Detection of HIV p17 antigen in lymphocytes but not epithelial cells from cervicovaginal secretions of women seropositive for HIV: implications for heterosexual transmission of the virus.

Human immunodeficiency virus (HIV) has been isolated from cervicovaginal secretions from infected women and is thought to be cell associated. To identify which cells harbour viral antigen, we used monoclonal antibodies to OKT4 and a monoclonal antibody directed against HIV p17 core antigen to perform indirect immunofluorescence assays of genital secretions from 17 HIV seropositive and 17 HIV seronegative women with leucorrhoea. OKT4 positive lymphocytes were detected in all tested samples. HIV p17 antigen was detected in the genital fluid lymphocytes in nine out of 14 seropositive subjects from whom lymphocytes were available. No viral antigen was detected in genital fluid lymphocytes of seronegative subjects, nor in any cervicovaginal epithelial cells. This study shows that lymphocytes are the major source of HIV in cervicovaginal secretions of infected women. Conditions that increase the lymphocyte population in the female genital tract, such as sexually transmitted disease (STD), chronic inflammation of the cervix, and menstruation, may facilitate the transmission of HIV during sexual intercourse.

Cell receptors for baboon endogenous virus recognized by monoclonal antibodies.

Hybridomas from mice immunized with baboon endogenous virus (BaEV) from A204(M7) cells produced several antiviral monoclonal antibodies and, in addition, antibodies D-12 and E-4, which appeared to be virus specific because they reacted with BaEV but not with Mason-Pfizer virus or RD-114 virus. However, they also bound to human virus-free cells, and they did not recognize BaEV from bat or canine host cells. Cell membrane targets for these antibodies comigrated with an 18,000-dalton protein, which may contain specific determinants of BaEV receptors since antibody masking of these cell sites prevented BaEV but not Mason-Pfizer virus or RD-114 virus adsorption. However, RD-114 virus interfered with BaEV adsorption. Thus, the two viral receptors must be adjacent, but the antibody D-12 and E-4 targets are not within the active site of RD-114 virus receptor. Conversely, cell coating with BaEV from bat or canine hosts inhibited antibody D-12 binding. Noncultivated human lymphocytes and cells from fetal organs bound much less antibody D-12 than did cells from established cell lines, with a correlation between amounts of antibody D-12 acceptor sites and BaEV receptors. Thus, in vivo, BaEV infection of human cells may be inefficient. In vitro, antibody D-12 treatment of chronically infected A204(M7) cells caused intracellular accumulation of viral proteins and decreased virus release, with no such effect on RD-114 virus-producing cells. Canine cells bound antibody D-12 only if coated with BaEV from A204(M7) cells, indicating that the human determinant coadsorbed with the virions to animal cells. Possibly, determinants of cell receptors participate in BaEV maturation and become associated with the virions.