Immunotherapy for Infectious Diseases

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Gene Therapy for HIV-1 Infection 239 Fig. 1. Life cycle of HIV-1, which is similar to that of all retroviruses studied. HIV-1 attaches to the target cell mainly by binding to the CD4 molecule. After fusion of the viral and cellular membranes, retroviral core particles are released into the cytoplasm. The RNA genome is converted into a double-stranded DNA by the viral reverse transcriptase (RT) and ribonuclease H (RNaseH) and actively transported into the nucleus, probably aided by the viral protein Vpr. The viral DNA is integrated into the genome of the host cell by the viral integrase (in). The integrated DNA form of the virus is called the provirus. In contrast to other retroviruses, transcription and RNA splicing of the provirus is regulated by viral accessory proteins. For example, the viral protein Tat must bind to a specific sequence in the HIV genome (termed TAR) to enable highly efficient transcription of the provirus. Rev is required to control RNA splicing and the transport of RNAs into the cytoplasm. Finally, in the cytoplasm, virus core particles are assembled by encapsidating full-length genomic viral RNAs (recognized by specific encapsidation sequences). At the cell membrane, virus particle assembly is completed by the interaction of the core with the viral membrane proteins, and new particles “bud” (are released) from the infected cell. For more details regarding regulatory proteins, see also Figure 5. Env, envelope; ER, endoplasmatic reticulum. fourth criteria, is that the antiviral agent has to be tolerated by the immune system. It would not make much sense to endow immune cells with an antiviral agent that elicits an immune response against itself, leading to the destruction of the HIV-1-resistant cell after a short period.
240 Dornburg and Pomerantz Fig. 2. Overview of possible genetic targets to block HIV-1 replication. The different approaches are described in detail in the text. GENETIC ANTIVIRALS TO BLOCK HIV-1 REPLICATION Protein-Based Inhibitors Transdominant Negative Mutant Proteins Replication of the HIV-1 virus depends on several regulatory proteins. Replication, however, is greatly impaired when certain mutant forms of such proteins are present. Thus, mutant viral proteins have been used to block HIV-1 replication. Transdominant (TD) negative mutants still bind to their targets but are unable to perform their actual function. They compete with the corresponding native, wild-type protein inside the cell and greatly reduce virus replication, especially when they are expressed from strong promoters (e.g., the cytomegalovirus immediate early promoter [CMV-IE]) (1).
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Immunotherapy for Infectious Diseas
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In f e c t i o u s . D i s e a s e
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© 2002 Humana Press Inc. 999 River
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vi Preface I am grateful to all of
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viii Contents 11 Passive Immunother
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x Contributors BARBARA G. MATTHEWS,
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From: Immunotherapy for Infectious
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Humoral Immunity 5 Fig. 1. Humoral
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Humoral Immunity 7 Table 1 Properti
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Humoral Immunity 9 minal complement
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Humoral Immunity 11 ficity. In ligh
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Humoral Immunity 13 Fig. 7. VDJ joi
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Humoral Immunity 15 Fig. 9. Messeng
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Humoral Immunity 17 In contrast to
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Humoral Immunity 19 advantage to tr
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Humoral Immunity 21 32. Allman DM,
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Some Basic Cellular Immunology Prin
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Cellular Immunology Principles 25 i
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Cellular Immunology Principles 27 s
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Cellular Immunology Principles 29 d
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Cellular Immunology Principles 31 f
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Cellular Immunology Principles 33 F
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Cellular Immunology Principles 35 R
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Cellular Immunology Principles 37 1
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INTRODUCTION Immune Defense at Muco
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Immune Defense at Mucosal Surfaces
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II Molecular Basis for Immunotherap
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64 Kunert and Katinger IMMUNOGLOBUL
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66 Fig. 2. Monomeric, dimeric, and
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68 Kunert and Katinger Fig. 4. Humo
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70 Kunert and Katinger remove prote
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72 Kunert and Katinger Fig. 6. Diff
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74 Kunert and Katinger persons of a
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76 Kunert and Katinger that so-call
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78 Kunert and Katinger whereas sele
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80 Kunert and Katinger Different pr
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82 Kunert and Katinger HUMAN/MOUSE
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84 Kunert and Katinger are expresse
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86 Kunert and Katinger missing meta
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88 Kunert and Katinger Fig. 8. Sche
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90 Kunert and Katinger include a se
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92 Kunert and Katinger 32. Lee S, e
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94 Kunert and Katinger 72. Abbs IC,
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96 Kunert and Katinger 117. Wright
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Dendritic Cells 101 several organis
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Dendritic Cells 103 tion that infec
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Dendritic Cells 105 chaperones such
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Dendritic Cells 107 CD8� CTLs, th
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Dendritic Cells 109 complete tumor
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Dendritic Cells 111 19. Holland SM,
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Dendritic Cells 113 mouse pneumonit
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Dendritic Cells 115 dendritic cells
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INTRODUCTION Cytokines, Cytokine An
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Cytokines, Cytokine Antagonists, an
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Principles of Vaccine Development F
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Principles of Vaccine Development 1
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INTRODUCTION Immunopathogenesis of
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Immunopathogenesis of HIV Disease 1
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164 Connick counts ranged from 73 t
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166 Connick retinitis in an individ
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168 Connick A novel method of ident
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170 Connick occurs quite early in i
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172 Connick 2. Delta Coordinating C
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174 Connick 39. Hurni MA, Bohlen L,
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176 Connick 76. Dolan M.J., Clerici
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178 Connick 114. Komanduri KV, Visw
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Active Immunization for HIV Infecti
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Page 211 and 212: 200 Jacobson changes of gp120 alter
Page 213 and 214: 202 Jacobson is reduced (54,55). A
Page 215 and 216: 204 Jacobson Table 2 Potential Prot
Page 217 and 218: 206 Jacobson from the SIV/17E-Cl-in
Page 219 and 220: 208 Jacobson Several groups have de
Page 221 and 222: 210 Jacobson HUMAN STUDIES Polyclon
Page 223 and 224: 212 Jacobson clinical isolates, whi
Page 225 and 226: 214 Jacobson 22. Beasley RP, Hwang
Page 227 and 228: 216 Jacobson 59. Yoshiyama H, Mo H,
Page 229 and 230: 218 Jacobson 95. Prince AM, Reesink
Page 231 and 232: 220 Jacobson 133. Stiehm ER, Lamber
Page 233 and 234: 222 Kilby and Bucy Although clinica
Page 235 and 236: 224 Kilby and Bucy can infect human
Page 237 and 238: 226 Kilby and Bucy the proinflammat
Page 239 and 240: 228 Kilby and Bucy CD3/CD28, and th
Page 241 and 242: 230 Kilby and Bucy of viral replica
Page 243 and 244: 232 Kilby and Bucy 21. Cao Y, Qin L
Page 245 and 246: 234 Kilby and Bucy 64. Pantaleo G,
Page 247 and 248: 236 Kilby and Bucy 101. Clements-Ma
Page 249: 238 Dornburg and Pomerantz cells (5
Page 253 and 254: 242 Dornburg and Pomerantz domains
Page 255 and 256: 244 Dornburg and Pomerantz GENETIC
Page 257 and 258: 246 Dornburg and Pomerantz Fig. 5.
Page 259 and 260: 248 Dornburg and Pomerantz 6. Balti
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Page 264 and 265: Viral Infections Other than HIV 253
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Page 288 and 289: Bacterial Infections and Sepsis 277
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Page 295 and 296: 284 Wallis and Johnson replication
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290 Wallis and Johnson peripheral b
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292 Wallis and Johnson (A. Hise and
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294 Wallis and Johnson infections,
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296 Wallis and Johnson 37. Boom WH.
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298 Wallis and Johnson 77. Ellner J
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300 Wallis and Johnson 113. Raad I,
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302 Wallis and Johnson 154. Anonymo
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304 Table 1 Major Fungal Infections
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306 Casadevall species suggest that
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308 Casadevall transfusions from G-
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310 Casadevall Table 3 Augmentation
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312 Casadevall There has been some
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314 Casadevall effective in achievi
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316 Casadevall CONCLUSION AND FUTUR
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318 Casadevall 16. Boutati EI, Anai
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320 Casadevall 52. Gallin JI, Malec
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322 Casadevall 91. Kowanko IC, Ferr
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324 Index Blastomycosis, see Fungal
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326 Index C-type retrovirus vectors
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328 Index K Klebsiella, intravenous
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330 Index Vaccine Recombinant vecto
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Infectious Disease IMMUNOTHERAPY FO
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