Pathophys - Exam 3 (1 Of 2) - Aids/hiv

Front 1

What immune cells (and subsets) are infected by HIV?

Back 1

CD4+ T-cells (Th1, Th2)
Macrophages / Dendritic cells

Front 2

What cells are directly destroyed (through the lytic cycle) by HIV?

Back 2

CD4+ T-Cells

(Indirectly destroyed through cytotoxic immune system)

Front 3

Which cells acts as a "reservoir" for viral replication?

Back 3

Macrophages

Front 4

Which cell transports HIV to lymphoid tissue?

Back 4

Macrophages
Dendritic cells

Front 5

What are the three main transmission routes of HIV?

Which two have the highest "act risk" for acquisition of HIV?

What is advocated in reducing the risk of spreading HIV through sexual transmission?

Back 5

1. Sexual Route
2. Blood or Blood Product Route (includes needle Sharing (IDU)
3. Mother-to-Child Transmission

2 Highest Risk: Mother-to-Child Transmission, and Blood or Blood Product route

Teaching Safe Sex!!!!

Front 6

What is the risk of transmitting AIDS though saliva, tears, and urine? Why?

Back 6

No documented account of transmitting AIDS through saliva, tears, or urine unless there is a significant amount of blood and direct contact of this.

Front 7

What roles do the following play in the "binding, fusion, and infection" steps in the life cycle of HIV:

GP120, GP41, co-receptors CCR5, CXCR4, and CD4?

Back 7

Binding:
HIV gp120 "docks" to CD4 cell (CCR5) or macrophage (CXCR4)

Fusion:
-gp120 pulled away
-underlying gp41 "sticks" into cell membrane

Infection:
-HIV RNA, Reverse Transcriptase, Protease, Integrase enters the cell

Front 8

What specific roles do the following enzymes play in the HIV life cycle:

reverse transcriptase

Back 8

single strands viral RNA --->> double stranded DNA

Front 9

What specific roles do the following enzymes play in the HIV life cycle:

Integrase

Back 9

Integrase: insert viral DNA into host cell genome

Front 10

What specific roles do the following enzymes play in the HIV life cycle:

Protease

Back 10

AFTER transcription/translation of viral DNA

Protease: "slices and dices" the long HIV protein

Front 11

From the original infection, what is the usual period time before the clinical manifestations of aids occurs?

Can this time period be shorter?

Back 11

Left untreated: 8 to 10 yrs, but can be 2 yrs or less

~10% succumb to AIDS, 2 to 3 yrs.

Front 12

What are the three factors that can effect the period of time until onset of AIDs ?

Back 12

1. Nature of the exposure
(route, size of microbial inoculum)

2. "Virulence" of the microbe

3. Host immune status

Front 13

In what two phases of the course of AIDs is an infected person the most contagious? Why?

Back 13

Phase 1 and 3
b/c of the HIV levels are the HIGHEST

Front 14

How do fusion inhibitors differ from reverse transcriptase inhibitors and anti proteases in terms "before/after" infection?

Back 14

Before:
Fusion inhibitors blocked HIV to hook up to CD4 chemokine receptor

After:
Reverse transcriptase inhibitors and anit-protease prevents the process once the virus gets into the cells by preventing it from killing the CD4 cells.

Front 15

What 4 surface proteins do fusion inhibitors attach to?

Back 15

gp120/gp41
CCR5/CXCR4

Front 16

Why will the treatment of one RT inhibitor not continue to work over time?

Back 16

generations of HIV
result in mutated strains

Resistance develops after 6mo -1yr of drug use

Front 17

Explain how protease inhibitors work.

Back 17

Protease inhibitors block the action of protease and prevents the "Slicing and dicing" of long proteins into HIV functional proteins. Used with a combination with reverse transcriptase inhibitors.

Front 18

Explain how integrase inhibitors work.

Back 18

Integrase inhibitors block the action of integrase and prevents the incorporation of the viral genome into the target cell genome.

Front 19

Explain HAART

Back 19

Highly Active Anti-Retroviral Therapy (HAART): combo. of several antiretroviral drugs (3 or 4, with combo of 2-3 types of RTs and protease)

Front 20

During HAART therapy, what happens to the levels of HIV?

Are these persons still infectious?

Back 20

The use of HAART regimen of drugs can lead to undetectable levels of HIV in the bloodstream.

There is still is HIV in genital secretions so these people are still infectious.

Front 21

What are the three phases on the graph included in the graph?

Back 21

Phase 1: Acute
Phase 2: Clinically Latent
Phase 3: Crisis

Front 22

For phase 1: changes that are occurring and why for

CD4+ T Cell

Back 22

1. Initial rise in CD4 Cells (activiation of specific Th1 and Th2 against HIV, thus mounting both humoral and cytotoxic immune response)
2. Fall (destruction of CD4 by HIV though the lytic cycle)
3. Then a rise back to almost normal #'s (bone marrow activated to replace CD4 cells killed by HIV)

Front 23

For phase 1: changes that are occurring and why for

CD8 T cell

Back 23

1. Acutely rise due to activation of specific CD8 cells by Th1 against HIV
2. This "spike" will return to normal as the serum HIV declines

Front 24

For phase 1: changes that are occurring and why for

Anit-HIV CP120 antibodies

Back 24

1.It takes 3-4 months following initial infection for these antibodies to appear in the blood at high enough concentrations to be measured.
2. Begins to rise as humoral immune response is activated

Front 25

For phase 1: changes that are occurring and why for

HIV Blood/body fluid levels

Back 25

1. Immediately after infection, virus titer rises and 6 months into this phase, virus titers are very high
2. Strong cell-mediated and humoral mounted against HIV, the virus largely disappears from the circulation by the end of the first phase

Front 26

For phase 2: changes that are occurring and why for

CD4+ T Cell

Back 26

1. 5% or more are being killed, which about 1 trillion, A DAY!!
2. (bone marrow) is being severely stressed and over time, the immune system is slowly being annihilated

Front 27

For phase 2: changes that are occurring and why for

CD8 T Cell

Back 27

1. As long as there are sufficient amount of viable CD4 Th1 cells to activate the CD8 t cell, the levels of these will remain at the normal levels

Front 28

For phase 2: changes that are occurring and why for

Anti-HIV GP120

Back 28

1. if there are sufficient amount of viable CD4 Th2 cells to activate the B, these antibodies will remain high

Front 29

For phase 2: changes that are occurring and why for

HIV blood/fluid levels

Back 29

HIV blood levels stay constant, at a low level

Front 30

For phase 3 (Stage 1): changes that are occurring and why for

CD4+ T Cell

Back 30

1. CD4 cells fall below 500 per cu mm and cont. to fall towards 200 per cu mm

Front 31

For phase 3 (Stage 1): changes that are occurring and why for

CD8 T Cell

Back 31

1. CD8 expansions persist, and absolute #'s of CD8 cells stay relatively normal

Front 32

For phase 3 (Stage 1): changes that are occurring and why for

Anti-HIV GP120 Antibodies

Back 32

1. As Th2 CD4 cells drop, the levels of anti-HIV gp 120 antibody dramatically drop
2. Humoral arm of the immune system is becoming non-functional

Front 33

For phase 3 (Stage 1): changes that are occurring and why for

HIV blood/body fluid levels

Back 33

1. As CD4+ drops, significant rise in of HIV viral components in the blood and body fluid

Front 34

For phase 3 (Stage 2): changes that are occurring and why for

CD4+ T Cell

Back 34

CD4 cells fall below 200 mm^3 and the immune system, for all the extent and purposes ceases to function

Front 35

For phase 3 (Stage 2): changes that are occurring and why for

CD8 T Cell

Back 35

All CD8+ T Cell #'s begin to fall, which includes memory CD8+ T cells to other pathogens besides HIV

Front 36

For phase 3 (Stage 2): changes that are occurring and why for

Anti-HIV GP120 Antibodies

Back 36

When Th2 CD4 cells drop below 200 mm^3, the levels of anti-HIV gp 120 antibody in the patient's is low to almost non-existent

Front 37

For phase 3 (Stage 2):changes that are occurring and why for

HIV blood/body fluid levels

Back 37

As the T4 cells fall below 200 per cu mm, virus titers rise rapidly and immune activity drops precipitously

Front 38

For phase 1, explain the symptoms!!

Back 38

1. Mild "flu like" condition that is self-limiting
2. Half remain asymptomatic during the initial period of infection
3. Symptoms are "not specific" enough to be identified with HIV infection

Front 39

For phase 2, explain the symptoms!!!

Back 39

1. Presence of mild to moderate lymphandenopathy or asymptomatic

Front 40

For phase 3, Stage 1 explain the symptoms!!

Back 40

1. Weight loss approx. 10% of body weight
2. Chronic diarrhea
3. Recurrent upper respiratory tract infections (bacterial sinusitis, bacterial pneumonia)
4. Oral candidiasis (thrush)
5. Oral hairy leukoplakia

Front 41

For phase 3, Stage 2 explain the symptoms!!!

Back 41

1. Pneumocystis carinii pneumonia
2. Cytomogalovirus disease of liver, spleen, and lymph nodes
3. Candidiasis of esophagus, trachea, bronchi
4. Pulmonary and extrapulmonary tuberculosis
5. Kaposi's Sarcoma

Front 42

Which may be among the first cells to encounter HIV at mucosal surfaces?

Back 42

Epidermal dendritic cells (Langerhans cells)

Front 43

What exposure route has a 90% chance of infection?

Back 43

Blood or Blood product route

Front 44

What exposure route has a 25% chance of infection?

Back 44

Mother to Child