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FPP Block 1 > HIV/AIDS > Flashcards

HIV/AIDS Flashcards

1
Q

Describe how to ensure that someone is not going to tranmitt their HIV

A

once the viral load is undetectable it is untransmissable!

  • condoms
  • circumcision
  • ART
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2
Q

WHat s PrEP

A
  • pre-exposure prophylaxis
  • daily oral antiretroviral with a fixed -dosecombination of tenofovir fumarate (TDF) and emtricitabine(FTC)
  • safe and effective in reducing the risk of HIV acquisition in adults
  • only works if you take it!
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3
Q

WHich test is the most likely to detec HIV infection the EARLIEST?

A

HIV RNA NAAT

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4
Q

After a person is infected with HIV how long might it take before they have antibodies in their system

A

30 days!

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5
Q

what test does the CDC reccommend for warly HIV testing and how soon after infection can it detect HIV?

A
  • 4th/5th generation HIV Ag/Ab combination test which can detect both the p24 antigen and HIV antibody
  • test can be positive as early as 14 days post infection
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6
Q

What is the HIV RNA NAAT tets

A
  • a test that can detect HIV as early as 10 days post infection. The earliest test!
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7
Q

Dexcribe the transmission process of HIV

A
  • MOst infections occur at the mucosal surface (vaginal or rectal)
  • virus crosses the mucosal surface and infects target cell-activated CD4+ T Cells, Dendritic cells and macrophages
  • small foci of infection are established locally and then expand and disseminate infection through the draining lymph node and into the blood
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8
Q

Who from team host immune system is involved in the counter attack?

A
  • Innate
    • Dendritic cells (DCs)
    • Natural Killer (NK) cells
  • Intrinsic
    • antiviral restriction factors
  • adaptive
    • B cells
    • T cells
  • When HIV is recognized by the TCR is causes cytokine release which recruits mor CD4 T cells, but that is kind of bad bc T cells are what HIv infects
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9
Q

WHat is the main role of NK cells

A
  • lyse malignant or infected cells
  • NK cell activation is stimulated by innate cytokines including IFN-1, IL-15 and IL-18 and is regulated by receptor ligand interactions
  • they combat HIV-1 replication by killing infected cells (perforin and granzyme, Fas ligand mediated apoptosis, ADDC)
  • produce antiviral factors including IFNy, TNFa and B-chemokines
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10
Q

What is intrinsic immunity and what role does it play during HIV infection?

A
  • Intrinsic, intracellular restriction factors inhibit viral replication directly
  • main restriction factors in HIV: APOBEC3G, TRIM5a, tetherin (BST-2) and SAMHD1
  • HIV-1 counteracts some of these restriction factors via acessory proteins
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11
Q
  • Describe the role that B cells play in HIV and how HIV avoids this
A
  • adaptive immunity, an initial Ab response to Env occurs but it is non-neutralizing
  • neutralizing antibodies eventually develop but slowly, about 12 weeks after infection. this is too late
  • Abs to conserved areas of Enc are rare so excape from Abs occurs
  • HIV induces the lysis of follicular B cells and leads to the loss of germinal centers which results in defects in the ability to rapidly generate Abs
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12
Q
  • How do CD8 T cells fight HIV
A

the first specific CD8 T cell responses are seen as viremia peaks, initially specific for ENv and Nef

virsu sequence chnages dramatically w rapid selection of escape mutant but T cell seventually become more targetd to conserved epitopes

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13
Q

Describe how an individuals genetics may relate to their clinical significane of infection

A
  • Individuals with MHC class I alleles, KLA B57, HLA 27 are associated with control of viremia
  • the combination of NK receptors KIR3DS1 and KIR3DL1 with HLA-B57 has been associated with delayed progression to AIDS
  • alite controllers, a subset of HIV infected individuals who spontaneously control HIV may have more functional CD8 T cells (more perforin and granzyme)
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14
Q

WHy do we need a cure to HIV if we can suppress the viral load with ART?

A
  • Even when the viral loads are supressed ART does not fully restore normal health and immune dysregulation
  • cost and access to medications worldwide is an issue
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15
Q

Describe the pathogenesis of HIV if a person is being treated and what are the consequences of this?

A
  • chronic HIV infection is characterized by persistent infammation and immune dysfunction even whe patients are supressed on ART
  • consequences:
    • ongoign HIV replication
    • infection with co-pathogens such as CMV
    • dysfunctional immunoregulatory factors
    • mcrobial translocation
    • lymphoid fibrosis
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16
Q

Describe the process of microbial translocation

A
  • breakdown in tight junctions, loss of immune cells and alteration of gut flora leading to microbial translocation
  • exposure to the LPS microbial products results in immune activation/inflammation
  • loss of Th17 cells and leads to a shift to Treg phenotype
17
Q

Describe the cycle of inflmmation in HIV

A
  • ongoign inflammation occurs and immune dysfunction during art contribute to disease
  • disease causes inflammation, and drug causes inflammation, which causes tissue injury and leads to more inflammation and the cylcle continues
18
Q

Does ART restore health and normal immune function?

A
  • NO! pts are still at risk for developing several non-AIDS disorders including
    • CV disease
    • cancer
    • kidney disease
    • liver disease
    • osteopenia or osteoporosis
    • neurocognitive disease
19
Q

How does HIV infect

A

HIV integrates intself into the host DNA of CD4+ T cells

20
Q

WHat is the HIV latent reservoir?

A
  • CD4 T cell become infected with HIV an most die
  • Some don’t die and they become memory CD4 T cells (note HIV is in the DNA of these T cells)
  • Some persist but some continue to divid making more and more latent memory HIV CD4 t cells.
  • as long as a person is taking ART the replication stops and the viral load is suppressed. But once they stop taking ART and replication is able to continue again, their viral load increases significantly QUICKLY bc they have a whole army of CD4 t cells that are making virus!
  • integrated HIC DNA persists in lon-lived memory CD4+ T cells
  • latent infected cells live for YEARS. it is so slow for them to die
21
Q

How can we prevent a patient from developing a large laten reservoir?

A

early treatment!

22
Q

Why is it important for early treatment

A
  • limit the size of the latent reservoir
  • limit the development of viral escape mutants
  • increase the number of plasma memory B cells and improve B cell fucntion
  • preserve mucosal immune function (maintenance of Th17 cells)
23
Q

WHat is HIV resisiatcen and how does it occur

A
  • failure to respond to treatment with therapeutic agents. it arises from mutations in the viral genome in regions that encode molecular therapy
  • happens when ppl take meds spuratically
  • HIV reverse transcriptase makes a ton of mutations spontaneously.
  • You need to use mulitple classes of medication which target different parts of the HIV cycle and ideally are still active in the presence of mutations
  • if you you aren’t replicating ( are taking meds) then you wont mutate and develop resistance!
24
Q

How do you test for HIV resistance

A
  • HIV genotype
    • more common: assays asses the genetic composition of HIV variants to determine resistacne mutations
  • HIV phenotype
    • asseses the ability of drugs to inhibit viral replication in cultured cells
25
Q

what are the guidelines for HIV resistance testing

A
  • always test the genotype when entering care
  • resistance testing shoudl be completed with viral failure (RNA>1000 copies/mL) or suboptimal viral load reduction after treatment initiation
  • Phenotypic testiing may be needed when known to have compled drug-resistance mutaion ( testing in a test tube against drugs to ssee if virus responds)
26
Q

what can physicians do to prevent resistance

A

choose a drug regimen that is easy to follow and doesnt have a lto of side effects

27
Q

why do we need to be nervous about resistance

A
  • resistance mutatiosn persist with HIV subpopulations
    • if resistance develops med should NOT be used again
  • resistant viruses can be transmitted to others
  • patients require ART changes but on appropriate regimen can acheive suprresion, but its harder…
28
Q

WHat is Immune reconstitution inflammatory syndrome? ( IRIS)

A
  • paradoxical worsening of preexisting infection following the initiation of ART
    • may be an infection that is known and previously diagnosed or you could be unmasking of a previously subclinical and undiagnosed infection
29
Q

WHat is the diagnostic criteria for IRIS

A
  • low pretreatment CD4 count, less than 1000
  • a virologic and immunologic response to antiretroviral therapy
  • a temporal association with starting ART (usually weeks to months)
  • excluding new infections
30
Q

How do you treat IRIS

A
  • supportive
  • may need a course of steroids
  • continue ART (in almost all cases unless there is serious brain meningeal infection or somthing and yu don’t want to cause more inflammation)
31
Q

How does HIV overcome intrinsic antiviral mechansims?

A

it uses accessory proteins

32
Q

Describe the initial B cell response to HIV

A

it is ineffective and virus escapes both B and T cell response

33
Q

Are there any downsides to our innate immune system response to HIV

A

yes. some of the innate responses contribute to increased inflamation, immune activation which leads to more recruitment of target cells and immune dysfunciton

34
Q

WHat is the hallmark of chronic HIV pathogenesis?

A

persistent immune activation and immune dysfunction. this likely leads to excess non-AIDS defining illnesses, even in patients on effective ART

FPP Block 1 (18 decks)

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