Important note: Information in this article was accurate in 1989. The state of the art may have changed since the publication date.
AIDS: IMMUNOPATHOGENESIS AND IMMUNE RESPONSE TO THE HUMAN IMMUNODEFICIENCY VIRUS
AIDS: Etiology, Diagnosis, Treatment, and Prevention. Second Edition. DeVita VT Jr et al, eds. Philadelphia, Lippincott, p. 61-77, 1988.. Unique Identifier : AIDSLINE ICDB/89650900 Koenig A; Fauci AS; Lab. of Immunoregulation, Natl. Inst. of Allergy and Infectious; Diseases, NIH, Bethesda, MD
Abstract:
AIDS is unique among the clinical disorders caused by defects of the immune system. While patients with AIDS may share certain clinical and laboratory features with individuals with primary immunodeficiencies, especially the severe combined immunodeficiencies (SCID), the pathophysiology and spectrum of immunologic defects of AIDS are unparalleled. The etiologic agent of AIDS, HIV, causes a relentless depletion of the helper/inducer subset of T lymphocytes, phenotypically defined by the expression of the CD4 (T4) molecule on their surface, and undermines the generation and regulation of the immune response. The immunopathogenesis of HIV infection is summarized, including quantitative T-cell abnormalities; mechanisms of T4 cell depletion, defects in immune function (T-cells, monocytes and macrophages, B cells and immunoglobulin production, natural killer [NK] cells, and other humoral abnormalities), and immune responses to HIV (neutralizing antibodies, antibody-dependent cellular cytotoxicity, NK cells, and cytotoxic T cells). Except for the infrequent primary immunodeficiencies, and immunologic dysfunction iatrogenically induced by radiation and chemotherapy, the devastation of the immune system by HIV is unprecedented. While the hallmark of the disease is the depletion and functional impairment of T4-lymphocytes with the consequent loss of helper and inducer functions of B cells, T cells, and monocytes in patients with AIDS, many of the functional changes that occur early in the course of HIV infection remain unexplained. The mechanism(s) by which T4-lymphocytes are killed in vivo remains a mystery and may include virally induced cytotoxic and fusogenic processes and autoimmune processes. Although many cell types have been identified that can support the replication of the virus, precise knowledge of the important niches and reservoirs in vivo is lacking. Clearly, this information is critical for devising therapeutic strategies. (198 Refs)
Keywords: Acquired Immunodeficiency Syndrome/*IMMUNOLOGY Cytopathogenic Effect, Viral Cytotoxicity, Immunologic CD4-Positive T-Lymphocytes/IMMUNOLOGY Human HIV/*IMMUNOLOGY/PATHOGENICITY HIV Antibodies/*ANALYSIS/BIOSYNTHESIS HIV Seropositivity/IMMUNOLOGY Immunity, Cellular Interleukin-2/BIOSYNTHESIS Leukocyte Count Receptors, Virus/*IMMUNOLOGY T-Lymphocytes, Suppressor-Effector/IMMUNOLOGY MONOGRAPH REVIEW REVIEW, TUTORIAL
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Important note: Information in this article was accurate in 1989. The state of the art may have changed since the publication date.
