The acquired immunodeficiency syndrome (AIDS).

Abstract

This article discusses clinical, immunologic, and etiologic considerations in the acquired immunodeficiency syndrome (AIDS) and the relationship of AIDS to other immunodeficiency diseases. The outstanding clinical feature of AIDS is the occurrence of opportunistic infections in individuals with no prior known cause of immunodeficiency. Such infections have included Pneumocystis carinii, oral thrush from Candida albicans, cytomegalovirus, atypical mycobacteria, cryptosporidium, and Herpes simplex virus. Central nervous system invasion by Cryptococcus neoformans and Toxoplasma gondi has also been reported. Persistent quantitative and functional depression of T4 cells is the immunologic hallmark of full-blown AIDS. Another prominent feature is in vitro spontaneous hyperactivity of B cells. AIDS patients lose cutaneous delayed hypersensitivity reactions both to recall and to new antigens, and T-cell-mediated cytotoxicity is diminished. The mounting number of T8 cells and diminution in T4 cells causes an inversion in the normal T4:T8 ratio. It has been hypothesized that the host defense mechanism is the attempt of the cytotoxic T8 cells to destroy the virus-infected T4 cells. 2 groups of investigators have discovered a lymphocytotropic retrovirus from blood and node lymphocytes of AIDS patients: lymphadenopathy-associated virus (LAV) or human T-lymphotropic virus type III (HTLV-III). Among the primary immunodeficiencies, AIDS most closely resembles the defect observed in purine nucleoside phosphorylase deficiency, an inherited autosomal recessive phenomenon. There is evidence that multiple infections or antigen overload characterize all the risk groups for AIDS. Moreover, antigen overload in experimental animals and man has been shown to suppress immune responses and to down-regulate Ia antigen expression on monocytes. This may prove to be a necessary precondition for the development of AIDS.