The immune response is an essential part of the pathogenesis of most virus diseases. Infiltration of lymphocytes and macrophages, with accompanying release of cytokines and inflammation, is a regular feature of viral infection. Such common signs as fever, erythema, edema, and enlargement of lymph nodes have an immunologic basis. In some viral diseases the cardinal manifestations are attributable to the body's immune response. When pathologic
changes are ameliorated by immunosuppressive treatment, it can be assumed that immunopalhology makes an important contribution to the disease
For most viral infections it is not known whether immunopalhology makes a significant contribution to disease, and, if so, which particular immunologic mechanisms are implicated; nevertheless, it is instructive to speculate about their possible involvement. Immunopathologic mechanisms are traditionally classified into hypersensitivity reactions of types 1, II, III, and IV. Although advances in cellular immunology have blurred some of the distinctions, the classification is still convenient.
Type I—Anaphylactic Hypersensitivity
Type I hypersensitivity reactions depend on the interaction of antigens with IgE antibodies attached to the surface of mast cells and basophils via Fc receptors, resulting in the release of histamine, leukotrienes and heparin, and the activation of serotonin and plasma kinins Except for its possible contribution to some types of rashes and in some acute respiratory infections such as respiratory syncytial virus bronchiolitis, anaphylaxis is probably not particularly important in viral immunopathology.
Type II—Antibody-Dependent Cytotoxic Hypersensitivity
Type II cytolytic reactions occur when antibody, having combined with viral antigen on the surface of infected cells, activates the complement system, leading to cell lysis. Alternatively, binding of antibodies can sensitize virus-infected cells to destruction by Fc receptor-carrying K (killer) cells, polymorphonuclear leukocytes, or macrophages, via antibody-dependent cell-mediated cytotoxicity (ADCC). Although it has been clearly demonstrated that virus-infected cells are readily lysed by all of these mechanisms in mtro and there is some evidence that they may be operative in certain herpesvirus infections, the relative importance of antibody-dependent cytotoxic hypersensitivity in viral diseases in vivo is unclear.
Type HI—Immune Complex-Mediated Hypersensitivity
Antigen-antibody reactions cause inflammation and cell damage by a variety of mechanisms. If the reaction occurs in extravascular tissues there is edema, inflammation, and infiltration of polymorphonuclear leukocytes, which may later be replaced by mononuclear cells This is a common cause of mild inflammatory reactions. These immune complex reactions constitute the classic Arthus response and are of major importance, especially in persistent viral inlections. If they occur in the blood, they produce circulating immune complexes, which are found in most viral infections. The fate of the immune complexes depends on the ratio of antibody to antigen If there is a large excess of antibody, each antigen molecule is covered with antibody and removed by macrophages, which have receptors for the Fc component of the antibody molecule. If the amounts of antigen and antibody are about equal, lattice structures which develop into large aggregates are formed and removed rapidly by the reticuloendothelial system. However, in antigen excess, as occurs in some persistent infections, when viral antigens and virions are continuously released into the blood but the antibody response is weak and the antibodies are of low avidity or nonneutralizing, complexes continue to be
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