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Color Plates

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Color Plate 1

Schematic representation of gp120 HIV-1, showing disulfide and glycosylation sites. Glycosylation sites containing high-mannose-type and/or hybrid-type oligosaccharides are indicated, as well as the glycosylation sites with complex-type oligosaccharide structures. The variable regions are designated V1 to V5. The conserved regions are designated C1 to C5. Parts of the envelope exposed on the surface and those portions probably occluded by carbohydrates are demonstrated. The CD4 region contains a major attachment site for CD4 (2417). Also noted are other regions on gp120 that, according to studies with amino acid substitutions (3333), appear to be involved in binding to the CD4 molecule (3093). Reprinted from reference 2497 with permission. (See page 11.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 2

Interactions between HIV and the cell surface. (A) HIV interacts with a cell surface receptor, primarily CD4, and through conformational changes becomes more closely associated with the cell through interactions with other cell surface molecules, such as the chemokine receptors CXCR4 and CCR5. Alternatively, some viruses, such as certain strains of HIV-2, could attach to CXCR4 directly. (B to E) The likely steps in HIV infection are as follows. The CD4-binding site on HIV-1 gp120 interacts with the CD4 molecule on the cell surface. Conformational changes in both the viral envelope and the CD4 receptor permit the binding of gp120 to another cell surface receptor, such as CCR5. This attachment brings the viral envelope closer to the cell surface, allowing interaction between gp41 on the viral envelope and a fusion domain on the cell surface. HIV fuses with the cell. Subsequently, the viral nucleoid enters into the cell, most likely by means of other cellular events. Once this stage is achieved, the cycle of viral replication begins. Reprinted from reference 2524 with permission. Copyright © 1996 Massachusetts Medical Society. All rights reserved. (See page 60.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 3

Model of the gp41 transmembrane (TM) protein of HIV-1. A linear sequence of gp41 is shown in a planar projection of the proposed structure derived from computer modeling and based on the influenza virus HA2 scaffold. α-Helices are depicted as modified helical nets alternating three and four amino acids per turn connected by single lines. Hydrophobic amino acids are indicated as solid circles, charged amino acids as open circles, and neutral amino acids as partly filled circles. Nonhelical regions are shown as loosely coiled extended chains; strong turns are indicated by a T, the proposed intramolecular disulfide bond by a double line. Specific functional regions are noted. Figure courtesy of R. Garry. Modified from reference 1412 with permission. (See page 66.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 4

Common structural features of RNA virus fusion proteins. Similar motifs found in representatives of diverse virus families are depicted in “rainbow” order from amino terminus to carboxyl terminus. Each of these class I viral fusion proteins (α-penetrenes) has a fusion peptide (red) at the amino terminus and two extended α-helices (N-helix [orange-] and C-helix [yellow-]), and most have an aromatic rich domain (green) proximal to the transmembrane anchor (indigo). (Based on references 1412 and 1413.) Truncations: HIV gp41 transmembrane (TM) protein C-term; mumps virus F1 after N-helix; sudden acute respiratory syndrome-associated coronavirus (SARS CoV) S N-term. Provided by R. Garry. (See page 66.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 5

Hypothetical mechanism for HIV virion:cell fusion. (A) Binding of HIV-1 SU to the primary receptor (CD4) and coreceptor (chemokine receptor). (B) Rearrangement of the helical domains of TM. The rearrangement allows the putative fusion peptide (red) to interact with the cell plasma membrane. (C) The helical domains of TM “snap back,” bringing the viral and cell membrane in closer proximity and resulting in membrane deformation or “nipple” formation (2009a). Alternatively, the rearrangement of the S2 protein into the six-helix bundle conformation does not result in nipple formation, but rather the virion itself is drawn closer to the cell surface. The fusion peptide, aromatic domain, and transmembrane anchor then constitute a contiguous track of sequences (black outline) that can facilitate the flow of lipid between the two membranes. (D) Six-helix bundle formation drives cellular and viral membrane closer together, resulting in spontaneous hemifusion. Peptide mimics (e.g., T20-like peptides) of the paired helices and/or the aromatic domain blocks six-helix formation in this step or as in panel C. (E) Fusion pore permits cytoplasmic entry of the HIV-1 core. SU, surface gp120 protein; TM, transmembrane gp41 protein. Provided by R. Garry. (See page 66.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 6

HIV:cell fusion. The fusion molecule on the HIV envelope (i.e., gp41) interacts with a fusion receptor (F) on the cell surface (A and B). This process leads to an intermixing of the inner lipid membranes (hemifusion) (C), but unless the outer lipid membranes also undergo intermixing (D), the HIV core cannot enter into the cell cytoplasm. This nucleocapsid entry may also depend on specific viral and cellular factors. Figure derived from a design provided by L. Stamatatos. (See page 68.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 7

An HIV-infected T lymphocyte (HUT 78 cell) shown by immunofluorescence staining fuses with an uninfected HUT 78 T cell. This interaction permits virus transfer to the uninfected cell. Magnification, × 65. Photo courtesy of E. Lennette. (See page 73.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 8

Typical macular-papular rash on the surface of the skin occurring within days after acute (primary) HIV infection. Photograph courtesy of R. Hutt and C. Farling. (See page 79.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 9

HIV infection of lymphoid tissue. Using both in situ DNA and RNA PCR procedures, the presence of HIV infection in cells of the lymph node was evaluated (1193). (A) A large number of cells are infected, as demonstrated by in situ DNA PCR procedures. Note the green grains (designating reaction with the HIV probe) over virus-infected cells. (B) In the same lymph node, evaluated by in situ RNA PCR, only two cells replicating virus particles (dark grains indicate viral RNA) can be detected. It has been estimated that 1 in 300 to 1 in 400 infected cells in the lymph node produce virus (4824). Photomicrographs courtesy of A. Haase. (See page 96.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 10

Histologic section of a colon biopsy sample from an HIV-infected individual with a gastrointestinal disorder. In situ hybridization shows the presence of HIV-1-infected cells in the bowel epithelium. The presence of grains of radioactivity designates reaction of cells with the viral protein. Photomicrograph courtesy of J. Nelson. (See page 98.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 11

Anti-HIV effect of APOBEC3G. APOBEC3G is encapsidated into the virions in the absence of HIV-encoded Vif protein. Following infection, the encapsidated APOBEC3G induces C⟹U deamination at the minus-strand viral DNA during reverse transcription. The C⟹U is converted into a plus-strand G⇒A mutation during plus-strand synthesis. The uracil-containing viral DNA is mostly degraded by cellular enzymes. Vif prevents the encapsidation of APOBEC3G into virions by directing APOBEC3G towards a ubiquitin-dependent degradation pathway. Figure provided by N. Landau. (See page 117.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 12

The HUT 78 T-cell line (pretreated with dye) was mixed with Chinese hamster ovary (CHO) cells expressing the HIV-1 envelope glycoprotein. The resulting fusion between these two cells permitted dye transfer from the T lymphocyte into the CHO cells. Photomicrograph courtesy of C. Weiss. (See page 135.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 13

A superantigen is not processed by cells but can bind directly to either class II molecules or the Vβ portion of the T-cell receptor (see Color Plate 18). This interaction can lead to a nonspecific activation of T cells. Adapted from reference 900 with permission. (See page 147.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 14

Effects of HIV infection on lymphoid tissue. (A) Early stage. Follicular and paracortical hyperplasia can be seen secondary to an increase in the number of germinal centers associated with B-cell proliferation. Paracortical hyperplasia reflects the increase in the number of CD8 cells. (B) Follicular lysis stage. In the early advancement to symptomatic infection, germinal centers break down and follicular dendritic cell death occurs. Eventually, an involution of the germinal centers takes place. (C) Terminal stage. At this stage of infection, lymphoid tissue depletion is noted, with an absence of lymphocytes and a complete disruption of normal lymph node architecture. Photomicrographs courtesy of B. Herndier. (See page 175.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 15

Effects of HIV infection on lymphoid tissue. Panels indicate the changes in the lymph node germinal centers as determined by selective staining (top panels) and by the location of virus replication in lymph node tissue (bottom panels). HIV replication was detected by PCR procedures. The events are reflected for the early, intermediate, and late stages of HIV infection. Data provided by the HIV Information Network; figure derived from reference 3414 with permission from Elsevier. (See page 175.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 16

Signaling through receptors of the innate immune system. Upon interaction with pathogen-associated molecular patterns (PAMPs), pattern recognition receptors (PRRs) initiate signaling cascades leading to activation of transcription factors (such as NF-kB and IRF3), resulting in expression of inflammatory cytokines and other cellular activation events. A simplified pathway highlighting the main elements is shown, with receptors in green, adaptor proteins in yellow, kinases in purple, and transcription factors in blue. Ligation of different Toll-like receptors (TLRs) may induce distinct gene expression patterns (1086). IK, ItB kinase complex; IRAK, IL-1 receptor-associated kinase; IRF, interferon regulatory protein; MyD88, myeloid differentiation factor 88; RICK, receptor-interacting serine/threonine kinase; TAB1/2, TAK1 binding protein; TAK1, transforming growth factor; β-activated kinase; TBK1, TRAF family member-associated NFkB activator binding kinase 1; TIR, Toll-IL-1 receptor domain; TIRAP, TIR domain-containing adaptive protein; TRAF, TNF receptor-associated factor; TRAM, TRIF-related adaptor molecules; TRIF, TIR domain-containing adaptor protein inducing IFN-β. Reprinted with permission from Macmillan Publishers Ltd.: (3433), © 2005. (See page 211.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 17

Neutralizing antibody epitopes on a model of the Env spike of HIV-1 based on the structure of core gp120 (2368, 2369); three gp120 monomers are shown in gray, pale green, and pale blue. gp41 (pink) is shown schematically as three tubes. Carbohydrate chains are shown in yellow, and the oligomannose cluster proposed to interact with monoclonal antibody 2G12 is shown in cyan. Binding sites for other neutralizing monoclonal antibodies are indicated. Figure provided by D. Burton, R. Stanfield, and I. A. Wilson. Reprinted from reference 563 with permission. (See page 241.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 18

(A) Antigen (Ag) presentation to CD4 T cells. An exogenous antigen with various epitopes is endocytosed by an antigen-presenting cell and processed in intracellular vesicles such as acidified endosomes. These vesicles then fuse with other vesicles containing major histocompatibility complex (MHC) class II molecules, which transport the peptide to the cell surface. The antigen is subsequently presented to the CD4 cells through an interaction with the T-cell receptor (TCR) (generally the alpha and beta chains) and the CD4 molecule. (B) Presentation of antigen to CD8 cells. Endogenous antigens expressed by a cell are first processed by proteasomes into small peptides. These molecules are then transported by specific molecules (the TAP transporters) into the endoplasmic reticulum. In this organelle, MHC class I molecules are bound first to calnexin (Csc), a chaperone protein, and then to peptide antigen. Binding of the peptide to the α chain allows for stable interaction with β-microglobulin. The peptide bound to the MHC class I complex is transported through the Golgi complex to the cell surface. From this site, it interacts with the TCR and the CD8 molecule on the CD8 cell surface TAP, transporter associated with antigen processing. Adapted from reference 900 with permission. (See page 261.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 19

Kaposi’s sarcoma in a young HIV-infected man. Note the distribution of the lesions suggesting lymphatic involvement. Figure courtesy of P. Volberding. (See page 295.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 20

Histologic picture of Kaposi’s sarcoma. Magnification, ×100. Photomicrograph courtesy of B. Herndier. (See page 296.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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Color Plate 21

AIN grade 2 lesion observed at analscopy. A 3% acidic solution was applied to the surface of the anal canal. A well-circumscribed lesion that has turned white compared to the normal mucosa (“acetowhite”) is visualized through an anal scope at ×160 magnification. The lesion is smooth and has prominent vacuolization. Reprinted from reference 3388 with permission. (See page 311.)

Citation: Levy J. 2007. Color Plates, In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC.
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