Human immunodeficiency virus (HIV) infection leads, within about 10 years, to acquired immunodeficiency syndrome (AIDS), characterized by cell loss in several organs, including CD4+ T cells in the immune system, hematopoietic progenitors in the bone marrow and neurons in the brain (Everall et al. 1991; Fauci 1988, 1993; Levy 1993b). In the immune system, cell dysfunction is obseved before cell depletion is detected. These qualitative defects are characterized by a selective loss of CD4+ T cell memory function that includes, in vivo, a failure of CD4+ T cells to mediate delayed-type hypersensitivity reactions to self MHC class II-restricted recall antigens and, in vitro, a selective loss of the ability of T cells to proliferate in response to T cell receptor (TCR) stimulation by these recall antigens antibodies directed to the CD3/TCR complex, or defined polyclonal activators such as pokeweed mitogen (Clerici et al. 1989a,b; Hofmann et al. 1989; Lane et al. 1985; Miedema et al. 1988; Shearer et al. 1986). An additional and paradoxical feature of cell dysfunction in HIV-infected persons is the chronic activation state of the immune system, in spite of an apparent complete lack of CD4+ T helper (Th) cell function, that involves both HIV permissive (monocytes) and nonpermissive (B cells and CD8+T cells) cell populations (Fauci 1988,1993).