Infection with the human immunodeficiency virus results in a progressive immune deficiency involving many components of the immune system. The major target cells for infection are CD4 antigen-bearing cells, which include predominantly, but not exclusively, the helper T cell subset and the monocyte-macrophage cell system. Hypergammaglobulinemia is a common and early feature of human immunodeficiency viral infection but is often associated with an inability to mount specific antibody responses to neoantigens and decreased in vitro B cell differentiation responses. On the basis of our data and reports of others, a major component of B cell hyperactivity is related to the direct activity of the human immunodeficiency virus and its proteins. We and others have documented that B cells of these patients lose the capacity to respond to both T cell-dependent and T cell-independent stimuli in vitro. Thus the human immunodeficiency virus can profoundly influence B cells, causing both "stimulation" (vis-à-vis hypergammaglobulinemia) and "suppression" (poor specific antibody responses). However, the memory cells are probably not suppressed, and their dysfunction may be directly related to the extent of helper cell dysfunction. This explanation lends itself well to the clinical observation that children (who have not developed memory to recall antigens) with human immunodeficiency viral infection have more profound defects in specific antibody responses than do adults (who have an existing pool of memory cells). Thus the main rationale for intravenous immune globulin in acquired immune deficiency syndrome is to provide antibody replacement.(ABSTRACT TRUNCATED AT 250 WORDS)