Human B-lymphotropic (human herpesvirus-6) virus (HBLV), isolated from acquired immunodeficiency syndrome (AIDS) patients and patients with other malignancies and lymphopro-liferative disorders, known to possess B-cell surface markers, was also found to infect T-cells obtained from peripheral blood, bone marrow, spleen, thymus and tonsils. HBLV could also replicate and produce large quantities of virus or viral antigens in established B-, T- and megakaryocyte cell lines. Coincident infection by human immunodeficiency virus (HIV)-1 and HBLV of T-cells possessing T4 receptors showed enhanced cytopathic effects and enhanced reverse transcriptase activity of HIV. Both viruses could be found in the same T4 cell, suggesting that interaction between HIV-1 and HBLV could enhance impairment of immure function by accelerated destruction of target cells. These findings were supported by higher HBLV antibody in HIV-1-positive asymptomatic individuals (AIDS-related complex (ARC), persistent generalized lymphopathy (PGL) and AIDS) and the presence of HIV-l DNA in about 80% of peripheral lymphocytes from AIDS patients. We also found that HBLV could oriy infect Epstein-Barr virus (EBV)-genome-positive B-cell lines or B-cell lines converted to ESV positivity, suggesting that EBV induces a receptor common for HIV and HBLV. HBLV and EBV antibody titers in African Burkitt's lymphoma (BL) sera were elevated: seven of ten BL tumors contained ESV and HBLV DHA. This suggests that HBLV has a role as a cofactor in some B-ce11 tumors. HBLV DNA was a1so detected in two Sjogren's B-cell tumors and a large B-cell follicular lymphoma. These findings are compatible with the implication of HBLV in some malignant, lymphoproliferative and immunosuppressive disorders.
