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Chapter 19 : Immunology of AIDS

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Abstract:

Acquired immune deficiency syndrome (AIDS) is a secondary immune deficiency caused by infection with a human retrovirus called human immunodeficiency virus (HIV). HIV infects and kills CD4+ T-helper cells. This causes a profound, irreversible immunosuppression that, without treatment, rapidly progresses from opportunistic infections to death in almost all infected individuals. A critical factor in the progression of HIV infection is the way that HIV manages to subvert or avoid immune defense mechanisms. These mechanisms will be presented in more detail throughout this chapter. The process of immune activation, which is critical for protection against infection, may, in the case of HIV infection, actually serve to activate expression of HIV and accentuate progression of inapparent infection to AIDS. The major problem with the clinical application of polymerase chain reaction (PCR) is the well-known high risk of false-positive results. Loss of delayed-type hypersensitivity (DTH) skin reactivity to standard test antigens is an independent predictor of progression to AIDS in persons with HIV infection. Theoretically, infection with a retrovirus such as HIV could be controlled by interfering with some stage of the life cycle of the virus. The most effective therapy is directed to inhibition of reverse transcriptase (RT) using dideoxynucleosides. A list of the drugs approved by the U.S. Food and Drug Administration for the treatment of AIDS is given in this chapter. A table provides a list of some of the putative immunogens and adjuvants. An example of combination therapy is highly active antiretroviral therapy.

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Figures

Image of Figure 19.1
Figure 19.1

The HIV genome and its products. The HIV genome, its products, and the structure of the virion are related to the proteins identified by Western blot (see Fig. 19.8). The HIV genome consists of two long terminal repeats (LTR), structural (gag, pol, and env) regions, and split segments coding for controlling factors. The gag region codes for internal structural proteins, including nucleic acid binding proteins (p7 and p9), the major structural protein of the nucleoid (p24), and p17, which covers the inner leaflet of the viral envelope. pol codes for reverse transcriptase and other enzymes that are necessary for synthesis, processing, and assembly of virion. env codes for the extracellular (gp120) and transmembrane (gp41) glycoproteins of the virion membrane. vif, rev, tat, and nef code for activating and controlling factors for HIV synthesis (see text).

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.2
Figure 19.2

The HIV replication cycle. HIV replicates by entering the cell, using reverse transcriptase to synthesize complementary DNA copies of virion RNA, which insert into the host genome and then are used as templates for viral RNA synthesis. The integrated DNA may remain inactive for a long time but will be activated to synthesize viral RNA when the infected cell is stimulated to proliferate by mitogens, antigens, allogeneic cells, or other viral infections through transactivating factors. The newly synthesized viral RNA is then assembled into a nucleoid in the cytoplasm, and the virion is formed during budding from the cell, where the external glycoproteins are added along with host cell membrane structures, such as MHC markers. (Modified from D. D. Ho, R. J. Pomerantz, and J. C. Kaplan, N. Engl. J. Med. 317:278–286, 1987.)

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.3
Figure 19.3

Interaction and fusion of HIV with the cell membrane. (A) HIV external proteins gp41 and gp120 contain domains that react with receptors on CD4+ cells. (B) HIV first reacts with cell surface CD4 through a binding site on gp120. This is followed by conformation changes in gp41/120 that allow interaction with other cell surface receptors, such as the chemokine receptors CXCR5 and CCR5. Some strains of HIV-2 can attach directly to CD4 without chemokine receptor interaction. (C) This brings the viral envelope closer to the cell surface, where interaction of a domain on gp41 with a fusion domain on the cell surface results in fusion of the viral capsid with the cell surface membrane, followed by entry of the viral core into the cell cytoplasm. (Modified from J. A. Levy, HIV and the Pathogenesis of AIDS, 2nd ed., ASM Press, Washington, D.C., 1998.)

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.4
Figure 19.4

Cellular transmission of HIV infection. The most likely means of transmission of HIV infection is through HIV-infected CD4+ peripheral blood lymphocytes that enter the body through breaks in the epithelial surface. The infected CD4+ cells are phagocytosed by migratory dendritic cells, which localize in follicles in draining lymph nodes. The infection is passed from the DNA of the lymphocytes to the DNA of the migratory phagocytic cells. Infection may be increased by the presence of FcR, C3bR, and CD4 on the macrophages. During immune activation, the infection is passed to host CD4+ T-helper cells through class II MHC-antigen receptor interactions. During this process, HIV is passed from dendritic antigen-presenting cells to CD4+ T-helper cells, and stimulation of the infected T-helper cells activates virus production (see Figure 19.6). HIV infection eventually causes disintegration of the lymph node structure by destruction of CD4+ T cells and degeneration of follicular dendritic cells.

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.5
Figure 19.5

Natural history of HIV infection. The course of AIDS may begin with an acute febrile illness, during which there is systemic viral infection and a limited period of viral replication that is checked by an effective immune reaction. This is usually followed by a long latent period, followed by AIDS-related complex (ARC) and then full-blown AIDS, signaled by the diagnosis of an opportunistic infection. During the period of asymptomatic infection, HIV sequences may be detected in cells of the macrophage series in tissues by in situ hybridization, and antibody to HIV antigens, in particular anti-gp41 and anti-p24, can be detected during the asymptomatic latent period by Western blotting. Periodic cycles of HIV production at low levels may occur. Progression to ARC is signaled by development of systemic symptoms (e.g., fever, weight loss, and diarrhea), decreased numbers of CD4+ cells in the blood, lymphadenopathy, appearance of HIV antigen in the blood, and falling titers of anti-p24. CD8+ T cells may rise during the acute infection, then remain at stable levels until they also become depleted, but not to the same extent as CD4+ cells. Once ARC is recognized, progression to symptomatic AIDS may occur in a few months or several years. (Modified from D. P. Bolognesi, Microbiol. Sci. 5:236–241, 1988.)

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.6
Figure 19.6

Induction of immunity and immune activation of HIV infection. HIV infects antigen-presenting macrophages. HIV antigens are presented to CD4+ T-helper cells through class II MHC (exogenous processing). HIV antigens are also presented to CD8+ TCTL cells through class I MHC (endogenous processing). In addition, CD4+ cells are infected with viable virus through class II MHC and CD4, a receptor for the gp120 surface antigen of HIV.

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.7
Figure 19.7

Activation of HIV in stimulated lymphocytes. Stimulation of proliferation of HIV-infected T cells activates production of HIV virions. Nuclear activation factors in stimulated lymphocytes (NF-κB and NFAT) form an activation complex with Tat that promotes HIV messenger RNA (mRNA) synthesis and virion assembly, leading to the death of the HIV-infected cell. The insets show the Tat binding region (TAR) and a model of the activation complex. After RNA transcripts initiate, Tat binds to nascent transcripts at TAR. After this, cellular factors are recruited (?) that enhance transcription and/or elongation of the mRNA.

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.8
Figure 19.8

Western blot test for antibody to HIV proteins. HIV antigens are obtained from tissue culture and electrophoresed in a polyacrylamide slab gel; the separated proteins are transferred to a nitrocellulose membrane, and reaction with antibody is identified by a color reaction after incubation with the patient's serum, followed by peroxidase-labeled goat anti-human Ig. Antibodies reacting with the individual identifiable proteins can be detected. The separated antigens are transferred to a nitrocellulose membrane by electrophoretic blotting, and the blot is cut into strips that are incubated with test and control sera. During incubation, antibodies to HIV antigens will react with the antigens in the blot and can be visualized by addition of peroxidase-labeled anti-human immunoglobulin and enzymatic reaction with a colorless substrate that is converted to color. If antibody binds to the proteins on the nitrocellulose strip, a band of color will appear. In this way, antibodies to the different antigens of HIV can be identified.

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.9
Figure 19.9

Epitope map for Env.Hypervariable regions of gp120 appear to be the most likely candidates to provide immunogenic peptides. There are five of these regions, marked V1 to V5. Of these, a segment in the third region from aa 325 to 329 (EnvT3) is not only the immunodominant region with which neutralizing antibody reacts but also the site of one of the epitopes that stimulate proliferation of reactive lymphocytes, as well as a reactive site for CD8+ T-cytotoxic lymphocytes. There are three other T-cell-activating regions: aa 428 to 443 (EnvT1); aa 112 to 124 (EnvT2), and aa 834 to 848 (EnvT4). Of particular importance is EnvT1, because it also contains the CD4 binding site. Immunization of healthy volunteers with these peptides in alum induces in vitro responses measured by IL-2 production on exposure of peripheral blood lymphocytes to the peptide. (Modified from the NIH HIV epitope map and from D. F. Nixon, K. Broliden, G. Ogg, and P.-A. Broliden, Immunology 76:515–534, 1992.) Gray forked symbols indicate complex-type oligosaccharides; blue-green ones represent mannose-rich oligosaccharides.

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.10
Figure 19.10

Vaccination against HIV: a paradox. Antibody to HIV may neutralize the virus (block infection) or increase infectivity by providing aggregated Fcs or binding of C3b that increases adherence and infection of macrophages. CD8+ TCTL cells limit infection by killing virus-infected cells but also reduce the number of CD4 T-helper cells and produce immunosuppression. DTH reactions can activate macrophages to kill intracellular viruses but also stimulate HIV production in infected cells.

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Image of Figure 19.11
Figure 19.11

HIV vaccination and viral evolution. In natural infection, at the end of the asymptomatic stage, a wave of wild-type virus replication may occur in the absence of immunity, leading to the asymptomatic stage. Then specific immunity controls viral replication as new antigenic variants emerge. With development of ARC and AIDS, specific immunity is lost, and the viral load increases rapidly. (From P. Sonigo, M. Girard, and D. Dormont, Immunol. Today 11:465, 1990.)

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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References

/content/book/10.1128/9781555818012.chap19
1. Levy, J. A. 1998. HIV and the Pathogenesis of AIDS, 2nd ed. ASM Press, Washington D.C..
2. AIDS:anInternationalBimonthly Journal. Gower Academic Journals, London, United Kingdom.
3. AIDS Research and Human Retroviruses. Mary Ann Liebert, Inc., New York, N.Y..
4. DeVita, V. T.,, S. Hellman,, and S. A. Rosenberg (ed.). 1997. AIDS: Etiology, Diagnosis, Treatment and Prevention. Lippincott-Raven, Hagerstown, Md..
5. Ioachim, H. L. 1989. Pathology of AIDS. J. B. Lippincott Co., Philadelphia, Pa..
6. Neiburgs, H. E.,, and J. G. Bekesi. 1988. Immune Dysfunctions in Cancer and AIDS. Alan R. Liss, New York, N.Y..
7. Wormser, G. P. (ed.). 1992. AIDS and Other Manifestations of HIV Infection, 2nd ed. Raven Press, New York, N.Y..
8. Gao, F.,, E. Bailes,, D. L. Robertson,, Y. Chen,, C. M. Rodenburg, et al. 1999. Origin of HIV-1 in the chimpanzee Pan troglodytes troglodytes. Nature 397:436441.
9. Gotch, F. 1998. Cross-clade T cell recognition of HIV-1. Curr. Opin. Immunol. 10:388392.
10. Korber, B.,, J. Theiler,, and S. Wolinsky. 1998. Limitations of a molecular clock applied to considerations of the origin of HIV-1. Science 280:18681871.
11. Zhu, T.,, B. T. Korber,, A. J. Nahmias,, E. Hooper,, P. M. Sharp,, and D. D. Ho. 1998. An African HIV-1 sequence from 1959 and implications for the origin of the epidemic. Nature 391:594597.
12. Wong-Staal, F. 1988. Human immunodeficiency virus: genetic structure and function. Semin. Hematol. 25:189196.
13. Wyatt, R.,, and J. Sodroski. 1999. The HIV-1 envelope glycoproteins: fusogens, antigens and immunogens. Science 280:18841888.
14. Emerman, M.,, and M. H. Malin. 1998. HIV-1 regulatory/accessory genes: keys to unraveling viral host cell biology. Science 280:18801884.
15. Lefevre, E. A.,, R. Krzysiek,, E. P. Loret,, P. Galanuaud,, and Y. Richard. 1999. HIV-1 tat protein differentially modulates the B cell response of naive, memory, and germinal center B cells. J. ImmunoI. 163:11191122.
16. Swingler, S.,, A. Mann,, J. Jacque,, B. Brichacek,, V. G. Sasseville, et al. 1999. HIV-1 Nef mediates lymphocyte chemotaxis and activation by infected macrophages. Nat. Med. 5:9971003.
17. Grivel, J.-C.,, and L. B. Margolis. 1999. CCR5- and CXCR4-tropic HIV-1 are equally cytopathic for their T-cell targets in human lymphoid tissue. Nat. Med. 5:344346.
18. Kwong, P. D.,, R. Wyatt,, J. Robinson,, R. W. Sweet,, J. Sodroski,, and W. A. Hendrickson. 1998. Structure of an HIV gp120 envelope glycoprotein in complex with the CD4 receptor and a neutralizing human antibody. Nature 393:648659.
19. Tang, H.,, K. L. Kuhen,, and F. Wong-Staal. 1999. Lentivirus replication and regulation. Annu. Rev. Genet. 33:133170.
20. Baker, E. 1999. CD8+ cell-derived anti-human immunodeficiency virus inhibitory factor. J. Infect. Dis. 179(Suppl. 3):S485S488.
21. Collins, K. L.,, B. K. Chen,, S. A. Kalams,, B. D. Walker,, and D. Baltimore. 1998. HIV-1 Nef protein protects infected primary cells against killing by cytotoxic T lymphocytes. Nature 391:397401.
22. Desrosiers, R. C. 1999. Strategies used by human immunodeficiency virus that allow persistent viral replication. Nat. Med. 5:723725.
23. Reitter, J. N.,, R. E. Means,, and R. C. Desrosiers. 1998. A role for carbohydrates in immune evasion in AIDS. Nat. Med. 4:679684.
24. Stranford, S. A.,, J. Skurnick,, D. Louria,, D. Osmond,, S.-Y. Chang, et al. 1999. Lack of infection in HIV-exposed individuals is associated with a strong CD8(+) cell noncytotoxic anti-HIV response. Proc. Natl. Acad. Sci. USA 96:10301035.
25. Garry, R. F.,, M. H. Witte,, A. A. Gottlieb,, M. Elvin-Lewis,, M. S. Gottlieb, et al. 1988. Documentation of an AIDS virus infection in the United States in 1968. JAMA 260:20852087.
26. Jaffe, H. W.,, D. J. Bergman,, and R. M. Selik. 1983. Acquired immune deficiency syndrome in the United States: the first 1,000 cases. J. Infect. Dis. 148:339345.
27. O’Brien, T. R.,, J. R. George,, and S. D. Holmberg. 1992. Human immunodeficiency virus type 2 infection in the United States. JAMA 267:2775.
28. Cao, Y.,, P. Krogstad,, B. T. Korber,, R. A. Koup,, M. Muldoon, et al. 1997. Maternal HIV-1 viral load and vertical transmission of infection: the Ariel Project for the prevention of HIV transmission from mother to infant. Nat. Med. 3:549552.
29. Peckham, C.,, and D. Gibb. 1995. Mother to child transmission of the human immunodeficiency virus. N. Engl. J. Med. 333:298302.
30. Stahl-Henning, C.,, R. M. Steinman,, K. Tenner-Racz,, M. Pope,, N. Stolte, et al. 1999. Rapid infection of oral mucosal-associated lymphoid tissue with simian immunodeficiency virus. Science 285:12611265.
31. Armstrong, D. 1987. Opportunistic infections in the acquired immune deficiency syndrome. Semin. Hematol. 14:4047.
32. Cameron, P. U.,, P. S. Freudenthal,, J. M. Barker,, S. Gezelter,, K. Inaba,, and R. M. Steinman. 1992. Dendritic cells exposed to human immunodeficiency virus type-1 transmit a vigorous cytopathic infection to CD4+ T cells. Science 257:383387.
33. Daar, E. S.,, T. Moudgil,, R. D. Meyer,, and D. D. Ho. 1991. Transient high levels of viremia in patients with primary human immunodeficiency virus type 1 infection. N. Engl. J. Med. 324:961964.
34. Meltzer, M. S.,, D. R. Skillman,, P. J. Gomatos,, D. C. Kalter,, and H. E. Gendelman. 1990. Role of mononuclear phagocytes in the pathogenesis of human immunodeficiency virus infection. Annu. Rev. Immunol. 8:169194.
35. Sheppard, H. W.,, W. Lang,, M. S. Ascher,, E. Vittinghoff,, and W. Winkelstein. 1993. The characterization of non-progressors: long-term HIV-1 infection with stable CD4+ T-cell levels. AIDS 7:11591166.
36. Brodie, S. J.,, D. A. Lewinson,, B. K. Patterson,, D. Jiyamapa,, J. Keieger, et al. 1999. In vivo migration and function of transferred HIV-1 specific cytotoxic T cells. Nat. Med. 5:3441.
37. Finzi, D.,, M. Hermankova,, T. Pierson,, L. M. Carruth,, C. Buck, et al. 1997. Identification of a reservoir for HIV-1 in patients on highly active antiretroviral therapy. Science 278:12951300.
38. Herbein, G.,, U. Mahlknecht,, F. Batliwalla,, P. Gregersen,, T. Pappas, et al. 1998. Apoptosis of CD8+ T cells is mediated by macrophages through interaction of HIV gp120 with chemokine receptor CXCR4. Nature 395:189194.
39. Mohri, H.,, S. Bonherffer,, S. Monard,, A. S. Perelson,, and D. D. Ho. 1998. Rapid turnover of T lymphocytes in SIV-infected Rhesus macaques. Science 279:12231227.
40. Roquews, P. A.,, G. Gras,, F. Parnet-Mathieu,, A. M. Mabondzo,, C. Dollfus, et al. 1995. Clearance of HIV infection in 12 perinatally infected children: clinical, viral and immunological data. AIDS 9:F19F26.
41. Schmidt, J. E.,, M. J. Kuroda,, S. Santra,, V. G. Sasseville,, M. A. Simon, et al. 1999. Control of viremia in simian immunodeficiency virus infection by CD8+ lymphocytes. Science 283:857860.
42. Cheynier, R.,, S. Gratton,, M. Halloran,, I. Stahmer,, N. L. Letvin,, and S. Wain- Hobson. 1998. Antigenic stimulation by BCG vaccine as an in vivo driving force for SIV replication and dissemination. Nat. Med. 4:421427.
43. Psallidopoulos, M. C.,, S. M. Schnittman,, L. M. Thompson III,, M. Baseler,, A. S. Fauci,, H. C. Lane,, and N. P. Salzman. 1989. Integrated proviral human immunodeficiency virus type I is present in CD4+ peripheral blood lymphocytes in healthy seropositive individuals. J. Virol. 63:46264631.
44. Stellrecht, K. A.,, K. Sperber,, and B. G. T. Pogo. 1992. Activation of human immunodeficiency virus type 1 long terminal repeat by vaccinia virus. J. Virol. 66:20512056.
45. Centers for Disease Control. 1989. Interpretation and use of Western blot assay for serodiagnosis of human immunodeficiency virus type 1 infections. Morb. Mortal. Wkly. Rep. 38(Suppl. S-7):1.
46. Centers for Disease Control. 1992. Unexplained CD4+ T-lymphocyte depletion in persons without evident HIV infection—United States. Morb. Mortal. Wkly. Rep. 41:541.
47. Consortium for Retrovirus Serology Standardization. 1992. Serologic diagnosis of human immunodeficiency virus infection by Western blot testing. JAMA 260:674679.
48. Constantine, N. T.,, J. D. Callahan,, and D. M. Watts. 1992. Retroviral Testing: Essentials for Quality Control and Laboratory Diagnosis. CRC Press, Boca Raton, Fla..
49. Constantine, N. T.,, L. Zekeng,, A. K. Sangare,, L. Gurtler,, R. Saville,, H. Anhary,, and C. Wild. 1997. Diagnostic challenges for rapid human immunodeficiency virus assays. Performance using HIV-1 group O, HIV-1 group M, and HIV-2 samples. J. Hum. Virol. 1:4551.
50. Defer, C.,, H. Agut,, A. Garbatg-Chenon,, M. Moncany,, F. Morinet,, D. Vignon,, M. Mariotti,, and J.-J. Lefrere. 1992. Multicenter quality control of polymerase chain reaction for detection of HIV DNA. AIDS 6:659663.
51. Stute, R. 1988. Comparison in sensitivity of 10 HIV antibody detection tests by serial dilutions of Western blot confirmed samples. J. Virol. Methods 20:269273.
52. Janossy, G.,, B. Autran,, and F. Miedema. 1992. Immunodeficiency in HIV Infection and AIDS. S. Karger, Farmington, Conn..
53. Levy, J. A. 1993. Pathogenesis of human immunodeficiency virus infection. Microbiol. Rev. 57:183289.
54. Blatt, S. P.,, C. W. Hendrix,, C. A. Butzin,, T. M. Freeman,, W. W. Ward, et al. 1993. Delayed-type hypersensitivity skin testing predicts progression to AIDS in HIVinfected patients. Ann. Intern. Med. 119:177184.
55. Wormser, G. P. (ed.). 1992. AIDS and Other Manifestations of HIV Infection. Raven Press, New York, N.Y..
56. Cohen, J. 1999. Cheap treatment cuts HIV transmission. Science 283:916917.
57. Fleury, S.,, R. J. de Boer,, G. P. Rizzardi,, K. C. Wolthers,, S. A. Otto,, C. C. Welborn, et al. 1998. Limited CD4+ T-cell renewal in early HIV-1 infection: effect of highly active antiretroviral therapy. Nat. Med. 4:794801.
58. Gulick, R. M.,, J. W. Mellors,, D. Havlir,, J. J. Eron,, C. Gonzalez, et al. 1998. Simultaneous vs sequential initiation of therapy with indinavir, zidovudine, and lamivudine for HIV-1 infections: 100 week follow-up. JAMA 280:3541.
59. Hellerstein, M.,, M. B. Hanley,, D. Cesar,, S. Siler,, C. Papageorgopoulos,, E. Wieder, et al. 1999. Directly measured kinetics of circulating T lymphocytes in normal and HIV-1-infected humans. Nat. Med. 5:8389.
60. Wong, J. K.,, M. Hezareh,, H. F. Gunthard,, D. V. Havlir,, C. C. Ignacio,, C. A. Spina,, and D. D. Richman. 1997. Recovery of replication-competent HIV despite prolonged suppression of plasma viremia. Science 278:12911294.
61. Desrosiers, R. C. 1988. Simian immunodeficiency viruses. Annu. Rev. Microbiol. 42:607625.
62. Gardner, M. B.,, and P. A. Luciw. 1989. Animal models of AIDS. FASEB J. 3:25932606.
63. Kock, J. A.,, and R. M. Ruprecht. 1992. Animal models for anti-AIDS therapy. Antiviral Res. 19:8169.
64. McCune, J. M.,, R. Namikawa,, H. Kaneshima,, L. D. Schultz,, M. Lieberman,, and I. L. Weissman. 1988. The SCID-hu mouse: murine model for the analysis of human hematolymphoid differentiation and function. Science 241:16321639.
65. Morse, H. C.,, S. K. Chattopadhyay,, M. Makino,, T. N. Fredrickson,, A. W. Hugin,, and J. W. Hartley. 1992. Retrovirus-induced immunodeficiency in the mouse: MAIDS as a model for AIDS. AIDS 6:607621.
66. Schellekens, H.,, and M. Horzinek. 1990. Animal Models in AIDS. Elsevier, New York, N.Y..
67. Boyer, J. D.,, K. E. Ugen,, B. Wang,, M. Agadjanyan,, L. Gilbert,, M. L. Bagarazzi, et al. 1997. Protection of chimpanzees from high-dose heterologous HIV-1 challenge by DNA vaccination. Nat. Med. 3:526532.
68. Cooney, E. L.,, M. J. McElrath,, L. Corey,, S. L. Hu,, A. C. Collier, et al. 1993. Enhanced immunity to human immunodeficiency virus (HIV) envelope elicited by a combined vaccine regimen consisting of priming with a vaccinia recombinant expressing HIV envelope and boosting with gp160 protein. Proc. Natl. Acad. Sci.USA90:18821886.
69. Kennedy, R. C. 1997. DNA vaccination for HIV. Nat. Med. 3:501504.
70. Letvin, N. L. 1998. Progress in the development of an HIV-1 vaccine. Science 280:18751879.
71. Lubeck, M. D.,, R. Natuk,, M. Myagkikh,, N. Kalyan,, K. Aldrich, et al. 1997. Longterm protection of chimpanzees against high-dose HIV-1 challenge induced by immunization. Nat. Med. 3:651658.
72. Phoolcharoen, W. 1998. HIV/AIDS prevention in Thailand: success and challenges. Science 280:18731874.

Tables

Generic image for table
Table 19.1

Human and animal retroviruses

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
Generic image for table
Table 19.2

HIV-activating proteins

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
Generic image for table
Table 19.3

Stages of HIV infection

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
Generic image for table
Table 19.4

Infections associated with AIDS a

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
Generic image for table
Table 19.5

Laboratory tests for AIDS

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
Generic image for table
Table 19.6

Interpretive criteria for Western blot tests a

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
Generic image for table
Table 19.7

Immune dysfunctions in AIDS

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
Generic image for table
Table 19.8

Status of approaches to AIDS therapy

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Table 19.9

Licensed drugs for therapy of HIV a

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Table 19.10

Animal models for AIDS

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
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Table 19.11

Possible approaches to an AIDS vaccine

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19
Generic image for table
Table 19.12

Recombinant HIV vaccine prime-and-boost strategy

Citation: Sell S. 2001. Immunology of AIDS, p 590-627. In Immunology, Immunopathology, and Immunity, Sixth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818012.ch19

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