Figure 20-1 Immunodeficiency caused by defects in B and T cell maturation.

Primary immunodeficiencies caused by genetic defects in lymphocyte maturation are shown.

These defects may affect T cell maturation alone, B cell maturation alone, or both. CLP, common lymphoid progenitor; DP, double-positive; FoB, follicular B cells; HSC,
hematopoietic stem cell; MZB, marginal zone B cells.

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Figure 20-2 Immunodeficiency caused by defects in B and T cell activation. Primary immunodeficiencies may be caused by genetic defects in molecules required for T or
B lymphocyte antigen receptor signaling, for helper T cell-mediated activation of B cells and APCs, or for activation of cytotoxic T lymphocytes and NK cells. CVID,
common variable immunodeficiency; HLH, hemophagocytic lymphohistiocytosis.

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Figure 20-3 Structure of HIV-1. An HIV-1 virion is shown next to a T cell surface. HIV-1 consists of two identical strands of RNA (the viral genome) and associated
enzymes, including reverse transcriptase, integrase, and protease, packaged in a cone-shaped core composed of p24 capsid protein with a surrounding p17 protein
matrix, all surrounded by a phospholipid membrane envelope derived from the host cell. Virally encoded membrane proteins (gp41 and gp120) are bound to the envelope.
CD4 and chemokine receptors on the host cell surface function as HIV-1 receptors. (© 2000 Terese Winslow.)

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Figure 20-4 HIV-1 genome. The genes along the linear genome are indicated as differently colored blocks. Some genes use some of the same sequences as other
genes, as shown by overlapping blocks, but are read differently by host cell RNA polymerase. Similarly shaded blocks separated by lines indicate genes whose coding
sequences are separated in the genome and require RNA splicing to produce functional mRNA. (Modified from Greene W. AIDS and the immune system. Copyright 1993
by Scientific American, Inc. All rights reserved.)

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Figure 20-5 HIV life cycle. The sequential steps in the life cycle of HIV are shown, from initial infection of a host cell to viral replication and release of a new virion. For the
sake of clarity, the production and release of only one new virion are shown. An infected cell actually produces many virions, each capable of infecting cells, thereby
amplifying the infectious cycle.

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Figure 20-6 Mechanism of HIV entry into a cell. In the model depicted, sequential conformational changes in gp120 and gp41 are induced by binding to CD4. These
changes promote binding of the virus to the coreceptor (a chemokine receptor) and fusion of the HIV-1 and host cell membranes. The fusion peptide of activated gp41
contains hydrophobic amino acid residues that mediate insertion into the host cell plasma membrane.

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Figure 20-7 Progression of HIV infection. The progression of HIV infection correlates with spread of the virus from the initial site of infection to lymphoid tissues
throughout the body. The immune response of the host temporarily controls acute infection but does not prevent the establishment of chronic infection of cells in lymphoid
tissues. Cytokine stimuli induced by other microbes serve to enhance HIV production and progression to AIDS.

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Figure 20-8 Clinical course of HIV disease. A, Plasma viremia, blood CD4+ T cell counts, and clinical stages of disease. About 12 weeks after infection, blood-borne virus
(plasma viremia) is reduced to very low levels (detectable only by sensitive reverse transcriptase-polymerase chain reaction assays) and stays this way for many years.
Nonetheless, CD4+ T cell counts steadily decline during this clinical latency period because of active viral replication and T cell infection in lymph nodes. When CD4+ T
cell counts drop below a critical level (about 200/mm3), the risk for infection and other clinical features of AIDS is high. (From Pantaleo G, C Graziosi, and AS Fauci. New
concepts in the immunopathogenesis of human immunodeficiency virus infection. New England Journal of Medicine 328:327-335, 1993. Copyright © 1993
Massachusetts Medical Society. All rights reserved.) B, Immune response to HIV infection. A CTL response to HIV is detectable by 2 to 3 weeks after the initial infection
and peaks by 9 to 12 weeks. Marked expansion of virus-specific CD8+ T cells occurs during this time, and up to 10% of a patient's CTLs may be HIV specific at 12
weeks. The humoral immune response to HIV peaks at about 12 weeks.
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