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55 Cards in this Set
- Front
- Back
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HIV infection |
viral infection causing depletion of CD4+ cells |
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AIDS |
the advanced stage of HIV infection in which the immune system is deficient, making individuals susceptible to life-threatening opportunistic infections and certain cancers |
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the decline in incidence since 2008 is partly due to... |
< # of new infections amongst IDU group |
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incidence rates are greatest amongst... |
homosexual males (MSM=49.3% of N.I. in 2013) |
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women account for... |
21.9% of new HIV cases (2013) |
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30-39 y.o. represent... |
30% of new cases (2011) |
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age distribution differed in male and females ... |
more females being diagnosed at younger ages |
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aboriginal peoples are disproportionately affected |
- represent 4% of cdn pop, but 16% of new HIV infections |
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HIV is a... |
retrovirus |
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HIV carries genetic info in the form of... |
RNA |
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HIV is able to convert their RNA to DNA using an enzyme called... |
reverse transciptase |
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HIV is... |
very fragile-> cannot survive long outside host cell (half life in plasma 1-2 days) |
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HIV is capable of... |
long term latency within cells |
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HIV-1 |
responsible for the most infections worldwide |
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HIV-2 |
-relatively rare, endemic in West Africa -less aggressive, longer period of latency before onset of symptoms |
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Two genetic strains of HIV virus exist that differ in the... |
type of envelope glycoproteins |
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HIV virus structure core contains... |
-viral RNA -reverse transcriptase -intergrase -protease |
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HIV virus structure inner capsid.. |
-viral protein p24 -antibody and antigen of p24 can be measured |
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HIV virus structure viral envelope... |
-embedded with glycoproteins gp41 and gp120 |
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spread occurs through... |
exposure to body fluid (blood, semen, vaginal secretions, rectal secretions, breast milk) |
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transmission includes... |
-unprotected sex -blood -mother to infant |
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unprotected sexual contact |
-enters through: abrasions or sores in genital, oral or anal mucosa -direct contact with mucosal dendritic cells |
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Why is a female at greater risk of transmission via sexual contact than a male? |
-greater surface area -greater concentration of virus in seminal fluid |
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factors that increase risk of transmission with sexual contact |
-high viral load - coexisting STIs (genital ulcers or sores) -trauma (tears, abrasions) -menstruation -lack of male circumcision |
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How can risk of sexual transmission be reduced? |
-antiviral therapy -condom -lubricant |
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post-exposure prophylaxis (PEP) |
-combo of 2-3 ART drugs -taken within 72hrs -taken q day x4 weeks -prescribed by DR -meant to stop viral rep. at site of infection -not 100% effective |
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pre-exposure prophylaxis (PrEP) |
-taken by person at risk for HIV -Truvada in US -transmission can < by 90% if taken daily -less effective if other STIs are present -clinical trails in cdn |
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blood borne transmission |
-sharing infected needles/drug paraphernalia -infected blood or blood products (before 1985) -occupational exposure (needle stick) -infected needles used for tattooing/acupuncture |
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transfer of HIV between mother and infant can occur through... 1. 2. 3. |
1. delivery (most common) 2. pregnancy across the placenta 3. breast milk |
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HIV replication 1. gp120 and gp41 bind specifically to CD4 proteins on target cells (CD4+ cells). Which types of cells are affected? |
-dendritic cells -CD4 and T cells (helper) -macrophages |
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HIV replication 2. in order to enter a CD4+ cell, HIV must also bind to a... |
co-receptor on target cells -CCR5 on macrophages and dendritic cells -CXCR4 on helper T cells |
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HIV anti retroviral therapy (ART) drugs target the HIV replication cycle. Where do these drugs work? |
-fusion inhibitors -co-receptor inhibitor (CCR5/CXR4) -protease inhibitor -integrase inhibitor -nukes-> prevents RNA to DNA -non-nukes-> prevents formation of second strand, blocks transcriptase |
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Primary HIV infection occurs in... |
-dendritic cells or macrophages in mucous membranes -helper T cells or monocytes in the blood |
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Infection in lymph nodes 1. |
-dendritic cells carry virus to lymph nodes -cells in blood carries the virus to spleen -lymphoid tissues are filled with target cells for HIV |
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Infection in lymph nodes 2. |
-the virus replicated and releases new virus -invade other CD4+ cells in lymph nodes or spleen -enter the blood and spread throughout the body -> viremia (2-3 days of infection) |
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Infection in lymph nodes 3. |
HIV infection is established (billions of viruses are produced daily) |
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Infection in lymph nodes 4. |
-not all infected cells are productive-> some become sanctuary sites (inactive memory helper T cells) -viral DNA is integrated but not expressed -can remain inactive for many years-> infection by another pathogen activates the cell and HIV gene expressed |
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Immune response to infection |
-both humoral (B cell) and cell-mediated (T cell) immune responses activated -CD4+ helper T cells are both activated and infected with HIV |
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Humoral response to HIV infection 1. |
anti-p24 antibodies measured in dx (most readily detected) |
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Humoral response to HIV infection 2. |
anti-envelope antibodies (gp120 or gp41) are usually bound to the virus and not detectable |
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Humoral response to HIV infection 3. |
anti HIV antibodies function to: -neutralize extracellular viruses (block gp120 binding site) -recruit natural killer cells -ineffective-> virus mutates and develops resistance to antibodies |
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The two lab tests to detect the presence of antibodies... |
1. ELISA (immunoassay) -1st test, inexpensive, quick, sensitive) 2. Western blot- to confirm is ELISA is + (several weeks for result) -combined 99.99% specific |
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Tests to detect HIV itself... |
1. HIV p24 antigen test -10-14 days post, not after 5-6 weeks 2.HIV NNAT test -detects HIV RNA 7-14 days after |
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Tests to measure viral load.. |
-polymerase chain reaction (PCR) -measure RNA levels -hours to days of infection |
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Window period |
-time when antibodies not detectable-> pt is infectious -takes 1-3 months for measurable antibodies (seroconversion) |
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What will influence how long it takes for the immune system to create antibodies? |
-immune system health -blood transmission shows antibodies sooner -if exposed to high viral load |
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Cell-mediated response to HIV |
-cytotoxic T cells (CD8+) prolif. and attack and lyse infected cells -primary mode of viral killing |
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Cell-mediated response to HIV CD4 destruction occurs by: |
-destruction by cytotoxic T cells -cytotoxic effects of viral replication (macrophages and monocytes not killed by function impaired) -apoptosis of uninfected cells (gp120 shed and binds to cells stimulating apoptosis) |
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Stages of HIV infection 1. 2. 3. 4. |
1.primary infection (acute HIV syndrome) 2.clinical latency 3.symptomatic HIV infection 4. AIDS |
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Primary Infection |
80-90% show mild symptoms 2-4 wks after infection |
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Primary Infection |
-viral levels peak (greatest infectivity) -CD4+ count < -window period -symptoms resolve in 2-10wks |
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Clinical Latency |
-viral load drops to steady level -viral rep. balanced by viral destruction by cytotoxic T cells -bone marrow maintains adequate production of CD4+ cells |
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Symptomatic HIV Infection |
-virus starts to overburden immune system -ability of bone marrow to produce CD4+ cells declines -viral load increases |
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Symptomatic HIV Infection |
-symptoms develop -night sweats, fever, diarrhea, fatigue (>1mnth) -persistent generalized lymphadenopathy >3mnths in >2 locations -minor opportunistic infections (thrush, herpes zoster, persistent vaginal yeast infection) |
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AIDS |
-CD4+ counts decline causing immune deficiency -normal: 800-1000 cells/mm3 -AIDS: <200 cell/mm3 development to AIDS ave. 10y -antiviral drugs slow or halt progression -now called chronic HIV infection/HIV disease |
