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B&L Unit 3 > Immunology of AIDS (complete) > Flashcards

Immunology of AIDS (complete) Flashcards

1
Q

What is the difference between “HIV-seropositive” and “AIDS”?

A

S+: if a pt has Ab to HIV (first way to detect infection)

AIDS: symptoms of opportunistic infections or Kaposi’s sarcoma, their Th (CD4+) cells are <200/microL of blood

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2
Q

What is the virus that causes AIDS?

A

HIV-1

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3
Q

What is HIV-1’s classification?

A
  • A nontransforming retrovirus

- RNA virus that carries no oncogene

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4
Q

What is the origin of the AIDS virus?

A

Simian Immunodeficiency Virus (SIV)

Thought that HIV evolved from SIV in DRC

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5
Q

What is the approximate number of HIV cases in the US?

A

1.1 million

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6
Q

What is the approximate number of HIV cases in the world?

A

35 million

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7
Q

What is the rate of change in incidence?

A

16%

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8
Q

Discuss the pathogenesis of AIDS. Include target cells types, mode of entry of virus, mode of exit, and latency vs productive infection

A
  • After first exposure => high blood virus levels, peak at 6 weeks
  • loss of CD4 cells in gut => increased gut permeability => systemic spread
  • Ab peaks @ 9 wks, falls to almost 0 but at steady state
  • DCs w/ HIV = Trojan horse, go to lymph nodes
  • HIV gp120 bind to CD4 on Th cells => cause host cell CCR-5 binding as coreceptor
  • CCR-5 binds => conf change of gp41 => exposes hydrophobic region that melts T cell membrane
  • Th cell and virus fuse => vRNA and reverse transcriptase injected into cell => vDNA production
  • W/ viral integrase, vDNA inserts at random break of host DNA => latent virus
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9
Q

What is the role of Tfh cells in persistence of HIV latency?

A
  • They are able to suppress viral replication

- Can’t eliminate the virus DNA from their nuclei

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10
Q

What is the role of Tfh cells in persistence of active HIV infection?

A
  • If the Tfh cell w/ viral DNA is activated by its correct Ag => a clone of virus-producing cells
  • Accompanied w/ or leads to dysregulation o f B cells
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11
Q

What are the types of infections seen in patients w/ AIDS?

A

1) Viral infection
2) Fungal infection
3) Protozoan infection
4) OIs of intracellular bacteria

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12
Q

What is the immunological basis for the spectrum of infection types seen in patients w/ AIDS?

A
  • Virus targets T-cell mediated immunity

- More infections occur that require this

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13
Q

What are the possible reasons for which the total number of CD4 cells in patients w/ AIDS decline?

A
  • When infected w/ HIV, you have to replace your CD4 cells OFTEN
  • Simple exhaustion => decreased ability to produce more
  • This is when CD4s decline… => opportunistic infections w/ a weak immune system
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14
Q

What are the reasons for apparent ineffectiveness of Ab in HIV infection?

A
  • When virus is replicating => gp120/gp41 made early => inserted into plasma membrane of host
  • Helps w/ fusion of infected cell to nearby uninfected CD4 cells
  • Can spread w/o an extracellular phase
  • Abs can’t attack w/o extracellular presence
  • Abs bind to virus but can’t block attachment to/infection of Th cells
  • Neutralizing epitopes on virus are shielded by carb — if pt makes neutralizing Ab, virus mutates, escapes
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15
Q

Define “long term survivors” in HIV infection. Discuss

A
  • Those who survived longer than other in the time before the first HIV drug, pre-1987
  • Homozygous for 32-base pair deletion for CCR5 (chemokine, HIV coreceptor)
  • 10% frequency in caucasians
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16
Q

Define “elite controllers” in HIV infection. Discuss

A
  • Infected w/ HIV but didn’t progress to AIDS
  • 2/3 have HLA-B57 allele
  • They just make effective CTL to HIV peptides presented at HLA-B57
  • More HIV-specific CTL#s = better prognosis
17
Q

Describe the laboratory diagnosis of AIDS

A
  • Test for Ab to HIV
  • Measured by ELISA (can have false+) => confirmed w/ Western blot analysis — must bind to gp120/41 to be true positive

Also:
- Small amounts of RNA can be detected w/ PCR

18
Q

What are the prospects of AIDS vaccine development?

A

Broad neutralizing Ab!!

  • can block infection by almost all HIV strains/mutant forms
  • Trying to find a vaccine that can produce that
  • People (LTS) develop this Ab after having the disease for 20 years
19
Q

What are the problems of AIDS vaccine development?

A
  • Kind of like the flu vaccine
  • Epitopes/virus is always changing => how do you make a vaccine with that?

As Cohen says: an HIV vaccine would neutralize today’s virus but not tomorrow’s

20
Q

What are the three things that happen after HIV infects Tn cells?

A

HIV-infected T cells:

1) Die rapidly
2) Become persistent virus-producers
3) Enter latency

21
Q

Why do HIV-infected T cells die rapidly?

A
  • Viruses try to bud

- But it tears so many holes in membrane => cells dies

22
Q

What is the standard antiretroviral therapy for patients w/ HIV?

A
  • 2 NRTIs

- 1 drug from a different class (usually NNRTI)

23
Q

What are two drugs that target reverse transcriptase?

A

1) Nucleosides (NRTI)

2) Non-nucleosides (NNRTI)

24
Q

What are NRTIs?

A
  • Competitive inhibitors of reverse transcriptase

- Chain terminators!

25
Q

What are NNRTIs?

A
  • Bind a hydrophobic pocket on reverse transcriptase => changes conformation => changes activity of catalytic site
  • Escape common to these types of drugs
26
Q

What is the target for protease inhibitors?

A
  • The gag, pol, and env proteins

- These are made by cleaving a larger polyprotein using a viral protease

27
Q

What is Enfuviritide?

A
  • a fusion inhibitor

- binds to part og gp41 => can’t change conformations => no cell entry/fusion

28
Q

What is maraviroc?

A
  • A CCR5 antagonist
  • Blocks viral entry into CD4 cells
  • Binds to transmembrane part of CCR5 => changes conformation of external receptor
  • Can’t bind to gp120
29
Q

What is Raltegravir?

A
  • Integrase inhibitor

- Used in pts w/ reverse transcriptase inhibitor-resistant strains of HIV

B&L Unit 3 (12 decks)

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