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Document 3 Retroviral Integrase: Structure as a Foundation for Drug Design Alison B. Hickman and Fred Dyda National Institutes of Health, Bethesda, Maryland I. Introduction A. Retroviral Lifecycle Page 83 The human immunodeficiency virus (HIV) is one of only a few retroviruses known to infect humans. It is estimated that approximately twenty-two million people are now infected worldwide [1]. With only a tiny number of exceptions, infection ultimately leads to the development of the lethal condition of acquired immunodeficiency syndrome, or AIDS. To date, only a handful of drugs have been shown to have any effect on the course of the disease. These are, in general, relatively ineffective at significantly prolonging life, and drug resistance develops rapidly. Equally discouraging, vaccines have not yet been developed to prevent infection. The retroviral lifecycle presents several steps that can be targeted as possible sites of intervention by inhibitors. As shown in Figure 1, when a retrovirus encounters a host cell, specific recognition between proteins on the surface of the virus and receptors on the host cell surface leads to membrane fusion. The viral core then enters the cell cytoplasm where the process of reverse transcription begins. The requirement of the conversion of viral RNA to double-stranded DNA is a feature unique to retroviruses. With the recent exception of the protease inhibitor saquinavir, ritonavir, and indinavir, the drugs approved to date by the U.S. Food and Drug Administration (FDA) for the treatment of HIV infection have been nucleoside analogs targeted against the viral enzyme that carries out this conversion, reverse transcriptase. http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_83.html [4/5/2004 4:53:30 PM]
Document Figure 1 Retroviral lifecycle as summarized in Reference 67. Reprinted by permission of Springer-Verlag Publishing Co., New York, NY. Page 84 Although details of the timing of reverse transcription, nuclear localization, and integration are not yet clear, it is generally recognized that the movement of double-stranded viral DNA across the nuclear membrane is followed by insertion, or integration, of the viral genome into a host-cell chromosome. The viral DNA moves as part of a larger “preintegration complex,” a high-molecular-weight aggregate whose composition has not yet been completely defined. The end result of integration is the incorporation of the viral DNA into the DNA of the host cell. Once there, the provirus can serve as a template for the production of mRNA, allowing for the synthesis of viral proteins. These are assembled at the cell membrane to produce new viral particles, which then bud off to seek out new cells to infect. The integrated viral DNA is also necessarily copied whenever the host cell undergoes cell division. The insidious nature of http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_84.html (1 of 2) [4/5/2004 4:54:27 PM]
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Page 67 and 68: Document Page 54 Table 2) [12,54].
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Page 81 and 82: Document Page 67 Biochemical data s
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Page 85 and 86: Document Chris Tantillo. The work i
Page 87 and 88: Document Page 72 16. Goldman ME, Nu
Page 89 and 90: Document 30. Coffin JM. HIV populat
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Page 103 and 104: Document dine) and didanosine (dide
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Page 137 and 138: Document when metals are bound. Fin
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Page 149 and 150: Document 4 Bradykinin Receptor Anta
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Document D ddI, 152 tumour necrosis
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Document antistasin peptides, 281 c
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Document Phosphoglycerate kinase (P
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Document [Protease targets] serinyl
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