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46 Cards in this Set

  • Front
  • Back
where is HIV-2 endemic?
West Africa
does HIV have a viral oncogene? Is the virus defective?
no; no
what unique genes are present in HIV genome?
regualatory genes
what protein-protein interaction with HIV and T cells is important for adsorption?
gp120 with CD4 and cytokine receptor
what cells other than T helper cells is CD4 found on?
monocytes-macrophages, microglial cells, dendritic cells
which viral envelope protein mediates fusion of the viral envelope with the cell membrane, resulting in nucleocapsid entry?
once integrated into the host DNA, what are the 3 choices of the HIV provirus?
1) latency, 2) controlled HIV growth, or 3) extensive viral growth resulting in lysis of host cell
what impact do other STD's have on HIV transmission? Does receptive or penetrative intercourse carry a higher risk of HIV infection?
their presence increases risk of transmission and acquisition; receptive
what are the symptoms of primary infection with HIV? Is viremia high or low during this symptomatic phase?
mononucleosis-like or flu-like syndrome with fever, enlarged lymph nodes, tireness, and headache; high
what follows the symptomatic phase of an HIV infection? With what does this phase correlate?
a period of normal health with low serum virus levels; seroconversion
what does viral growth of CD4 T cells require?
activation of cells by antigen for which they are specific
how long is the clinically latent phase of HIV infection? What happens to CD4+ cells during this time?
3-10 years; they are lost at a steady rate
what occurs as CD4+ cell count declines?
increase in incidence of variety of infectious diseases
what is the CDC definitions of AIDS?
CD4+ T cell percentage of less than 14% total lymphos and an occurrence of one of the AIDS-defining infections or cancers
other than CD4+ cell count decline, what immune defects are seen in HIV infection?
chronic activation of immune system and impaired function of monocytes-macros
is the platelet count in HIV infections high or low? Are dimentia and brain diseases common in late HIV infections?
low; yes
what are two ways in which the number of CD4+ cells are eliminated in HIV infected patients?
apoptosis or CTL death
which phase of the HIV infection is responsible for spreading the infection to various organs?
the acute early phase with high viremia
what is an accurate and important marker in predicting the progression to AIDS in HIV-infected patients?
HIV viral load (measured with RT-PCR)
is more virus required for the HIV onset of AIDS in men or women?
men (women can get AIDS in the same time with half the viral load)
when is the latency period in an HIV infection?
there is no real latent period
how is ELISA performed to detect HIV in a patient? What is the specificity of this technique? The sensitivity?
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%
what is the range of HIV ag for which Ab can be detected with Western Blot?
25000 or 41000 molecular weight
what are the steps in performing a Western blot for Ab against HIV Ag? What is the specificity compared to ELISA? The sensitivity?
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
what is sensitivity? Specificity?
probability of a positive test in a positive infection; probability of a negative test in a negative infection
which tests must be performed to serologically confirm an HIV infection?
2 consecutive ELISAs and 1 Western blot
what viral infections are commonly seen in AIDS patients?
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)
what is the acronym for the current treatment strategy for HIV?
highly active antiretroviral therapy (HAART)
what is immune reconstitution syndrome?
when the immune system starts to recover from AIDS then attacks a pre-existing infection, only to exacerbate HIV infection
despite the potent effects of HAART, where is HIV likely to remain hiding?
lymph nodes, brain, testes, and retina of eye
what is neuroAIDS?
memory loss and cognitive damage in 20% of patients surviving through HAART therapy
RT inhibitor antivirals are analogs of what?
what is the mechanisms of RT inhibitors in HIV infections?
chain terminators
what class of antiviral is AZT?
chain terminator (RT inhibitor)
is the AZT triphosphate incorporated into DNA by RT?
how do HIV levels and CD4+ levels change after 2-4 months of AZT?
HIV down ten-fold and CD4+ levels rise by 50
what is the mechanism of action of non-nucleoside RT inhibitors? Is monotherapy with this adequate? Why or why not?
bind to an allosteric site on HIV RT to inhibit RT activity; no, because of resistant mutations
does HIV mutate more quickly to nucleoside RT inhibitors or non-nucleoside RT inhibitors?
non-nucleotide RT inhibitors
what is the mechanism of action of protease inhibitors?
competitive inhibitors of HIV protease -- prevent cleavage of gag-pol polypeptide into individual viral infections so virion particles made are not infectious
by how much do protease inhibitors reduce plasma HIV load? How effective are they in conjuction with other HIV inhibitors?
by 100-fold; very effective -- synergistic
what is triple therapy for HIV?
protease inhibitor plus two RT inhibitors
how to entry inhibitor antivirals work? What is the name of the one known drug of this family?
they bind to gp41 on the surface of HIV virion the prevent adsorption of virion; Fuzeon
how is Fuzeon administered? By how much does it reduce viral load? Can it be used alone?
2 daily injections; 10 fold; no, due to mutations
what specific cohort of AID patients can use Fuzeon?
those who have tried other HIV antivirals in the part and cannot keep their viral load down
what is the mechanism of action of integrase inhibitors? What is the the name of the only licensed drug in this family?
interferes with integrase activity thereby blocking integration of the proviral DNA into the host cell chromosomes; Isentress
how is Isentress administered? Is it used alone?
orally; no, always in conjunction with something else