Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
IMMUNOLOGY OF AIDS AND HIV INFECTION
Retrovirus Biology and Human Disease. Gallo RC, and Wong-Staal F eds. Marcel Dekker, New York, p. 285-316, 1990.. Unique Identifier : AIDSLINE ICDB/91676227 Koenig S; Fauci AS; Natl. Inst. of Allergy and Infectious Diseases, Bethesda, MD
Abstract:
The major advance in AIDS research has been the identification of the etiologic agent of this disorder, sometimes called lymphadenopathy-associated virus (LAV), human T-cell lymphotropic virus III (HTLV-III), AIDS-related virus (ARV), and, most recently, human immunodeficiency virus (HIV). Another human T-cell tropic retrovirus, LAV-2, has been implicated as the cause of AIDS in certain individuals in western Africa. Observations related to immunologic abnormalities detected in patients with AIDS and individuals infected with HIV are reviewed. Topics include the following: T lymphocytes (T-cell subpopulations, in vitro infection of T4 lymphocytes, mechanisms of T-cell depletion, T-cell function [proliferation to antigen and mitogen], and substances suppressing T-cell function), monocytes and macrophages, B cells, natural killer (NK) cells, miscellaneous immunologic defects, and immunity to HIV. Although understanding of the in vivo pathogenesis of AIDS is still fragmented, a model can be constructed based on clinical and laboratory observations on HIV and other lentiviruses. An individual may be infected initially with HIV in several ways, including direct transfer of infected hematopoietic cells or infection of nonhematopoietic cells as a result of sexual contact with an infected individual. The few infected and passaged cells would be sequestered primarily in lymphatic tissue, initiating a primary cellular and humoral immune response. During this response, virions are passaged to other lymphocytes, dendritic cells, and monocytes. After the primary HIV infection, a period of either true viral latency and/or low-level chronic infection occurs in most individuals. Infections with other organisms may precipitate HIV expression. Macrophages infected with various viral diseases will release lymphokines that could activate lymphocytes latently infected with HIV and induce virus replication. Also, coinfection of latently infected monocytes and lymphocytes with other pathogens may contribute to virus propagation. As a consequence of loss of T4 cells, the function of many other cells that require induction by T4 cells is impaired. T8-cell-mediated cytotoxicity, Ig production by B cells, and possibly NK responses are some of the immune functions that are impaired by T4-cell loss. An impaired specific humoral immune response may be a consequence of loss of T4-helper function plus coexisting polyclonal B-cell activation. The generation of polyclonal responses may occur by direct HIV stimulation, through T-cell products, and by other pathogens. (168 Refs)
Keywords: Acquired Immunodeficiency Syndrome/*IMMUNOLOGY B-Lymphocytes/IMMUNOLOGY Cytotoxicity, Immunologic/IMMUNOLOGY Human HIV Infections HIV-1/*IMMUNOLOGY HIV-2/*IMMUNOLOGY Lymphocyte Transformation/IMMUNOLOGY Macrophages/IMMUNOLOGY Monocytes/IMMUNOLOGY Receptors, Interleukin-2/IMMUNOLOGY T-Lymphocytes/IMMUNOLOGY Virus Replication/IMMUNOLOGY MONOGRAPH REVIEW
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Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
