HIV Flashcards

1
Q

Difference between prevalence and incidence

A
Prevalence = Cases per population
Incidence = No cases per unit time
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2
Q

Approx. new HIV cases per year?
New AIDS per year?
Deaths per year?

A

45,000
35,000
15,000

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3
Q

Until very recently HIV’s origins are typically __% Sexual and __% Affiliated with Drug Use

A

85% Sexual

15% Drug Associated

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4
Q

What race has the most disproportionately high rate of HIV trasnsmission

A

African American (esp. among women)

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5
Q

Leading case of HIV transmission

A

MSM

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6
Q

Why increasing MSM transmission?

A

Gen X never watched their generation die
Belief that low RNA levels will prevent transmission
Overall increase in MSM STD rate

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7
Q

The one cure for AIDS?

A

Bone Marrow transplant using a donor with a CCR5-delta32 mutation

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8
Q

___% of all cases of HIV/AIDS are in Subsaharan Africa

Prevalence there?

A

70

5%

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9
Q

How is HIV transmitted?

A

Exchange of bodily fluid
Allows for entry of a virus across a mucosal membrane
(or injected parenterally)

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10
Q

HIV transmission is documented via which bodily fluids

A

Blood, Semen, Vaginal Fluid, Breast Milk

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11
Q

T or F. Contaminated surfaces may be a high risk for contraction of HIV

A

F. Virus doesn’t survive in environment.

Drying = Near Zero levels of the virus

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12
Q

Only which types of condoms can effectively prevent AIDS transmission

A

Latex and Polyurethane

No lambskin allowed

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13
Q

Who is the higher occupational needle stick risk?

Hep B or HIV

A

Hep B

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14
Q

Three routes of pediatric infection

A

Transplacental
Infected Birth Canal
Ingestion of Breast Milk

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15
Q

How are pediatric infections with HIV avoided?

A

Universal HIV screening prior to week 36
Treat mom with HAART ( 30->2% transmission)
Cesarean Section decreases risk by half

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16
Q

Genetic Info about the HIV virus itself?

A

Retrovirus related to lentiviruses

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17
Q

Difference between HIV-1 and HIV-2

A

HIV-1 more aggressive
HIV-1 is in US/Central Africa
HIV-2 is in Western Africa and India

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18
Q

Important HIV virus Proteins to Remember? Why?

A

gp120 - Mediates CD4 binding
gp41 - Fusion to cell membranes
p24 - Major caspid protein in the core (diagnostic)

19
Q

Three viral enzymes necessary for HIV reproduction

A

Protease, Integrase, Reverse Transcriptase

20
Q

HIV has a tropism for what tissues

A

Hematopoetic, Nervous tissue

Binds CD4 on lymphocytes, macrophages, and Glial cells

21
Q

HIV proliferation is triggered by…

A

Cell Activation

Multiplication is cytotoxic to the host cell

22
Q

Normal CD4:CD8 Ratio

HIV CD4:CD8 Ratio

A

2: 1
1: 2

23
Q

In the first few weeks following infection, total body CD4 cells can drop by…

A

approx 80%

24
Q

Three ways you may see dying T cells in an HIV infection

A

Normal Death from Negative Selection
Death by cytopathic effect of virus
Killing of infected cells by virus specific T cells

25
Q

What happens to CD8 cells in HIV infection?

A

Activated by inflammation, die in LN

CD8s in chronic activation will eventually express CD69 and be retained in nodes

26
Q

Approach to HIV treatment

A

Inhibit Viral Replication

Inhibit activation of already infected cells

27
Q

Which tends to have higher viral load – genital secretions or plasma

A

Genital secretions

28
Q

Describe the process of HIV uptake

A

Virus binds to gp120 on CD4 molecules
Exposure of CCR5 or CXCR4
gp41 undergoes a conformational change that causes insertion of fusion peptide.

29
Q

Whats the deal with CCR5 and CXCr4

A

Gp120 initially binds to CCR5 (prev. in genital dendritic cells), but over the course of infection, Gp120 mutates and matches better with CXCR4 on lymphocytes

30
Q

HIV resistant individuals tend to be homozygoups for what mutation

A

CCR5

31
Q

What causes the switch from CCR5 to CXCR4?

How can this be delayed?

A

Switch due to hypervariable regions on gp120

Inhibitors of viral replication

32
Q

CXCR4 viruses are a cause of….

A

syncytia formation on lymphoid tissues
Rapid loss of lymphoid tissues
You’re fucked

33
Q

A natural method of blocking viral uptake?

A

Early on, inflammatory cytokines block CCR5 binding

You’re fucked when the switch to CXCr4 occurs

34
Q

Viral reservoir in an HIV patient?

A

Lymphoid tissue throughout the body

Virus can proliferate in macrophages with minimal cytopathic effect

35
Q

Role of a mucosal vs a follicular dendritic cell in HIV infection

A

Mucosal – Entry/Transport

Follicular – Reservoir

36
Q

Cause of the initial decay in plasma virus?

Cause of slower secondary decay?

A
  1. Virus specific CD8 T cell response

2. Loss of longer lived viral reservoirs

37
Q

Can HIV proliferate without significant plasma RNA?

A

Yes, more prolif in lymphoid tissue reservoirs

38
Q

Three main factors contributing to the development of immune deficiency

A

Loss of CD4 cells
Loss of CD8 fxn
Evolutionary changes in the virus

39
Q

How do the LNs change over the course of continued loss f immune fxn

A

Loss of fxn, architecture
Enlarged, then CD4 atrophy
Later scarred/fibrotic (burn out)

40
Q

What happens with extensive, early loss of CD4 cells from Peyer’s patches

A

Products from gut pathogens are released into the blood stream. Increase in Ag-specific and non-specific activation of cells

41
Q

With chronic activation, CD8 cells eventually express _____, which makes them stick in lymph nodes

A

CD69

Even if they weren’t stuck in nodes, they’d be pretty crappy without CD4s to get them to turn up

42
Q

Alternate mechanisms for decreased immune fxn

A

Apoptosis of uninfected cells caused by soluble gp120 bound to CD4
Killing by CD8s specific for gp120

43
Q

The evolution of drug resistant strains of HIV has resulted in what two maxims:

A
  1. Maximal inhibition of virus replication should decrease resistance.
  2. Treatment should always include multiple agents