Dictionary of Allergies .. AIDS, Acquired Immune Deficiency Syndrome

AIDS, Acquired Immune Deficiency Syndrome

A lethal, infectious viral disease caused by the human immunodeficiency virus (HIV), formerly called the human t-lymphotropic, type III (HTLV-III). AIDS may be transmitted through contact with infected blood, semen, or other body fluids. The virus causes profound weakening of the immune system that leaves the body vulnerable to opportunistic disorders and infections, such as Kaposi's sarcoma and pneumonia caused by Pneumocystis carinii. A brief review of the immunologic mechanisms affected by the human immunodeficiency virus (HIV), the causative agent in AIDS, provides penetrating insight into the functional intricacies of the immune system.

The T4-helper cell is a critical mediator of overall immune responses. The T4-helper cell has the ability to recognize antigens, produce clonal proliferation of T cells, secrete lymphokines, facilitate cytotoxic/suppressor functions, and promote B-cell production of specific antibody. The tremendous variety of complications associated with AIDS can be appreciated by reviewing the ramifications of HIV effects on the T4 cell. Normal immune responses are dependent upon precise, intricate, and complex interactions among a variety of different immunologic elements. Reduction of the absolute number of T4 cells, producing lymphopenia and a decreased or altered ratio of T4 to T8 cells, renders AIDS patients susceptible to a wide range of opportunistic infections and neoplasms.  In the AIDS patient, the ratio of T4 to T8 cells is greatly reduced (generally greater than 1.0 in normal persons, often 0.5 or less in the AIDS patient). As a result, delayed hypersensitivity is decreased or absent; natural killer and cytotoxic T-cell activity are impaired; proliferative responses to specific antigens are reduced; lymphokine production is reduced, and macrophages demonstrate reduced chemotaxis, cell killing and impaired production of interleukin-1 (IL-1) in antigenic response. 

B-cell function is also severely impaired in the AIDS patient. As just described in T-cell functional impairment, B cells lose their ability to mount effective responses to foreign antigens. This promotes heightened susceptibility to infection from common bacteria normally overcome by intact humoral immunity. Ironically, while B cells demonstrate poor antibody responses to antigenic stimulation, there occur in the AIDS patient increased serum levels of immunoglobulins. Unregulated B cells produce the elevated levels of serum immunoglobulin. This lack of an organized humoral defence leaves the patients vulnerable to infection. The presence of antibodies against HIV does not appear to bestow protection against AIDS and, at present, serves only as a diagnostic marker for the infection. The use of IGIV treatment has thus far not demonstrated an increased capacity of directly influence the course of AIDS in adults, though in preliminary studies, it has produced positive results in children, reducing recurrent serious bacterial infections. The mechanism of action of IGIV in the pediatric AIDS patient is unknown but may be attributed to the elimination of antigenic stimuli for B-cell proliferation, or to a more direct feedback inhibition of B-cell proliferation. (See T cells). Programs to prevent mother to child transmission and to provide appropriate treatment to families living with HIV/AIDS must be a public health priority.

References

Samayoa B, Anderson MR, Grazioso C, Rivera BE, Harrison M, O'Brien W, Arathoon E. Experience of a pediatric HIV clinic in Guatemala City. Rev Panam Salud Publica. 2009 Jan;25(1):51-55.