31 fig 82 approaches to anti hiv therapy fusion

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31 Fig 8.2 Approaches to anti-HIV therapy Fusion Inhibitors Integrase Inhibitors Protease Inhibitors Reverse Transcriptase Inhibitors
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32 The History of AZT For many viral diseases therapeutic drugs are the exception rather than the rule Viral diseases effectively prevented by vaccination In 1964, AZT was initially developed as anti-cancer drug = not effective so shelved for 20 years In 1984, Mitsuya and Broder obtained a sample of HIV from Gallo and began testing > 300 drugs Inhibition of HIV infection of human T cell cultures AZT was potent inhibitor at conc. of minimal toxicity to human cells
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33 Reverse Transcriptase Inhibitors (RTI) (A) Reverse Transcriptase (B) Inactive Reverse Transcriptase (C) Mutated Reverse Transcriptase Active site RTI in active site RTI does not fit in active site
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34 How drug resistance emerges in an HIV population
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35 Nucleoside Analogues Thymidine Azidothymidine Azido- group
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36 Properties of AZT that make it a good inhibitor • Binds RT irreversibly = RT is non-functional • Permeable to cells / bind PO 4 gp at 5’ position • Has higher affinity for RT than host cell polymerases • Stability • Administered orally
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37 Figure 08.T03: Benefits and Obstacles to Use of AZT
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38 Action of Reverse Transcriptase Inhibitors (A) Nucleoside Analogue (B) Non-Nucleoside Analogue Nucleoside Analogue is a DNA chain terminator Newly formed HIV DNA Inactivated Reverse Transcriptase Inhibitor
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39 Protease Inhibitors A. Why HIV Protease is essential for HIV Replication B. How HIV Protease Inhibitors inhibit viral protease function Active/cutting site of enzyme
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40 Protease Paunch
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41 Buffalo Hump
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