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Virology > HIV > Flashcards

HIV Flashcards

1
Q

gp41, HIV

A 
transmembrane protein(hookshot)
associates with gp120 on envelope surface
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2
Q

p17, HIV

A

matrix proteins

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3
Q

p24, HIV

A

capsid proteins

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4
Q

p7, HIV

A

nucleocapsid proteins

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5
Q

transmission of HIV

A

mucosal: sex or mother»child @birth
parenteral: direct injection

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6
Q

how does HIV invade the body when it goes the mucosal route?

A
  • DCs trap HIV and pass to/infect CD4+ Tcells
  • Breach in endothelium
  • Transcytosis
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7
Q

describe HIV cell surface interactions when infecting a cell

A

gp120 binds CD4

gp120 transforms and binds CCR5 or CXCR4

gp41 is exposed and extends to target cell, initiating fusion

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8
Q

tRNA lysine role in HIV infection

A

primer for RT

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9
Q

structural genes for HIV

A

gag, pol, env

gag and pol code polyproteins that are cleaved into respective structural proteins after translation

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10
Q

trans-activator genes?

what do they do?

A

tat and rev

tat - essential for HIV transcription; binds tat-activation region on all species; activates cellular promoters

rev - essentially binds and chaperones RNA out of the nucleus that hasnt been spliced(or just single spliced) and would otherwise be degraded w/out rev

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11
Q

what is the greatest hurdle(at the molecular level) for HIV eradication?

A

integration into the genome; there is a large pool of latent virus just sitting in cells which there isnt a good drug target for

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12
Q

role of Nef gene in HIV

A

down-regulates CD4, MHCI

induces FasL expression

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13
Q

role of Vif gene in HIV

A

targets APOBEC3G which is then degraded; otherwise it would cause massive inactivating mutation in HIV genome

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14
Q

role of Vpu gene in HIV

A

targets CD4 at the ER, preventing it from being expressed

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15
Q

role of Vpr gene in HIV

A

can keep cell in G2 phase which is ideal for RNA production

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16
Q

hurdles to producing a Vaccine for HIV

A

variably glycosylated envelope

highly mutagenic virus

integrates genome; latency

neutralizing epitopes only transiently expressed

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17
Q

most common transmission of HIV in US

most common transmission of HIV ww

A

US - MSM

WW - heterosexual transmission

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18
Q

fluids that transmit HIV

A

blood
breast milk
semen
vaginal/rectal fluids/secretions

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19
Q

what would cause a false negative for HIV serologic testing

A

“window period”

time between infection and antibody/antigen production

20
Q

about how much time does it take for p24 antigen and HIV antibodies to appear after infection

A

p24 ~15 days (2 weeks)

antibodies ~25 days (3 weeks)

21
Q

when is pro-viral DNA tested for by PCR?

A

diagnosis of infants < 18 months of age

22
Q

symptoms of acute HIV infection

A

fever, lymphadenopathy, pharyngitis, rash, myalgia/arthralgia

**CD4 drops/viral load spikes @ start of HIV infection

23
Q

normal CD4 cnt

A

800-1050 cells/mm3

can range from 500-1400 in uninfected individuals

24
Q

HIV OI
pneumocystitis(PCP)

CD4 indication?
prophylaxis and when it should be given(primary/secondary)

A

CD4<200

give TMP-SMX as primary/secondary prophylaxis

25
Q

HIV OI
toxoplasmosis

CD4 indication?
prophylaxis and when it should be given(primary/secondary)

A

CD4<100 and toxo IgG+

give primary/secondary prophylaxis of TMP-SMX

26
Q

HIV OI
cryptococcus

CD4 indication?
prophylaxis and when it should be given(primary/secondary)

A

CD4<100

give only secondary prophylaxis of fluconazole

27
Q

HIV OI
m. avium complex(MAC)

CD4 indication?
prophylaxis and when it should be given(primary/secondary)

A

CD4<50

give only primary prophylaxis of azithromycin

28
Q

HIV OI
CMV

CD4 indication?
prophylaxis and when it should be given(primary/secondary)

A

CD4<50

give only secondary prophylaxis of valganciclovir

29
Q

OIs for HIV most comon at CD4 200-500

A

TB
Oro-pharyngeal candidiasis
VZV(shingles)
kaposi’s sarcoma(HHV-8)

30
Q

maraviroc(MVC) mechanism

A

binds CCR5 coreceptor; blocks HIV from entering cell

wont work on mixed or CXCR4 virus profiles

31
Q

enfuvirtide(T-20) mechanism

A

prevents change in gp41 that allows fusion of HIV to cell membrane

32
Q

NRTIs

A 
zidovudine
stavudine
didanosine
tenofovir
abacavir
lamivudine
emtricitabine

zestdla

33
Q

NRTI toxicity

A

mitochondrial toxicity causing neuropathy, myopathy, LAcidosis, hepatic steatosis, pancreatitis, lipoatrophy

34
Q

NRTI mechanism

A

stop chain elongation of RT

35
Q

NNRTI mechanism

A

binds at non-catalytic site on RT; inhibits functionality

36
Q

NNRTIs

A

nevirapine
efavirenz
etravirine
rilpivirine

37
Q

resistance problems for NNRTIs

A

single mutations can cause cross-class resistance

38
Q

NNRTI toxicities

A

rash; can progress to stevens-johnson

liver transaminase elevations/hepatitis

39
Q

efavirenze toxicity

A

CNS effects(hallucinations, insomnia) on top of class-common rash/liver enzyme elevation

40
Q

t1/2 of NNRTIs

A

VERY LONG; need to keep other meds going if stopping treatment to not cause resistance from NNRTI monotherapy due to long t1/2

41
Q

integrase inhibitors

A

raltegravir
elvitegravir
doultegravir

ralph is an elite dueler

42
Q

ritonavir mechanism; indications

A

protease inhibitor

cyp450 34a inhibitor; combined with other drugs to “boost” them

43
Q

are NNRTI’s effective against HIV-2

A

NO, NO THEY ARENT

44
Q

protease inhibitor class toxicities

A

metabolic dysregulation

  • hyperlipidemia
  • increased potentiation of glucose intolerance

GI upset - nausea, diarrhea

Fat redistribution

  • buffalo hump
  • central/visceral adiposity
45
Q

ART treatment in naive patient should be composed of which drug classes?

A

2 NRTIs +….

  • 1 NNRTI or
  • 1 PI(w/ritonavir boost)
  • 1 II
46
Q

what is the goal for the viral load after 1-4 months of therapy

A

see a log decrease in initial viral load

Virology (13 decks)

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