Virology Quiz 2 Hiv/aids

Front 1

where is HIV-2 endemic?

Back 1

West Africa

Front 2

does HIV have a viral oncogene? Is the virus defective?

Back 2

no; no

Front 3

what unique genes are present in HIV genome?

Back 3

regualatory genes

Front 4

what protein-protein interaction with HIV and T cells is important for adsorption?

Back 4

gp120 with CD4 and cytokine receptor

Front 5

what cells other than T helper cells is CD4 found on?

Back 5

monocytes-macrophages, microglial cells, dendritic cells

Front 6

which viral envelope protein mediates fusion of the viral envelope with the cell membrane, resulting in nucleocapsid entry?

Back 6

gp41

Front 7

once integrated into the host DNA, what are the 3 choices of the HIV provirus?

Back 7

1) latency, 2) controlled HIV growth, or 3) extensive viral growth resulting in lysis of host cell

Front 8

what impact do other STD's have on HIV transmission? Does receptive or penetrative intercourse carry a higher risk of HIV infection?

Back 8

their presence increases risk of transmission and acquisition; receptive

Front 9

what are the symptoms of primary infection with HIV? Is viremia high or low during this symptomatic phase?

Back 9

mononucleosis-like or flu-like syndrome with fever, enlarged lymph nodes, tireness, and headache; high

Front 10

what follows the symptomatic phase of an HIV infection? With what does this phase correlate?

Back 10

a period of normal health with low serum virus levels; seroconversion

Front 11

what does viral growth of CD4 T cells require?

Back 11

activation of cells by antigen for which they are specific

Front 12

how long is the clinically latent phase of HIV infection? What happens to CD4+ cells during this time?

Back 12

3-10 years; they are lost at a steady rate

Front 13

what occurs as CD4+ cell count declines?

Back 13

increase in incidence of variety of infectious diseases

Front 14

what is the CDC definitions of AIDS?

Back 14

CD4+ T cell percentage of less than 14% total lymphos and an occurrence of one of the AIDS-defining infections or cancers

Front 15

other than CD4+ cell count decline, what immune defects are seen in HIV infection?

Back 15

chronic activation of immune system and impaired function of monocytes-macros

Front 16

is the platelet count in HIV infections high or low? Are dimentia and brain diseases common in late HIV infections?

Back 16

low; yes

Front 17

what are two ways in which the number of CD4+ cells are eliminated in HIV infected patients?

Back 17

apoptosis or CTL death

Front 18

which phase of the HIV infection is responsible for spreading the infection to various organs?

Back 18

the acute early phase with high viremia

Front 19

what is an accurate and important marker in predicting the progression to AIDS in HIV-infected patients?

Back 19

HIV viral load (measured with RT-PCR)

Front 20

is more virus required for the HIV onset of AIDS in men or women?

Back 20

men (women can get AIDS in the same time with half the viral load)

Front 21

when is the latency period in an HIV infection?

Back 21

there is no real latent period

Front 22

how is ELISA performed to detect HIV in a patient? What is the specificity of this technique? The sensitivity?

Back 22

virion antigens fixed to plastic bead, bead reacted with patient's serum, Ab from serum attached to bead, unbound Ab washed, enzyme-linked Anti-HIV Ab added to detect presence of HIV Ab; 99%; 99%

Front 23

what is the range of HIV ag for which Ab can be detected with Western Blot?

Back 23

25000 or 41000 molecular weight

Front 24

what are the steps in performing a Western blot for Ab against HIV Ag? What is the specificity compared to ELISA? The sensitivity?

Back 24

resolve HIV ag by molcular weight using gel electrophoresis, xfer to nitrocellulose paper, react sheets with pt serum, wash unbound Ab, detect human Ab with suitably labeled Anti-Ig Ab; greater than ELISA; less than ELISA

Front 25

what is sensitivity? Specificity?

Back 25

probability of a positive test in a positive infection; probability of a negative test in a negative infection

Front 26

which tests must be performed to serologically confirm an HIV infection?

Back 26

2 consecutive ELISAs and 1 Western blot

Front 27

what viral infections are commonly seen in AIDS patients?

Back 27

zoster (varicella zoster virus), oral hairy leukoplakia (EB virus), herpes infection of skin, esophagus, and mucous membranes (HSV), cytomegalovirus disease of retina, esophagus, and colon (CMV), human papilloma virus, and kaposi's sarcoma (herpes virus)

Front 28

what is the acronym for the current treatment strategy for HIV?

Back 28

highly active antiretroviral therapy (HAART)

Front 29

what is immune reconstitution syndrome?

Back 29

when the immune system starts to recover from AIDS then attacks a pre-existing infection, only to exacerbate HIV infection

Front 30

despite the potent effects of HAART, where is HIV likely to remain hiding?

Back 30

lymph nodes, brain, testes, and retina of eye

Front 31

what is neuroAIDS?

Back 31

memory loss and cognitive damage in 20% of patients surviving through HAART therapy

Front 32

RT inhibitor antivirals are analogs of what?

Back 32

dideoxynucleosides

Front 33

what is the mechanisms of RT inhibitors in HIV infections?

Back 33

chain terminators

Front 34

what class of antiviral is AZT?

Back 34

chain terminator (RT inhibitor)

Front 35

is the AZT triphosphate incorporated into DNA by RT?

Back 35

yes

Front 36

how do HIV levels and CD4+ levels change after 2-4 months of AZT?

Back 36

HIV down ten-fold and CD4+ levels rise by 50

Front 37

what is the mechanism of action of non-nucleoside RT inhibitors? Is monotherapy with this adequate? Why or why not?

Back 37

bind to an allosteric site on HIV RT to inhibit RT activity; no, because of resistant mutations

Front 38

does HIV mutate more quickly to nucleoside RT inhibitors or non-nucleoside RT inhibitors?

Back 38

non-nucleotide RT inhibitors

Front 39

what is the mechanism of action of protease inhibitors?

Back 39

competitive inhibitors of HIV protease -- prevent cleavage of gag-pol polypeptide into individual viral infections so virion particles made are not infectious

Front 40

by how much do protease inhibitors reduce plasma HIV load? How effective are they in conjuction with other HIV inhibitors?

Back 40

by 100-fold; very effective -- synergistic

Front 41

what is triple therapy for HIV?

Back 41

protease inhibitor plus two RT inhibitors

Front 42

how to entry inhibitor antivirals work? What is the name of the one known drug of this family?

Back 42

they bind to gp41 on the surface of HIV virion the prevent adsorption of virion; Fuzeon

Front 43

how is Fuzeon administered? By how much does it reduce viral load? Can it be used alone?

Back 43

2 daily injections; 10 fold; no, due to mutations

Front 44

what specific cohort of AID patients can use Fuzeon?

Back 44

those who have tried other HIV antivirals in the part and cannot keep their viral load down

Front 45

what is the mechanism of action of integrase inhibitors? What is the the name of the only licensed drug in this family?

Back 45

interferes with integrase activity thereby blocking integration of the proviral DNA into the host cell chromosomes; Isentress

Front 46

how is Isentress administered? Is it used alone?

Back 46

orally; no, always in conjunction with something else