT involved in transcription. REV - Regulates Expression of Virion proteins

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8
Q

what does HIV cause in the gut during the ‘fast slow phase’ (2)?

A

loss of peyers patches. breakdown of tight junctions

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9
Q

3 stages of HIV infection

A

primary, asymptomatic, symtpmatic (and aids)

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10
Q

what is acute HIV characterized by (cellularly)?

A

a rapid massive loss of body’s CD4 T cells

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11
Q

what is a HIV viral load?

A

amount of RNA in plasma

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12
Q

name 3 ways HIV avoids immune response

A

high mutation rate, latency, altered antigen presentation

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13
Q

4 targets for anti HIV drugs

A

fusion/entry inhibitors, reverse transcriptase inhibitors, integrase inhibitors, protease inhibitors

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14
Q

dif b/w NRTI and NNRTI

A

(Non) Nucleoside Reverse Transcriptase Inhibitors. The non dont bind to the nucleotide binding site of reverse Transcriptase and arent DNA analogues. NRTIs are DNA analgoues

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15
Q

rationale for combination treatment?

A

reduce drug resistance. drugs are thus more potent

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16
Q

why does HAART fail to cure HIV?

A

a small proportion of virus remain latent. Resting memory T cells and in resorvoirs (Brain, gut , testis)

17
Q

what does HAART stand for?

A

highly active antiretroviral therapy

18
Q

chronic immune activation may contribute to elevated risk of non-AIDS co-morbidities. name 5

A

cardiovascular, cancer, liver failure, kidney failure, bone/osteoporosis