CD4+ T cells and monocytes are the primary targets for HIV-1 infection. Interaction of these cell types is important in the normal immune response. Studies were undertaken to investigate the potential alteration of the normal regulatory signals by HIV-1 infection in cell to cell communication. Antibodies to cell surface structures that activate T cells increase the levels of infection. Alternatively, antibodies that interfere with accessory adhesion molecules and therefore disrupt cell to cell communication inhibit T cell infection. Studies are underway to characterize the virus-like particle(s) seen in Kaposi's sarcoma (KS) tissue biopsies from individuals in a cohort who are seronegative for HIV- 1, HIV-2, HTLV-I, and HTLV-II. Polymerase chain reaction primers having common sequences with different classes of retroviruses in the long terminal repeat, polymerase, gag and envelope regions were used to amplify DNA from biopsy specimens from KS lesions. The immunoglobulin antibody class and subclass responses to HIV-1 proteins were assessed in sera from infected mothers that gave birth to infected and non-infected infants. IgG2 antibodies to envelope protein alone or in combination with IgG and IgG3 were more frequent in transmitting mothers. No class or subclass antibody appeared to be protective. An investigation of methods to assess viral load in peripheral blood by flow cytometry was initiated. A fluoresceinated probe capable of detecting one copy of viral RNA per cell was used in in situ hybridization studies of infected cell populations.
