Studies are being conducted to investigate the immunobiology of human immunodeficiency virus (HIV-1) infection. Cells that bear the CD4 molecule are the primary targets for infection of HIV-1. In sequential measurement of the numbers of these cells in a cohort of HIV-infected hemophiliacs, disease progression to AIDS was found to be associated and therefore could be predicted by the loss of CD4 positive T cells. Cells of the monocyte/macrophage lineage serve important functions in initiating the immune response and, in addition, are the primary reservoir for HIV-1 in the infected host. We have studied these cells, infected in vitro, to determine if HIV-1 alters the ability of these cells to process and present antigen to T cells. Antibodies to major histocompatibility complex (MHC) class II antigens were shown to inhibit infection and antigen presentation to T cells by the infected monocytes/ macrophages. Monoclonal antibodies that react with cell surface structures that interact in antigen presentation and signaling to the T cells also inhibited infection. In contrast, augmentation of T cell response by antibodies to CD3 enhanced infection. Soluble recombinant CD4, known to inhibit infection of T-cells by cell-free virus, was not capable of inhibiting T cell infection by monocytes/ macrophages when the monocytes/macrophages were simultaneously presenting exogenous antigen. Studies are underway to isolate and identify the virus-like particle(s) seen in Kaposi's sarcoma tissue biopsies from individuals in a cohort of Greek individuals. Studies are underway to investigate the nature of the antibody response to HIV-1 proteins in infected mothers and their infants. The antibody response in these individuals is varied with the detection of a number of immunoglobulin class- and subclass-specific antibodies to different viral proteins. The most striking finding thus far is the presence of IgD antibodies to these proteins.
