Term
| What are the two types of HIV and from what species did they originate? |
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Definition
HIV-1 (principle cause of AIDS in most countries) from chimpanzees
HIV-2 much slower disease progression in west Africa and Asia that came from sooty mangabeys probably |
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Term
| 67% of people with AIDS live in which country? |
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Definition
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Term
| In Africa, what characterizes common oportunistic infections due to AIDS? |
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Definition
| they are usually enteropathic (diarrhea and wasting) instead of respiratory like pneumocystic carinii in developed countries |
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Term
| What opportunistic infection due to AIDS causes the most fatalities? |
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Definition
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Term
| What is the risk of getting AIDs with infected blood transfusion? needlestick? |
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Definition
| blood transfusion is 100%; needlestick is .3% (compared to HepB which is 30% |
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Term
| What increases your risk of contracting HIV through a mucosal surface? |
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Definition
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Term
| What type of molecule is the HIV genome? |
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Definition
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Term
| T/F HIV has a relatively low mutation rate. |
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Definition
| FALSE, it has a very high mutation rate |
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Term
| What viral family is HIV a part of? |
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Definition
| Lentivirus family (lentus=slow, reflecting progressive disease) |
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Term
| The Gp120 envelope protein of HIV binds to what? |
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Definition
| CD4 and CCR5 (and CXCR4 late in the course of infection) |
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Term
| How many gp160 are there on an HIV envelope? |
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Definition
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Term
| What are the parts of gp160 and their functions? |
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Definition
| gp 120 mediates binding and gp41 mediates fusion |
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Term
| Describe the inner core inside the envelope of the HIV virus? |
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Definition
| inner core is a shell made of the p24 major capsid protein which contains teh RNA genome and enzymes (like reverse transcriptase, protease and integrase) |
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Term
| Name the three important genes common to all retroviruses (including HIV). |
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Definition
1) gag (group specific antigens)-core and matrix proteins
2) pol (polymerase)- reverse transcriptase, protease, and integrase enzymes
3) env (envelope)- transmembrane glycoproteins (like gp120 for HIV) |
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Term
| What is the function of the nef gene in the HIV genome? |
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Definition
| "negative regulation factor"- augments viral replication and downregulates CD4 and MHC class I and II |
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Term
| What do you call the cocktail of drugs that inhibit different stages of the HIV life cycle? |
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Definition
| HAART (highly active antiretroviral therapy) combination therapy |
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Term
| How does HIV virus leave the host cell? |
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Definition
| by budding off whereby the immature virus pushes out of the cell, taking some cell membrane with it. |
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Term
| Characterize "R5"-tropic HIV viruses. |
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Definition
| These HIV viruses bind to CD4+ and CCR5 and are easily transmitted and prevalent throughout most of infection |
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Term
| Characterize the "X4"-tropic HIV viruses. |
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Definition
| These viruses bind to CD4 and CXCR4 and are more active in endstage disease |
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Term
| What gene deletion can result in HIV resistance? |
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Definition
| homozygous CCR5delta32 base pair deletion. occurs in less than 1% of caucasians |
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Term
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Definition
| highly exposed persistently seronegative individuals--term used to describe some people who just don't get HIV despite mutliple exposures |
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Term
| T/F HIV infects any and all CD4 T cells but only some macrophages. |
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Definition
| false! it can only infect activated or memory CD4 T cells because naive T cells make an enzyme that degrades HIV |
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Term
| Why can't HIV infect mucosal macrophages? |
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Definition
| mucosal macrophages are refractive due to an NFKB modification. CD4+ langerhan's cells degrade HIV |
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Term
| Can dendritic cells be infected by HIV? |
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Definition
| not really. dendritic cells bind HIV then transfer infection virus to T cells (this is called transinfection) |
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Term
| Why are mucosal CD4 T cells (including gastrointestinal) more susceptible to HIV infection? |
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Definition
| increased expression of CCR5 |
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Term
| T/F HAART is designed to eliminate latent reservoirs of the HIV virus. |
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Definition
| FALSE, they halt production of viral proteins |
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Term
| Where are the major reservoirs of latent HIV? |
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Definition
| GALT and other mucosal lymphoid tissue |
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Term
| In what ways does HIV "kill" CD4 T cells? |
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Definition
| 1) direct virus-induced cytolysis 2) lysis of infected T cells by CD8 or NK cells 3) killing of infected T cells through ADCC (antibody and NK or other FcR+ cell)and 4) apoptosis (virus-specific or nonspecific) |
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Term
| T/F HIV infection decreases thymopoiesis of CD4+ cells. |
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Definition
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Term
| CD4 T cell loss in HIV infection is probably mainly due to.. |
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Definition
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Term
| How long is the asymptomatic phase of HIV infection? |
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Definition
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Term
| At what CD4 levels does the symptomatic phase of HIV infection start? |
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Definition
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Term
| At what CD4 count does AIDS occur? |
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Definition
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Term
| When is HAART generally started? |
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Definition
| at the onset of AIDS but starting ART at higher CD4 (like 350 cells/uL) reduces mortality rates |
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Term
| T/F Liver and spleen enlargement are symptoms of acute HIV infection. |
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Definition
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Term
| How long after exposure can you detect an antibody response to HIV? |
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Definition
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Term
| If an ELISA gives a positive HIV test result, what test should be done to confirm it? |
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Definition
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Term
| Why are new ELISA kits able to detect HIV infection sooner? |
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Definition
| they are able to detect IgM against HIV not just IgG |
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Term
| OraQuick HIV test is based on the presence of ________ in oral fluid. |
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Definition
| HIV env- and p24 gag-specific antibody |
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Term
| T/F If OraQuick test is positive, you should confirm with a laboratory ELISA. |
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Definition
| FALSE, oraquick is just as accurate as ELISA and you need to do a western blott to confirm either test |
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Term
| Which MHC allotypes are associated with slower progression of HIV infection? |
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Definition
HLA B27 and HLA B57
they stimulate stronger CD8 responses due to better presentation of HIV peptide |
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Term
| What are HIV-infected "elite controllers"? |
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Definition
| an unknown immune mechanism not related to genes or an attenuated virus whereby a patient is able to maintain CD4 count without anti-retrovirals. THe immune system keeps viral loads at almost undetectable levels and there is no disease progression. |
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Term
| How does HIV evade neutralizing antibodies? |
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Definition
| latency, cell-to-cell transmission, mutations in Env, and low availability of Env proteins (little surface gp160) |
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Term
| How does HIV evade being destroyed by CD8 cells? |
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Definition
| downregulation of class I MHC, point mutations, apoptosis, and latency |
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Term
| Roughly __% of individuals cannot take HAART due to severe side effects. |
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Definition
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Term
| Why has it been so difficult to develope an HIV vaccine? |
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Definition
| correlates of immune protection aren't clear, IM injection isn't effective for mucosal immunity, poorly designed immunogens because it is difficult to mimic env proteins, T cell vaccines cannot prevent transmission, better adjuvants are needed |
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Term
| Describe the most effective HIV vaccine that we've come up with. |
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Definition
| 30% efficacy with a vaccine that uses ALVAC (canarypox) as a viral vector to induce non-neutralizing Env antibody capable of mediating ADCC (part of the RV 144 Thai trial) |
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Term
| What's the worst HIV vaccine we've created? |
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Definition
| Made 30% more susceptible to HIV and was a T cell vaccine in STEP trial that prevented T cells from responding against HIV infection in patients who were exposed/infected by HIV after vaccination |
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