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

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
What happens to CD8 cells in HIV infection?
Activated by inflammation, die in LN | CD8s in chronic activation will eventually express CD69 and be retained in nodes
26
Approach to HIV treatment
Inhibit Viral Replication | Inhibit activation of already infected cells
27
Which tends to have higher viral load -- genital secretions or plasma
Genital secretions
28
Describe the process of HIV uptake
Virus binds to gp120 on CD4 molecules Exposure of CCR5 or CXCR4 gp41 undergoes a conformational change that causes insertion of fusion peptide.
29
Whats the deal with CCR5 and CXCr4
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
HIV resistant individuals tend to be homozygoups for what mutation
CCR5
31
What causes the switch from CCR5 to CXCR4? | How can this be delayed?
Switch due to hypervariable regions on gp120 | Inhibitors of viral replication
32
CXCR4 viruses are a cause of....
syncytia formation on lymphoid tissues Rapid loss of lymphoid tissues You're fucked
33
A natural method of blocking viral uptake?
Early on, inflammatory cytokines block CCR5 binding | You're fucked when the switch to CXCr4 occurs
34
Viral reservoir in an HIV patient?
Lymphoid tissue throughout the body | Virus can proliferate in macrophages with minimal cytopathic effect
35
Role of a mucosal vs a follicular dendritic cell in HIV infection
Mucosal -- Entry/Transport | Follicular -- Reservoir
36
Cause of the initial decay in plasma virus? | Cause of slower secondary decay?
1. Virus specific CD8 T cell response | 2. Loss of longer lived viral reservoirs
37
Can HIV proliferate without significant plasma RNA?
Yes, more prolif in lymphoid tissue reservoirs
38
Three main factors contributing to the development of immune deficiency
Loss of CD4 cells Loss of CD8 fxn Evolutionary changes in the virus
39
How do the LNs change over the course of continued loss f immune fxn
Loss of fxn, architecture Enlarged, then CD4 atrophy Later scarred/fibrotic (burn out)
40
What happens with extensive, early loss of CD4 cells from Peyer's patches
Products from gut pathogens are released into the blood stream. Increase in Ag-specific and non-specific activation of cells
41
With chronic activation, CD8 cells eventually express _____, which makes them stick in lymph nodes
CD69 | Even if they weren't stuck in nodes, they'd be pretty crappy without CD4s to get them to turn up
42
Alternate mechanisms for decreased immune fxn
Apoptosis of uninfected cells caused by soluble gp120 bound to CD4 Killing by CD8s specific for gp120
43
The evolution of drug resistant strains of HIV has resulted in what two maxims:
1. Maximal inhibition of virus replication should decrease resistance. 2. Treatment should always include multiple agents