HIV/AIDS Flashcards

1
Q

What are the methods of HIV prevention?

A
  1. Antiretroviral treatment (ART; prevention or pre/post-exposure prophylaxis)
  2. Condom use
  3. Male circumcision (decreases transmission to men)
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2
Q

What is the U=U campaign?

A

undetectabl=untransmittable (treatment is prevention; it can reduce transmission by up to 96%)

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3
Q

What is PrEP?

A

Pre-exposure prophylaxis

Daily oral antiretroviral combo pill

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4
Q

What tests detect HIV infection? (earliest possible to latest)

A
  1. HIV RNA NAAT (nucleic acid amplification test)
    **detects as early as 10 days
  2. 4th/5th gen Ab/Ag test (detect both the p24 antigen and HIV antibody) **detects as early as 14 days
  3. ELISA
  4. Western blot
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5
Q

Describe HIV transmission

A
  • Occurs at a mucosal surface (vaginal/rectal)
  • Virus crosses mucosal surface and infects CD4+ T cells, DCs, and macrophages
  • Small foci of infection are established locally and then expand/disseminate through lymph and blood
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6
Q

What is the DC role in responding to HIV infection?

A

Initial surge of IL15/IFNs

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7
Q

What is the NK cell role in responding to HIV infection?

A
  • NKs activated by IFN-1, IL-15, IL-18, and receptor/ligand interactions
  • Lyse malignant or infected cells (via perforin/granzyme, fas ligand mediated apoptosis, ADCC)
  • Produce antiviral factors (IFNγ, TNFα, β-chemokines)
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8
Q

What is the B cell role in responding to HIV infection?

A

Initial Ab response to Env protein, but is non-neutralizing

Neutralizing Ab response develops too slowly (~12 weeks) to be effective

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9
Q

What is the T cell role in responding to HIV infection?

A
  • First HIV specific CD8+ T cell responses are seen as viremia peaks, initially specific for Env and Nef
  • Virus sequence changes with rapid selection to escape
  • Eventually T cells become more targeted to conserve epitopes

**“Immune system is always one step behind HIV mutations”

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10
Q

What genetics can help individuals control HIV?

A
  • Certain MHC class I alleles are associated with control of viremia
  • Certain NK receptors have been associated with delayed progression to AIDS
  • “Elite controllers” may have more functional CD8+ T cells (i.e. more perforin, granzyme, and cytokine production)
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11
Q

Do we need an HIV cure?

A

Yes,

even when viral loads are suppressed ART doesn’t fully restore normal health and immune dysfunction,

and cost/access to meds is still a barrier for many HIV infected individuals worldwide

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12
Q

What causes the persistent inflammation and immune dysfunction even in patients suppressed by ART?

A
  • ongoing HIV replication
  • infection with co-pathogens such as CMV
  • dysfunctional immunoregulatory factors
  • microbial translocation
  • lymphoid fibrosis
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13
Q

What leads to microbial translocation?

A

Breakdown in tight junctions, loss of immune cells (Th17), and alteration of gut flora

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14
Q

What is microbial translocation?

A

The passage of viable bacteria from the GI tract to extraintestinal sites, such as the liver, spleen, kidney, and bloodstream.

**Results in increased immune activation, inflammation, and collagen deposition in lymphatic tissue

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15
Q

What cells harbor the latent HIV reservoir?

A

Long-lived memory CD4+ T cells (HIV integrates into DNA)

**established very early in the HIV infection; early treatment can limit the size of the reservoir

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16
Q

How can early treatment help HIV patients?

A
  • limit size of the latent reservoir
  • limit the development of viral escape mutants
  • increase the number of plasma and memory B cells and improve B cell function
  • preserve mucosal immune function (by maintaining Th17 cells)
17
Q

How do mutations arise in HIV?

A

HIV-1 reverse transcriptase makes spontaneous errors

**important to get replication to zero in treatment to prevent mutation

(1 in 10,000 and the genome is 10,000 bp long -> 1 error each time it is replicated)

18
Q

Describe the 2 types of resistance testing

A
  1. HIV genotype (assay assesses the genetic composition of HIV variants to determine resistance -> more common)
  2. HIV phenotype (assses the ability of drugs to inhibit replication in cultured cells -> less common, only for patients with many complicated mutations)
19
Q

What is IRIS?

A

Immune reconstitution inflammatory syndrome

**Paradoxical worsening of preexisting infection following the initiation of ART (may be an already diagnosed infection or an unmasking of previously subclinical infection)

20
Q

What are the diagnostic criteria for IRIS? What is the treatment?

A
  • low pretreatment CD4 count (usually <100)
  • a virologic/immunologic response to ART
  • a temporal association with starting ART (usually weeks to months)
  • excluding other new infections

**usually supportive treatment… CONTINUE ART, may need a course of steroids