Term
| The absence or failure of the immune system function is called |
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Definition
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Term
| autosomal dominant, autosomal recessive and X linked are all ____ immnodeificiencies |
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Definition
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Term
| lack of T cells in immunodefiency makes patinet at more risk for |
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Definition
| intracellular pathogens like virus, fungi and parasites |
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Term
| what is severe combined immunodeifiency SCID |
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Definition
| Most likely a lack of funct thymus; so now cell mediated immune responses, no T cell dependent Ab responses. AT risk to intracellular pathogens |
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Term
| What is Digeorge syndrome |
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Definition
| deletions on chromosome 22 and results in lack of T box transcription factor. Very lock T cell numbers. Associated with congeital problems |
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Term
| Chediak-Higashi syndrome is? |
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Definition
| mutation of protein that lets phagoctosed material be transported to lysosomes. Can't do a good job with engulfing bacteria. Also less phagocytes in general |
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Term
| leukocyte adhesion deficiency (LAD) Is? |
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Definition
| Problem with beta chain in adhesion molecules resulting in a decreased ablity for leukocytes to bind to the endothelium and migrate to invasion. Person susceptible to bacterial and fungal infections |
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Term
| 5x things that contribute to secondary immunodeficiencies |
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Definition
1. acquired 2. drugs 3. naturitional defi 4. virus or bacterial causes 5. young and old |
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Term
| is AIDS a primary or secondary immunodeficiency |
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Definition
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Term
| most common spread of HIV infection is via what cells |
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Definition
| T cells, macrophages and dendritic cells. |
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Term
| HIV more spread by free virus or infected cells |
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Definition
| INFECTED CELLS not free virus in blood or other fluids. |
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Term
| causative agent identified as aids is called |
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Definition
| causative agent identified as human retrovirus |
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Term
| Is HIV-1 or HIV-2 more pathogenic? Which one is human version and which one primate version |
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Definition
HIV-1 > HIV-2. HIV-1: humans HIV-2: Primates |
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Term
| is HIV closely related to HTLV I |
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Definition
| NO. They are both retroviruses but not closely related. |
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Term
| retroviruses use what as their genetic material |
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Definition
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Term
| The core of the HIV virus is |
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Definition
| 2 strands of single stranded RNA (ssRNA) |
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Term
| what enzymes makes double stranded DNA from single stranded RNA |
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Definition
| reverse transcriptase enzyme |
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Term
| Reverse transcriptase enzyme makes DNA that contains no |
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Definition
|
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Term
| Other internal proteins include |
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Definition
1. p10(Protease) 2. P32 (Integrase) 3. P9 4. P7 |
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Term
| what is the purpose of integrase with DNA/RNA/HIV |
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Definition
| integrase helps with the isnertion of viral DNA into the host cell DNA. When the host now infected divides it makes copies of this virus DNA |
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Term
| Once the HIV virus is turned into VIRAL DNA and it invades a cell as a double stranded DNA it is now called |
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Definition
| a provirus.(B/c its origins was a double stranded RNA virus that had to become activated first through reverse transcriptase enzyme activity to be turned into a double stranded DNA) Now this active double stranded DNA is a provirus infecting other cells) |
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Term
| purpose of proteases during virus replications |
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Definition
| cleaves large viurs polypeptides into smaller peptides and for final virus formation and budding from host cell |
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Term
| the hiv virus is enveloped by what |
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Definition
| lipid bilayer which was from the original host cell it previously infected. So the lipid bilayer that is taken may have MHCI and MHCII on its surface dpeending on what kind of cell it infected. |
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Term
| once the enveloped virus is out on its own it begins to put more things on its stolen lipid bilayer such as these two viral glycoproteins |
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Definition
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Term
| Which viral glycoprotein spans the entire lipid bilayer? |
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Definition
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Term
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Definition
1. CD4 2. chemokine receptors on host cells |
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Term
| Describe the HIV mutation rate |
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Definition
| HIV mutations are at a greater rate than other viruses such as influenza, and a million times greater rate than human DNA |
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Term
| Is the HIV virus from one person then infected into the next the same? |
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Definition
| NO. Different in each infected individual and then it even mutates further in that same person |
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Term
| what contributes to the extremely high mutation rate of the HIV virus |
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Definition
| reverse transcriptase makes errors in the sequencing of the Double stranded DNA From single stranded RNA of the HIV virus thereofore making additions, deletions and substitutions of bases leading to different varieties of the HIV and its amino acids |
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Term
| whats the differences between reverse transcriptase and DNA Polymerase |
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Definition
| DNA polymerase makes more accurate replications and has "proof-reading" ability unlike reverse transcriptase which makes many mistakes when it converts virus RNA to DNA |
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Term
| Why HIV surface glycoprotein is associated with more protein mutations |
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Definition
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Term
| What cells does HIV have a high affinity to and why? Give 3 x examples of these type of cells |
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Definition
CD4 T cells because its GP 120 wants to bind to the CD4 on the TCR of T cells. So cells with high # of CD4 on their surface are 1. Monocytes 2. macrophages 3. APC (Dendritic cells) in the lymph nodes and skin. |
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Term
| What is the sequence for HIV binding to cells |
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Definition
1. First GP 120 binds to CD4 on host cell -GP 120 which previously was covering GP41 binds to CD4 on host cell. This then means GP 41 now open to bind too. 2. GP 120 next need to aslo bind to chemokine receptors on host cell. 3. Now GP41 will fuse to host cell membrane via hydrophobic fusion and invade it |
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Term
first receptor needed for HIV fusion is? Second receptor needed for HIV fusion is? |
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Definition
1. first is GP120 to CD4 then CD41 available 2. CD120 binds to Chemokinreceptor 3. now the available CD41 can fuse to host cell and bomb it with enveloped virus |
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Term
| Chemokine receptors are classified as |
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Definition
| 7-membrane G protein-coupled receptor |
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Term
| what does GP41 do in the invasion of a host cell |
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Definition
| once GP120 gets off of it (from CR and CD4 binding) then GP41 can cause fusion of virus to host cell and inject its poision |
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Term
| on ACTIVATED T cells what chemokine receptor is expressed |
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Definition
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Term
| T tropic HIV-1 cells bind to what kind of chemokine receptor on host cells |
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Definition
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Term
| The CCR5 receptor is in vivo or in vitro? What chemokines can bind to it |
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Definition
In Vivo 1. RANTES: Regulated on Activation, Normal T Expressed & Secreted 2. MIP-1 alpha and MIP-1 Beta Macrophage inflammatory protein. |
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Term
| CCR5 chemokine receptors used by? CXCR4 Chemokine receptor used by? |
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Definition
CCR5 chemokine receptors used by M Tropic HIV-1 virus to enter macrophages and dendritic cells
CXCR4 Chemokine receptor used by T cell-tropic HIV-1 for entry into T cells and dendritic cells in vitro |
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Term
| how can chemokines block HIV-1 into cells |
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Definition
| by competitively binding to the same receptors. |
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Term
| if cytokines were to induce expression of more chemokine receptors would HIV be worse or less |
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Definition
| WORSE! B/c more chemokine receptors then more chance for HIV-1 to bind to those chemokine receptors. |
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Term
| which WBC has both CCR5 and CXCR4 co-receptors? What's the importance of this cell? |
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Definition
| TH17 cells. They get knocked out and no longer can block pathogens from crossing gut. SO gut diseases! |
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Term
| after the provirus of HIV made from replication of ssRNA to dsDNA, then it is spread by what mechanisms |
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Definition
| HIV is picked up by dendritic cells and hten spread HIV to more TH cells. |
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Term
| IS M tropic HIV or T-Tropic HIV more common in early HIV infected people compared to Late HIV infected |
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Definition
Early HIV Infected > M-tropic HIV using CCR5. Late HIV Infected > T-Tropic HIV using CXCR4 |
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Term
| is T tropic HIV or M-tropic HIV associated with hte faster decrease in CD4 T cells and progression to AIDS |
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Definition
| T-tropic HIV which we know are more predominant in late HIV infection. |
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Term
| what is syncytia formation in regards to HIV spread |
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Definition
| A form of spread via cell-to-cell transmission with fusion. When an infected cell fuses with a healthy cell it is called a syncytium. 50-500 cells can form together in this syncytium. |
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Term
| syncytium formation of HIV cells with other cells can be as large as ____ cells fused together |
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Definition
| 50-500 cells fused together. |
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Term
| syncitia formation of HIV occurs with T cells or macrophages |
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Definition
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Term
| silent HIV infected cells are more common in what type of WBC |
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Definition
1. memory CD4 T cells 2. Dormant macrophages |
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Term
| a dormant HIV infected cell means |
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Definition
| the cell is not replicating |
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Term
| Which cells are hard for HIV to kill? And therefore act as a reservoir for the virus |
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Definition
1. macrophages 2. dendritic cells |
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Term
| after a cell is infected by HIV why does that kill die and via what mechanism |
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Definition
| Budding of the newly replicated HIV virus as it tries and eject out of the host cell may weaken that host cells membrane since the ejecting cell may release GP120 which puts holes in the host cell. |
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Term
| Which type of cells are more at risk for death when the HIV virus buds |
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Definition
| Cells with more CD4 since the mechanism for which the host cells die is from HIV virus GP120 binding to CD4 and causing holes. Cells with more CD4 (T cells > macrophages) are at more risk |
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Term
| how does GP 120 play a role in CD$ T cell maturation and budding |
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Definition
GP120 can be left on host cell's membrane of budding HIV virus. This will bind to CD4 if its on that particular cell and cause holes which kill the host cell. 2. GP 120 can also be freely floating around in the body and on its own bind to T cells in lymphoidal tissues and distort them thereby preventing them from further maturation. |
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Term
| are circulating CD4 TH cells or CD4 TH cells in lymphoidal tissues more at risk for HIV Infection |
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Definition
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Term
| name other ways other than budding that INFECTED host CELLS may be killed as a result of infection |
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Definition
immune system! Will recognize GP120 and GP41 as foreign and kills via 1. Ab and Complement mediated cell lysis 2. compelment mediated opsonization 3. Ab mediated opsonization 4. Tc cells kill infected cells |
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Term
| How can body kill free gp120 |
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Definition
1. Ab and complement mediated lysis or opsonization can kill free gp120 that may bind to CD4 of UNIFECTED cells. 2. The unifected cell ITSELF can commit suicide via apoptosis b/c free GP120 binds to its CD4 it realizes its been hacked when it goes to bind with an Ag and self-destructs |
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Term
| how does syncytia formation of HIV and other cells result in a mechanism of cell death |
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Definition
| those clusters of infected cells can act as a superantigen which has mitogenic effect causing an extreme immune response. |
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Term
| you can have an INCREASE in HIV replication from |
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Definition
1. infected CD4 cells that stimulated by an Ag and then increase their syntehsis of everything. 2. If a HIV proviurs (ssDNA) is incorporated into a cell and that cell uses its transcription factor such as nuclear factor kB then it makes LOTS of copies. |
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Term
| Transcription of Provirus by a cell is made possible by what transcription factors |
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Definition
| Nuclear factor KB. Remember the proviurs is in a ssDNA form not ssRNA form. That DNA is then trascribed to MRNA/RNA to make LARGE AMTS of viurs copies. |
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Term
| if a provirus is using a host cells apparatus to increase its copies via transcription factors then it goes from a latency state to a lytic state and this is correlated with a conversion of its promoters from a ___ to a ___ |
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Definition
| from a weak promoter to a strong promoter signifies the virus is stronger at binding to host cells RNA (higher promoter) Transciptase factors make this possible. |
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Term
| what is NF=kB (Nuclear factor kB)? What cells may increaase it? what does it do |
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Definition
| Nuclear factor kB is important cause it makes the HIV provirus go from being a weak promoter to a strong promoter. The stronger hte promoter of the proviurs than the higher chances it will be read by RNA and replicated with its apparatus. It also increases replication of IL-2. This NF-kB is increased from TH cell-APC interactions. |
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Term
| what co-infections may increase transciptase factors which means more HIV inadvertantly made |
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Definition
1. herpes 2. Hep B 3. Cytomegaolovirus |
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Term
| clinical course of HIV infection can be graded based on |
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Definition
|
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Term
| what clinical phase of HIV infection is there no Ab to HIV |
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Definition
|
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Term
| Describe CD4 and HIV levels during acute phase compared to chronic phase |
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Definition
Acute phase: High HIV, Low CD4 Chronic Phase: Low HIV, Higher CD4 at first, then opposite happens. |
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Term
| Describe characteristics of the AIDS Syndrome |
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Definition
1. CD4 T cell count <200cells/uL 2. Large #s of HIV cells 3. Impaired or absent Cell-mediated resposne 4. opportunistic infections |
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Term
| In an unifected individual the normal CD4 T cell count is? |
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Definition
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Term
| The healthy person CD4 T cell: CD8 Tcell is |
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Definition
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Term
In HIV infected individual with AIDS what is the: 1. CD4 level 2. CD4-CD8 T cell ratio |
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Definition
1. CD4 level < 200 cells / ul 2. CD4:CD8 ratio < 1.0 |
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Term
| Ab are made against HIV components and this takes how long? what is the name for this |
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Definition
| CAlled sero-conversion; it takes 6 weeks for Ab to be made against HIV |
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Term
| describe the early Ab response to HIV |
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Definition
There are two types in early Ab attack. 1. Early Ab- envelops glycoproteins around 2-3 weeks, but cant completely prevent 2. Neutralizing Ab: effective in preventing virus from infection and this takes several weeks. |
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Term
| First Ab produced against HIV is? Then followed by more of ___Ab |
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Definition
| First Ab is IgM then IgG replaces it as the main effector. |
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Term
| later Ab responses are less effective and IgG not working why? |
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Definition
| b/c of the loss of TH cells you can't get specific and tailored or even stimulation of Ab. |
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Term
| what can we measure that correlates with the clinical course of HIV infection |
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Definition
| Ab correlates with the clincal course of HIV infection |
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Term
| chronic phase occurs during what period of HIV |
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Definition
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Term
| TH1 delayed type hypersensitivity responses occur during the progression of the chronic phase which results in? |
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Definition
Early effects: reduced ability to activate TH1 cells Later effects: opportunistic infections can help |
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Term
| a decrease in TH1 activity is also associated with an increase in what other immune cells |
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Definition
| increase TH2 activity and Ab response causes decrease TH1 and lack of delayted type hypersensitivity. |
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Term
| The relationship of progression of HIV and cell mediated response is? |
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Definition
| Decrease CD4 TH cells, means less TH1 cells, which means less TH1 cytokines such as IL2 and IFN gamma which means decrease Tc cell activation which means decrease DTH and IFN gamma |
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Term
| what is Tc cell relationship to HIV and its progression |
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Definition
| Tc Cell can kill effectively and decrease viral loads. But to be activated it needs IL2 signalling from CD4 cells and since HIV directly kills CD4 cells then Tc cells stop attacking eventually. |
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Term
| in HIV there is an increase of what cytokines |
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Definition
1. IL2 2. IL6 3. TNF Alpha 4. GM-CSF = more reverse transciptase 5. TNF Beta - more phag and chemotaxis |
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Term
| what happens to cytokines during HIV progression |
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Definition
1. the immune response changes resulting in decrease TH1 activity. If you decrease TH1 then you indirectly decrease Tc Cells and delayed type hypersensitivity. Which means decrease levels of IL2, IFN gamma. Also decrease NK cells from decrease levels of those cytokines.
2. increase TH2 cells and the release of their cytokines |
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Term
| what are three tests for HIV detection |
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Definition
1. ELISA assay detects serum Ab to HIV proteins) 2. Western Blot: confirms 3. Polymerase chain (PCR) confirms, measures viral load in plasma. |
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