ABSTRACT
The Acquired Immunodeficiency Syndrome (AIDS) has emerged as the most critical health care problem of the century. The syndrome was first recognized in 1981 among young sexually active male homosexuals who presented with Pneumocystis carinii pneumonia or Kaposi's sarcoma (KS) and profoundly depressed cellular immunity (Gottlieb et al., 1981; Siegal et al., 1981). Several populations, including sexually active homosexual men, intravenous drug users, recipients of blood products, and sexual partners, have been identified to be at increased risk. AIDS, which has no known cure and no adequate treatment, is caused by a retrovirus, the human immunodeficiency virus (HIV–1), formerly called lymphadenopathy associated virus (LAV) or the human T-cell lympho-tropic virus type III (HTLV III) now designated HIV–1 (Barre – Sinoussi et al., 1983; Gallo et al., 1983). As can be inferred from its name, the disease is marked by a progressive loss of immunocompetence, with resulting susceptibility to infections and to malignancy. The patterns of immune dysfunction which were first recognized in the immunodeficiency states of AIDS and ARC (AIDS-related conditions) included lymphopenia, decreased numbers of T-cells, inverted ratio of T-helper/inducer (CD4) lymphocyte to cytotoxic/suppressor (CD8) and depressed cell-mediated immunity as evidenced by cutaneous anergy to common recall antigens, loss of T-cell cytotoxic responses to virus-self antigen, depressed lymphocyte proliferation in response to mitogen/antigen stimulation (Gottlieb et al., 1981; Lane & Fauci, 1985; Lane et al., 1985; Shearer et al., 1985; Siegal et al., 1981).
