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Chapter 10 : Humoral Immune Responses to HIV Infection

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Humoral Immune Responses to HIV Infection, Page 1 of 2

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Abstract:

This chapter describes four processes involving circulating antibodies that react against HIV and HIV-infected cells: neutralizing antibodies, antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cytotoxicity (ADC), and complement binding antibodies. The evolution of antibody responses in HIV infection begins with the early presence of antibodies to the Gag protein followed by Nef, Rev, and finally Env. Generally neutralization by IgG is higher than that by IgA. The HIV envelope is the major target for such humoral antibody responses. The viral proteins primarily involved in antibody neutralization have been localized to the envelope gp120 and the external portion of the transmembrane envelope protein, gp41. Enhancing antibodies were recognized during evaluation of sera for neutralizing activity against HIV. Two types of antibody-dependent enhancement (ADE) were detected: complement mediated and Fc mediated. Both involve binding of antiviral antibodies to the virion and infection of cells by this immune complex via the complement or Fc receptor. Antibodies (primarily IgG1 isotypes) to both the gp120 and gp41 envelope proteins induce ADCC. Some studies have indicated that certain neutralizing and non-neutralizing antibodies can lyse HIV via complement fixation. With neutralizing antibodies, the antiviral titer can sometimes be increased up to 10-fold by the addition of high levels of complement to the assay. Since HIV disturbs the balance of the immune system, it is not surprising that autoimmune disorders can accompany this viral infection. Vasculitis has been linked in HIV infection to immune complexes, but immune complex glomerulonephritis is not commonly found.

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10

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Figures

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Figure 10.1

Mechanism of antibody-dependent enhancement of HIV infection. The antiviral antibody binds to the viral envelope glycoprotein. This virus-antibody complex can then enter cells (T cells and macrophages shown here) through an interaction of the Fc portion of the antibody with either the cellular Fc receptor or the complement receptor (after complexing with complement). Reprinted from reference 2519 with permission.

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
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Image of Figure 10.2
Figure 10.2

Neutralization or enhancement of infection by sequential homotypic HIV-1 isolates. HIV-1 strains recovered from the same individual were tested for enhancement or neutralization by the corresponding sera obtained early or late in the infection. The sera were evaluated at fivefold dilutions (1:10 to 1:1,250). Normal control serum was used at similar dilutions. The clinical status of the individual at the different time points is indicated (ARC, AIDS-related complex). The extent of neutralization is shown below the bar; the enhancement index (EI) is shown above the bar. The response is defined as the ratio of the viral reverse transcriptase activity in supernatants of cultures receiving virus preincubated with homotypic serum to that in supernatants of cultures receiving virus preincubated with control serum. Modified from reference 1881.

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
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Image of Figure 10.3
Figure 10.3

The V3 loop in virus-antibody neutralization versus enhancement. Using a monoclonal antibody to a small epitope in the HIV-1 V3 loop, differences in response of various virus strains can be appreciated. Some are neutralized (Neut.), others are enhanced (Enhan.), and still others are resistant (Resist.). As demonstrated, only one amino acid change appears to affect the serologic response, but the results are strain specific. If the amino acid is modified by site-directed mutagenesis (arrows), the mutant virus appears to become resistant. Data from reference 2239.

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
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Image of Figure 10.4
Figure 10.4

The V loop of HIV-1 with the amino acid substitutions (present on HIV-1) that make this strain neutralizable by an anti-HIV-1 monoclonal antibody (see Figure 10.3 ).

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
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Image of Figure 10.5
Figure 10.5

Mechanisms for neutralization versus enhancement. The concept is proposed that neutralization involves a strong binding of antibody to the viral envelope with the subsequent removal of gp120, resulting in virus inactivation. Enhancement would involve binding to the virus without removal of the envelope glycoprotein. Conformational changes would subsequently occur that enhance infection by the virus, presumably via virus:cell fusion.

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
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Image of Figure 10.6
Figure 10.6

HIV molecular mimicry and autoimmunity. If the viral envelope protein has a similarity to an MHC domain (class I or II), antibodies to this portion of the viral envelope could induce an anti-MHC reaction at the cell surface even with uninfected cells.

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
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Image of Figure 10.7
Figure 10.7

Possible mechanisms for autoimmune responses in HIV infection. HIV infection of T cells could lead to T-cell disorders (step 1), with subsequent loss of T-cell control of B-cell proliferation. Similarly, infection of macrophages by HIV could lead to enhanced production of IL-6, with resultant B-cell proliferation (step 2). B-cell proliferation could eventually lead to lymphomas through chromosome changes and establishment of a transformed state (see Chapter 12). The presence of cellular antigens on the surface of HIV virions or expressed together with viral antigens on the cell surface (step 3) might induce immune responses (e.g., antibodies) against normal cellular antigens (step 3) in a carrier-hapten fashion (2612) (step 4), leading to autoimmune cellular reactions. Antiviral responses by B cells could also lead to autoantibodies through molecular mimicry (step 5) ( Table 10.6 ). By this phenomenon, viral proteins may resemble normal cellular proteins sufficiently to cause an autoimmune response against these cellular components.

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
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References

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Tables

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Table 10.1

Regions of HIV sensitive to antibody neutralization

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
Generic image for table
Table 10.2

Neutralization of HIV-1 infectivity by anti-HIV-1 sera

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
Generic image for table
Table 10.3

Factors influencing virus sensitivity to neutralization

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
Generic image for table
Table 10.4

Autoantibodies detected in HIV infection and associated clinical condition

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
Generic image for table
Table 10.5

Potential mechanisms for induction of autoimmunity by retroviruses

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10
Generic image for table
Table 10.6

Regions of HIV that resemble normal cellular proteins

Citation: Levy J. 2007. Humoral Immune Responses to HIV Infection, p 237-258. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch10

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