Neutralization of Sensitized Virus by Purified Components of Complement
01 Mar 1970-Proceedings of the National Academy of Sciences of the United States of America (National Academy of Sciences)-Vol. 65, Iss: 3, pp 528-535
TL;DR: Herpes simplex virus which had been sensitized with immunoglobulin M antibody was neutralized by serum deficiencies in the fifth and sixth components of complement (C) but not by serum deficient in the fourth component C (C4).
Abstract: Herpes simplex virus which had been sensitized with immunoglobulin M antibody was neutralized by serum deficient in the fifth and sixth components of complement (C) but not by serum deficient in the fourth component C (C4). The sequential addition of the functionally purified components of C showed that the activated first component of C (C1[unk]) failed to neutralize sensitized virus. However, in the presence of an optimal concentration of C1[unk], the addition of C4 resulted in neutralization. The amount of virus neutralized was dependent upon the concentration of immunoglobulin M used to sensitize the virus and the concentration of C1[unk] and C4. The addition of the second component of C (C2) to reaction mixtures containing an optimal concentration of C1[unk] and a limiting concentration of C4 resulted in increased neutralization and the amount of virus neutralized was dependent upon the concentration of C2. The addition of the third component of C (C3) to reaction mixtures containing an optimal concentration of C1[unk] and limiting concentrations of C4 and C2 also resulted in increased neutralization and the amount of virus neutralized was dependent upon the concentration of C3.
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TL;DR: This chapter summarizes the data presented in two reviews of experimental acute and chronic immune complex disease produced by nonliving antigens and discusses in detail more recent studies.
Abstract: Publisher Summary No experimental model has provided greater insight into the mechanism of immune complex disease than the experimental serum sickness. The morphological, immunohistological, and serological features of the laboratory models have provided a basis for understanding the pathogenic mechanisms responsible for human glomerulonephritis, vasculitis, and a variety of systemic connective tissue diseases. The subject of experimental acute and chronic immune complex disease produced by nonliving antigens has received extensive review in this series. This chapter summarizes the data presented in these two reviews and discusses in detail more recent studies. Experiments to study acute immune complex disease (serum sickness) have been performed in rabbits almost exclusively. Experimental chronic immune complex disease has proved to be a most useful model in understanding human glomerulonephritis. When injected daily with heterologous serum protein antigens, rabbits with strong antibody responses develop chronic membranous glomerulonephritis in about 5 weeks.
539 citations
TL;DR: A large number of these abnormalities are related to Epstein-Barr virus infection, and the use of chemotherapy to correct these problems is a natural progression of disease.
Abstract: Acquired Abnormalities Alterations in the complement system associated with human disease have been appreciated since early in this century,152 but only within recent years have measurements of ser...
329 citations
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09 Jul 1993TL;DR: In this paper, the authors describe the immunoglobulin G neutralization mechanism which operates after attachment of the virus-antibody complex to a cell Receptor Unit. But, they do not discuss the role of the cell in neutralization.
Abstract: 1 Introduction.- 2 Immunoglobulin G Neutralization by Inhibition of Attachment of Virus to the Cell.- 3 Immunoglobulin G Neutralization Which Does Not Inhibit Attachment of Virus to the Cell.- 4 Immunoglobulin G Neutralization by Aggregation of Virions . ..- 5 Immunoglobulin G Neutralization Mechanisms which Operate After Attachment of the Virus-Antibody Complex to a Cell Receptor Unit.- 5.1 Inhibition of Fusion at the Plasma Membrane.- 5.2 Inhibition of Endocytosis.- 5.3 Inhibition of Fusion of Viral and Cellular Membranes.- 5.4 Inhibition of Non-fusion Uncoating.- 5.5 Inhibition of Events which Occur After Primary Uncoating.- 6 Neutralization which Occurs by Virus Binding Antibody After It Has Attached to a Cell.- 7 Role of the Cell in Neutralization.- 8 Antibody-Dependent Enhancement of Infectivity by Neutralizing Antibody: Fc and Complement Receptors.- 9 Neutralization by Polymeric Immunoglobulin A.- 10 Neutralization by Immunoglobulin M.- 11 The Relevance of Immunoglobulin Isotype to Neutralization.- 12 Viral Carbohydrates, Proteins and Neutralization.- 12.1 Carbohydrates and Neutralization.- 12.2 Proteinsand Neutralization.- 13 Properties of Protein and Peptide Antigens Which Elicit Neutralizing Antibody.- 14 Neutralization In Vivo.- 15 Complement and Neutralization.- 16 Neutralization by Inhibition of Release of Progeny Virus from the Infected Cell.- 17 Changes in Virus Proteins and Virion Structure on Binding Antibody, Including Synergistic Neutralization.- 18 Reversibility of Neutralization.- 19 Neutralization by Fragments of Antibody.- 20 Quantitative Aspects of Neutralization.- 21 Unconventional Neutralization.- 21.1 Genetic Engineering of Antibodies and Viruses.- 21.2 Anti-idiotype Antibodies and Neutralization.- 22 The Evolutionary Significance of Neutralization Sites.- 22.1 Why Do Viruses Have Neutralization Sites?.- 22.2 Strategies which Avoid or Minimize Expression of, or Response, to Neutralization Sites.- 22.2.1 Relating to the Virus Particle.- 22.2.2 Relating to the Immune System.- 23 Neutralization of Poliovirus and Rhinovirus: A Summary.- 23.1 Introduction.- 23.2 Attachment.- 23.3 Internalization.- 23.4 Post-internalization.- 23.5 Aggregation.- 23.6 Conformational Changes on Binding Antibody.- 24 Neutralization of Type a Influenza Virus by Immunoglobulins M, A and G: A Summary.- 24.1 Introduction.- 24.2 IgM Neutralization.- 24.3 IgA Neutralization.- 24.4 IgG Neutralization.- 24.5 Discussion.- 25 Neutralization of HIV-1: A Summary.- 26 Conclusions.- References.
184 citations
TL;DR: Bipolar bridging was shown to occur even when small concentrations of immune IgG were present in physiologic concentrations of nonimmune IgG, which provides insight into the role of the HSV-1 FcR in pathogenesis and may help explain the function of F cR detected on other microorganisms.
Abstract: We describe a novel function of the Fc receptor of herpes simplex virus type 1 (HSV-1), its ability to participate in antibody bipolar bridging. This refers to the binding of a single immunoglobulin G (IgG) molecule by its Fab end to its antigenic target and by its Fc end to an Fc receptor (FcR). We demonstrate that various immune IgG antibodies, including polyclonal rabbit antibodies to HSV-1 glycoproteins gC1 and gD1 and monoclonal human antibody to gD1 blocked rosetting of IgG-coated erythrocytes at IgG concentrations 100- to 2,000-fold lower than required for rosette inhibition with nonimmune IgG. Steric hindrance did not account for the observed differences between immune and nonimmune IgG since rabbit anti-gC1 F(ab')2 fragments did not block rosetting. Murine anti-gC1 or anti-gD1 IgG, a species of IgG incapable of binding by its Fc end to the HSV-1 FcR, also did not block rosetting. When cells were infected with a gC1-deficient mutant, anti-gC1 IgG inhibited rosetting to the same extent as nonimmune IgG. This indicates that binding by the Fab end of the IgG molecule was required for maximum inhibition of rosetting. Bipolar bridging was shown to occur even when small concentrations of immune IgG were present in physiologic concentrations of nonimmune IgG. The biologic relevance of antibody bipolar bridging was evaluated by comparing antibody- and complement-dependent virus neutralization of an FcR-negative mutant and its parent HSV-1 strain. By engaging the Fc end of antiviral IgG, the parent strain resisted neutralization mediated by the classical complement pathway. These observations provide insight into the role of the HSV-1 FcR in pathogenesis and may help explain the function of FcR detected on other microorganisms.
172 citations
Cites background from "Neutralization of Sensitized Virus ..."
...Complement enhances HSV neutralization by antibody (12, 53, 56, 57)....
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01 Jan 1980
160 citations