Virsuses: Human Immunodeficiency Syndrome & Acquired Immunodeficiency Syndrome. Outline we may need to save some topic in lecture. Origins of HIV based on scientific evidence HIV viral particle Mechanism of infection Transmission Treatment AIDS Prevention Clinical Detection and Diagnosis.
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Greater spot nose monkey
SIV cpz almost identical to HIV 1
Simian Virus (SIV cpz) almost identical to HIV 1
Simian Virus corresponds to HIV2
mechanism of replication
Infects Th cell
Integrates into host DNA
HOST CELLS:helper T lymphocyte, macrophages
Binds naturally occurring chemokines
CCR5 or CXCR4 (fusin)
Indirect evidence of HIV exposure
Directly measures HIV
Identifies HIV proteins
Antibodies are directed against specific antigens.
Labelled 2nd Ab
Color inducing substrate
NO COLOR CHANGE
(similar test is also available for blood samples, see next slides).
OraQuick Rapid Anti-HIV Blood Test
20 minute test
Cost app. $15.00
Onto the ELISA lab Antibodies
Normal CD4+ count Antibodies
Normal CD4+ (%)
<350/mm3 begin anti-viral treatment
<14% serious immune damageAcquired Immunodeficiency Syndrome
Experimental drugs are Antibodiesitalicized, and approved drugs are in regular, non-italicized type)
Experimental drugs are Antibodiesitalicized, and approved drugs are in regular, non-italicized type)Brand NameGeneric NameAbbreviationExperimental Code Pharmaceutical Company Fuzeon™enfuvirtideENFT-20Trimeris and Hoffmann-La Roche BMS-488043Bristol-Myers SquibbGSK-873,140GlaxoSmithKlinePRO-542Progenics PharmaceuticalsSCH-DSchering-Plough CorporationTNX-355Tanox and Biogen IdecUK-427,857Pfizer What are Entry Inhibitors (including Fusion Inhibitors)?Entry inhibitors work by preventing HIV from entering healthy T-cells in the body. They work differently than many of the approved anti-HIV drugs – the protease inhibitors (PIs), the nucleoside reverse transcriptase inhibitors (NRTIs), and the non-nucleoside reverse transcriptase inhibitors (NNRTIs) – which are active against HIV after it has infected a T-cell. Entry inhibitors work by attaching themselves to proteins on the surface of T-cells or proteins on the surface of HIV. In order for HIV to bind to T-cells, the proteins on HIV's outer coat must bind to the proteins on the surface of T-cells. Entry inhibitors prevent this from happening. Some entry inhibitors target the gp120 or gp41 proteins on HIV's surface. Some entry inhibitors target the CD4 protein or the CCR5 or CXCR4 receptors on a T-cell's surface. If entry inhibitors are successful in blocking these proteins, HIV is unable to bind to the surface of T-cells and gain entry into the cells. Only one entry inhibitor has been approved by the U.S. Food and Drug Administration (FDA): Fuzeon™ (T-20). This drug targets the gp41 protein on HIV's surface. Some experimental drugs target proteins on T-cells: BMS-488043 targets the gp120 protein, PRO-542 and TNX-355 target the CD4 protein, and SCH-D, GSK-873,140 and UK-427,857 target the CCR5 protein. HIV-positive people who have become resistant to PIs, NRTIs, and NNRTIs will likely benefit from the entry inhibitors because they are a different class of drugs. This is good news for HIV-positive people who have tried and failed many of the currently approved anti-HIV medications.To learn more on how HIV infects a T-cell and begins to create more viruses, and where each class of anti-HIV drugs blocks this process, click on the following lesson link:The HIV Life Cycle (and the targets of each class of anti-HIV drugs)