Test 2 Guide Questions

Front 1

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

Back 1

Primarily infects vital components of the human immune system such as CD4+ Tcells (Th1, Th2), macrophages and dendritic cells.

Front 2

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

Back 2

Directly destroys CD4+ T cells through lytic cycle and indirectly through thecytotoxic immune system.

Front 3

Which cells act as a “reservoir” for viral replication?

Back 3

Macrophages

Front 4

Which cell transports HIV to lymphoid tissue?

Back 4

Macrophages and dendritic cells

Front 5

What are the three main transmission routes of HIV?

Back 5

Sexual Route, Blood or Blood Product Route to include needle sharing (IDU),Mother-to-Child Transmission, and needle sharing (IDU)

Front 6

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

Back 6

Mother-to-Child Transmission and Blood or blood product route

Front 7

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

Back 7

Teaching of safe sex

Front 8

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

Back 8

There has been no documented account of AIDS being transmitted by saliva, tears, urine, ornasal fluids. These body fluids do not contain enough HIV to infect a person, unless theyhave blood mixed in them and one has significant and direct contact with the bloodcontaminatedsaliva, urine or nasal fluids.

Front 9

What roles do the following play in the “binding, fusion, and infection” steps in the lifecycle of HIV: gp120; gp41, co-receptors CCR5, CXCR4, and CD4?

Back 9

HIV gp120gp “docks” to CD4 protein and two other co-receptors (CCR5 or CXCR4) onCD4 cell (CCR5) or macrophage (CXCR5); 120gp is “pulled” away from underlying gp41by CD4 protein and coreceptors. Gp41 “sticks” into CD4 cell membrane, “breaches” the cellmembrane and HIV RNA along with reverse transcriptase, protease and integrase enters CD4cell.

Front 10

What specific roles do the following enzymes play in the HIV life cycle: reversetranscriptase, integrase, and protease?

Back 10

Reverse Transcriptase will take the viral RNA and make a copy of it DNA and then it willcopy the DNA structure and therefore form a DNA pro virus.Integrase will take the pro virus and stick it into the genome of the host cell and then it isactivated and made into mRNA and translated into long chains of amino acids.Protease: The long chains of proteins must be “sliced and diced” into the correct proteins thatwill form the new HIV virus. This is where protease plays a major role (i.e., in the slicingand dicing)

Front 11

From the original infection, what is the usual period of time before the clinical manifestationsof AIDs occurs?

Can this time period be shorter?

What are the three factors that can effect this period of time?

Back 11

-If left untreated, it usually takes 8 to 10 years but it may be two years or less

-Approximately 10% of patients succumb to AIDS within 2 to 3 years

-Nature of the exposure (e.g., the route, the size of the microbial inoculum), the“virulence” of the microbe (some HIV viruses, because of mutation, are more potent than 41others), and the nature of the host susceptibility to infection (i.e., the immune status of theindividual).

Front 12

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

Back 12

Phase one and three because the HIV levels are highest of AIDS

Front 13

How do fusion inhibitors differ from reverse transcriptase inhibitors and anti proteases interms “before/after” infection? What two surface proteins do fusion inhibitors attach to?

Back 13

-The fusion inhibitors blocked HIV to hook up to CD4 chemokine receptor whichprevents the entrance of the protein core with its reverse transcriptase, integrase andprotease proteins. Reverse transcriptase inhibitors and anti-protease prevent the processonce the virus gets into the cells by preventing it from killing the CD4 cells.

-Gp41 and chemokine receptor on the CD 4 cell

Front 14

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

Back 14

Resistance develops after 6 months to one year after use and occurs more rapidly in patientsthat have been infected for a longer time. This is because they have a greater burden of morediverse forms of the virus. Resistance results from mutations in reverse transcriptase whichquickly arises because of the enormous proliferation rate of virus.

Front 15

Explain how protease inhibitors work. Do the same for integrase inhibitors.

Back 15

-Protease inhibitors block the action of protease and thus prevent the “slicing anddicing” of long proteins into HIV functional proteins. These are usually used on acombination with reverse transcriptase inhibitors.

-Integrase inhibitors block the action of integrase and thus prevent the incorporation ofthe viral genome into the target cell genome.

Front 16

Explain HAART. During this therapy, what happens to the levels of HIV? Are thesepersons still infectious?

Back 16

Combination of several (typically three or four, with a combination of 2-3 types of RTs andprotease) antiretroviral drugs is known as Highly Active Anti-Retroviral Therapy (HAART)The use of the HAART regimen of drugs can lead to undetectable levels of HIV in thebloodstream but there is still HIV in genital secretions so these people are still infectious.