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      <image:title>News - Can HIV be Cured? - Make it stand out</image:title>
      <image:caption>The human immunodeficiency virus has inspired decades of intensive research into virology, immunology, and vaccines. © iStockphoto</image:caption>
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      <image:title>News - Can HIV be Cured? - Make it stand out</image:title>
      <image:caption>Figure 2. Prevalence, new cases, and deaths from HIV/AIDS Deaths reached a peak in 2005 and 2006 and continue to fall, as do new infections, while the number of people living with HIV continues to rise. (Note: To fit all three metrics on the same graph, the number of people living with HIV has been divided by 10). © IHME, Global Burden of Disease</image:caption>
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      <image:title>News - Can HIV be Cured? - Figure 3. HIV replication cycle This illustration, which we also saw in the Week 2 essay “Viral Life Cycles,” shows the steps by which a HIV viral particle uses a host cell’s machinery to replicate itself. © NIAID</image:title>
      <image:caption>Figure 3. HIV replication cycle This illustration, which we also saw in the Week 2 essay “Viral Life Cycles,” shows the steps by which a HIV viral particle uses a host cell’s machinery to replicate itself. © NIAID</image:caption>
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      <image:title>News - Can HIV be Cured? - Make it stand out</image:title>
      <image:caption>Figure 4. HIV Progression. During the early, acute phase of HIV infection, the virus multiplies rapidly. Multiplication slows as the infection progresses to chronic infection, but as chronic infection progresses, CD4 cells decrease, and the immune system is increasingly damaged, HIV rises again until the disease progresses to AIDS. © NIH</image:caption>
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      <image:title>News - Can HIV be Cured? - Make it stand out</image:title>
      <image:caption>Figure 5. Antiretroviral agents for HIV (A) Entry inhibitors work outside the cell. They prevent HIV from entering the CD4 cell by blocking binding or fusion of HIV with the CD4 cell membrane. If HIV cannot enter the CD4 cell, it is unable to replicate. (B) Non-nucleoside reverse transcriptase inhibitors bind to reverse transcriptase and inhibit the enzyme, stopping HIV replication by preventing formation of HIV DNA. These drugs act in a completely different way from nucleoside/nucleotide analogues. (C) Nucleoside/nucleotide analogues act as false substrate for reverse transcriptase, causing chain termination. The resulting DNA is incomplete and prevents HIV replication. (D) Integrase inhibitors block the integration of HIV and cell DNA. This process prevents HIV replication. (E) Protease inhibitors work at the last stage of the HIV replication cycle. They prevent HIV from being successfully assembled and released from the infected CD4 cell. © NIAID / QPP (adapted by AMNH)</image:caption>
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      <image:title>News - Can HIV be Cured? - Make it stand out</image:title>
      <image:caption>Figure 6. HIV infection and resistance When CCR5-delta32 is present instead of CCR5, the HIV particle is unable to use it to enter the cell, thus protecting the cell against infection. © NIAID (adapted by AMNH)</image:caption>
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      <image:title>News - Can HIV be Cured? - Make it stand out</image:title>
      <image:caption>Figure 7. Cytotoxic T-cells (CTL) A group of killer T-cells (outer three cells) surround a cancer cell (center, blue). All the cells in this image are tagged with fluorescent dyes. Signaling molecules (pink) indicate that the CTLs have found a target. To kill it, they will use cytotoxic chemicals stored in vesicles (red), which they will deliver through the microtubule cytoskeleton (green). © NIH</image:caption>
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      <image:title>News - Can HIV be Cured? - Make it stand out</image:title>
      <image:caption>Figure 8. At work in the Jones lab At left, Brad Jones performs an assay called digital droplet PCR to measure the levels of residual HIV infection in people treated with antiretroviral therapy. At right, Evan McNeil (top), Eva Stevenson (center), and Uche Chukwukere (bottom) isolate and grow cytotoxic T-cells (CTL), which they will use to study mechanisms of CTL resistance. © Brad Jones</image:caption>
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