Primary human macrophages infected with a monocytotropic human immunodeficiency virus type-I (HIV-1) isolate were found to secrete one or more factors which had a significant effect on the rate of proliferation of cells derived from the synovial lining of uninfected donors. Quantitation of the cytokine present in the supernatants from infected macrophages showed that although several cytokines were expressed, none were present in amounts adequate to explain the proliferation of the test cells. These data suggest that not only may HIV-1 infected macrophages mediate disease expression in infected individuals, but that, individually, substimulatory concentrations of cytokines may operate addictively or synergistically. The interaction of human herpesvirus-6 (HHV-6) and the pathogenic human retroviruses, human T lymphotropic virus type-I and HIV-1, was shown to result in both an expanded host cell range due to phenotypic mixing of the viruses as well as the modulation of CD antigens on infected cells. Although HHV-6 infection occurred only after cellular activation, the virus receptor appeared to be present continuously. Further studies showed that HHV-6 infection increased the surface density of the CD4 antigen as well as de novo expression on otherwise CD4- cells.
