Important note: Information in this article was accurate in 1985. The state of the art may have changed since the publication date.
VIRUSES, IMMUNE DYSREGULATION, AND ONCOGENESIS: INFERENCES REGARDING THE CAUSE AND EVOLUTION OF AIDS
AIDS. The Epidemic of Kaposi's Sarcoma and Opportunistic Infections. Friedman-Kien AE, Laubenstein LJ, eds. New York, Masson, p. 7-21, 1984.. Unique Identifier : AIDSLINE ICDB/85610684 Levine AS; National Inst. of Child Health and Human Development, NIH,; Bethesda, MD 20205
Abstract:
The roles of immunologic dysfunction and viral infections in the development of the Acquired Immune Deficiency Syndrome (AIDS) are discussed in this article. The weight of the evidence favors the hypothesis that a single transmissible viral agent causes the immune dysfunction of AIDS. This dysfunction is characterized by depletion and dysfunction of T-helper cells; a relative increase in the number of T-suppressor cells; polyclonal B-cell hyperactivity (PBH); diminished activity of natural killer cells and macrophages; defective interferon induction; circulating alpha-1-thymosin; anti-sperm antibodies; a soluble inhibitory factor; and a graft versus host diathesis. Because the T-helper cell is central to normal immune function, a defect in this cell is hypothesized to be the principle abnormality in AIDS. Numerous virus groups are known to cause nonspecific immune modulation. Cytomegaloviruses cause T-suppressor proliferation and PBH. Epstein-Barr virus causes PBH, secondary T-suppressor proliferation, and autoantibody production. Retroviruses suppress lymphocyte activity, enhance T-suppressor cells and induce neutralizing antibodies. Among these, human T-cell leukemia virus (HTLV) and murine leukemia virus interact specifically with the T-helper population. Hepatitis B virus decreases suppressor cell levels and is not immunosuppressive. A parvovirus may be the AIDS agent, since these viruses mutate frequently and cross species barriers, and since some are specific for T-cells. Successive viral infections have been hypothesized to account for T-helper cell defects and secondary epiphenomena. Implications of the congenital immune deficiency syndromes for AIDS also are discussed. Among renal transplant recipients, decreases in the ratio of helper to suppressor cells are associated with opportunistic infections and Kaposi's sarcoma, while increases in this ratio are associated with early graft rejection. Immune dysfunction is hypothesized to permit tumor growth because of deficient surveillance; secondary B-cell proliferation; autoantibody production; or induction of oncogenes. (87 Refs)
Keywords: Acquired Immunodeficiency Syndrome/COMPLICATIONS/*IMMUNOLOGY Animal Antibody Formation B-Lymphocytes/IMMUNOLOGY Female Herpesviridae Infections/IMMUNOLOGY Human Immunity, Cellular Immunologic Deficiency Syndromes/CONGENITAL/COMPLICATIONS/ IMMUNOLOGY Kidney/TRANSPLANTATION Kidney Transplantation Lymphoma/*COMPLICATIONS/IMMUNOLOGY Male Phenotype Retroviridae Infections/IMMUNOLOGY Sarcoma, Kaposi's/*COMPLICATIONS/IMMUNOLOGY T-Lymphocytes/IMMUNOLOGY Transplantation Immunology Tumor Virus Infections/*IMMUNOLOGY MEETING PAPER REVIEW
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Important note: Information in this article was accurate in 1985. The state of the art may have changed since the publication date.
