Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
THE IMMUNE SYSTEM: PATHOPHYSIOLOGY
The Epidemiology of AIDS: Expression, Occurrence, and Control of Human Immunodeficiency Virus Type 1 Infection. Kaslow RA and Francis DP, eds. New York, Oxford University Press, p. 18-41, 1989.. Unique Identifier : AIDSLINE ICDB/90668109 McDougal JS; Mawle AC; Nicholson JK; CDC, Bldg. 1, Rm. 1202 (A25), Atlanta, GA 30333
Abstract:
The pathogenesis of few immunologic diseases is as well understood as that of AIDS. However, confounding the study of immune function in patients with AIDS is the fact that many of the opportunistic infections and malignancies that complicate the clinical course may affect the immune system, making a distinction between primary and secondary effects difficult. Pathophysiology of the immune system in AIDS is reviewed, including relationships between immunologic and clinical manifestations of immunodeficiency; cellular tropism of HIV; significance and use of CD4+ T cell count and CD4+/CD8+ ratio; co-determinants of progressive immunodeficiency; the major components of the immune system in HIV-1 infection (CD4+ T cells, suppressor/cytotoxic cells, B cells, Igs, antibody response to vaccination, monocytes/macrophages, and lymphokines and other soluble serum substances); and immune responses to HIV infection. Current knowledge of the pathogenesis of immune deficiency due to HIV-1 infection provides for consistent interconnections between molecular, cellular, and clinical observations. The virus has evolved an affinity for the human CD4 molecule and a replication cycle that is cytopathic for host cells. HIV-1 binds, penetrates, replicates in, and destroys CD4+ T cells. The result is numerical/functional depletion of CD4+ T cells occurring over time. Decline of CD4+ T cells results in progressive paralysis of immune responses, rendering the infected person susceptible to opportunistic infections and malignancies. People infected with HIV-1 mount and sustain a vigorous antibody response to HIV-1. In advanced immunodeficiency, antibody titers to most viral proteins diminish, with the exception of those for the transmembrane protein gp41. In established infection, it is not clear what role antibody plays in limiting infection, although it is clear that progression often occurs despite the presence of antibody. For many viral diseases, antibody induced by vaccination or as a result of primary infection protects against infection upon subsequent exposure, but it is the cellular response that is primarily responsible for resolution of infection. HIV-1 is unique in that the cells that initiate a response to HIV-1 are the cells destroyed by the virus. The sustained antibody response to HIV-1, which most certainly requires T-B collaboration, suggests that HIV-1-specific T cells do exist, and other observations suggest there may be phenotypic or functional immune profiles that indicate an attempt by the immune system to eliminate infection. (191 Refs)
Keywords: Acquired Immunodeficiency Syndrome/*IMMUNOLOGY Cytopathogenic Effect, Viral/IMMUNOLOGY CD4-Positive T-Lymphocytes/IMMUNOLOGY Human HIV Antibodies/ANALYSIS HIV Infections/*IMMUNOLOGY HIV-1/*IMMUNOLOGY Immunity, Cellular/PHYSIOLOGY Leukocyte Count T-Lymphocytes, Helper-Inducer/IMMUNOLOGY T-Lymphocytes, Suppressor-Effector/IMMUNOLOGY Viral Vaccines/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.
