Term
What immune cells (and subsets) are infected by HIV?
What cells are directly destroyed (through the lytic cylcle) by HIV?
Which cells act as a "reservoir" for viral replication?
Which cells transports HIV to lymphoid tissue? |
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Definition
-Primarily infects vital components of the human immune system such as CD4+ T cells (TH1, TH2), macrophages and dendritic cells
-Directly destroys CD4+ T cells through lytic cycle and indirectly through the cytotoxic immune system
-Macrophages
-Macrophages and dendritic cells |
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Term
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? |
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Definition
-Sexual route, Blood or Blood Product Route, Mother-to-Child Transmission, and needle sharing (IDU)
-Mother-to-Child Transmission and Blood or blood product route
-Teaching of safe sex |
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Term
| What is the risk of transmitting AIDS through saliva, tears, and urine? Why? |
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Definition
| There has been no documented account of AIDS being transmitted by saliva, tears, urine, or nasal fluids. These body fluids do not contain enough HIV to infect a person, unless they have blood mixed in them and one has significant and direct contact with the blood-contaminated saliva, urine or nasal fluids |
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Term
| 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? |
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Definition
| HIV gp120gp "docks" to CD4 protein and two other co-receptors (CCR5 or CXCR4) on CD4 cell (CCR5) or macrophage (CXCR5); 120gp is "pulled" away from underlying gp41 by CD4 protein and coreceptors. Gp41 "sticks" into CD4 cell membrane, "breaches" the cell membrane and HIV RNA along with reverse transcriptase, protease and integrase enters CD4 cell. |
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Term
| What specific roles do the following enzymes play in the HIV life cycle: reverse transcriptase, integrase, and protease? |
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Definition
| Reverse Transcriptase will take the viral RNA and make a copy of it DNA and then it will copy the DNA structure and therefore form a DNA pro virus. Once that's formed, the integrase will take the pro virus and stick it into the genome of the host cell and then it is activated 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 that will form the new HIV virus. This is where protease plays a major role (i.e., in the slicing and dicing) |
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Term
From the original infection, what is the usual period of time before the clinical manifestations of AIDs occurs?
Can this time period be shorter?
What are the three factors that can effec this period of time? |
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Definition
-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, becuase of mutation, are more potent than others), and the nature of the host susceptibility to infection (i.e., the immune status of the individual). |
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Term
| In what two phases of the course of AIDS in an infected person the most contangious? Why? |
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Definition
| Phase one and three because the HIV levels are highest of AIDS. |
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Term
| How do fusion inhibitors differ from reverse transcriptase inhibitors and anti proteases in terms "before/after" infection? What two surface proteins do fusion inhibitors attach to? |
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Definition
-The fusion inhibitors blocked HIV to hook up to CD4 chemokine receptor which prevents the entrance of the protein core with its reverse transcriptase, integrase and protease proteins. Reverse transcriptase inhibitors and anti-protease prevent the process once the virus gets into the cells by preventing it from killing the CD4 cells.
-Gp41 and chemokine receptor on the CD4 cell |
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Term
| Why will the treatment of one RT inhibitor not continue to work over time? |
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Definition
| Resistance develops after 6 months to one year after use and occurs more rapidly in patients that have been infected for a longer time. This is because they have a greater burden of more diverse forms of the virus. Resistance results from mutations in reverse transcriptase which quickly arises because of the enormous proliferation rate of virus. |
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Term
| Explain how protease inhibitors work. Do the same for integrase inhibitors. |
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Definition
-Protease inhibitors block the action of protease and thus prevent the "slicing and dicing" of long proteins into HIV functional proteins. These are usually used on a combination with reverse transcriptase inhibitors.
-Integrase inhibitors block the action of integrase and thus prevent the incorporation of the viral genome into the target cell genome. |
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Term
| Explain HAART. During this therapy, what happens to the levels of HIV? Are these persons still infectious? |
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Definition
Combination of several (typically three or four, with a combination of 2-3 types of RTs and protease) antiretroviral drugs is known as Highly Active Anti-Retroviral Therapy (HAART).
The use of HAART regimen of drugs can lead to undetectable levels of HIV in the bloodstream but there is still HIV in genital secretions so these people are still infectious. |
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Term
| For Phase I, explain the symptoms, and changes that are occuring, and why, for the following: CD4 T cell; CD8 T cell; Anti-HIV gp120 antibodies; and HIV blood/body fluid levels |
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Definition
Symptoms:
-Mild "flu like" condition that is self-limiting
-Half remain asymptomatic during the initial period of infection
-Symptoms are not specific enough to be identified with HIV infection
CD4 T cells:
-Initial rise in CD4 cells (activation of specific TH1 and TH2 against HIV, thus mounting both humoral and cytotoxic immune response)
-Fall (destruction of CD4 by HIV through the lytic cycle)
-Then a rise back to almost normal numbers (bone marrow activated to replace CD4 cells killed by HIV)
Anti-HIV gp120 antibody:
-It will take 3-4 months following initial infection for these antibodies to appear in the blood at high enough conc. to be measured
-Begins to rise as humoral immune response is activated
CD8 T cells:
-Acutely rise due to activation of specific CD8 cells by TH1 against HIV
-This "spike" will return to normal as the serum HIV declines
HIV virus:
-Immediately after infection, virus titer rises and 6 months into this phase, virus titers are very high
-A strong cell-mediated and humoral mounted against HIV, the virus largely disappears from the circulation by the end of the first phase
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Term
| For Phase II, explain the symptoms, and changes that are occuring, and why, for the following: CD4 T cell; CD8 T cell; Anti-HIV gp120 antibodies; and HIV blood/body fluid levels |
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Definition
Symptoms:
-Presence of mild to moderate lymphandenopathy or asymptomatic
CD4 T cells:
-5% or more are being killed, which is about one trillion, a day
-(bone marrow) is being severely stressed and over time, the immune system is slowly being inhibited
Anti-HIV gp120 antibody:
-As long as there are a sufficient amount of viable CD4 TH2 cells to activate the B, these antibodies will remain high
CD8 T cells:
-As long as there are sufficient amount of CD4 TH1 cells to activate the CD8 T cells, the level of CD8 T cells will remain at the normal levels
HIV virus:
As long as there is a sufficient cell-mediated and humoral mounted response against HIV, the level of virus in the blood will stay low to non-detectable |
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Term
| For Phase III, stage 1, explain the symptoms, and changes that are occuring, and why, for the following: CD4 T cell; CD8 T cell; Anti-HIV gp120 antibodies; and HIV blood/body fluid levels |
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Definition
Symptoms (4 of the 5):
-Weight loss ≈ 10% of body weight
-Chronic diarrhea
-Recurrent upper respiratory tract infections (eg., bacterial sinusitis, bacterial pneumonia)
-Oral candidiasis (thrush)
-Oral hairy leukoplakia
CD4 T cells:
-CD4 cells fall below 500 per cu mm and continue to fall towards 200 per cu mm.
Anti-HIV gp 120 antibody:
-As TH2 CD4 cells drop, the levels of anti-HIV gp 120 antibody dramatically drop
-Humoral arm of the immune system is becoming non-functional
CD8 T cells:
-CD8 expansions persist, and absolute numbers of CD8 cells stay relatively normal
HIV virus:
-As CD+4 drops, significant rise in of HIV viral components in the blood and body fluid
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Term
For phase III, stage 2, explain the symptoms, and changes that are occurring, and why, for the following: CD4+ T cell; CD8 T cell; Anti-HIV GP120 antibodies; and HIV blood/body fluid levels.
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Definition
Symptoms (4 of the 5):
-Pneumocystis carinii pneumonia
-Cytomegalovirus disease of liver, spleen and lymph nodes
-Candidiasis of esophagus, trachea, bronchi
Pulmonary and extrapulmonary tuberculosis
-Kaposi’s sarcoma
CD4 T cells:
-CD4 cells fall below 200 mm3 and the immune system, for all extent and purposes, ceases to function
Anti-HIV gp 120 antibody:
-When TH2 CD4 cells drop below 200 mm3, the levels of anti-HIV gp 120 antibody in the patient’s is low to almost non-existent
CD8 T cells:
-All CD8+ T cell numbers begin to fall, which includes memory CD8+ T cells to other pathogens besides HIV.
HIV virus:
-As the T4 cells fall below 200 per cu mm, virus titers rise rapidly and immune activity drops precipitously.
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