Epstein-Barr virus (EBV) associated with B-cell lymphomas was recently isolated from the plasma of AIDS patients in our laboratory. In view of this development and recent reports of a 30-fold increase in B-cell lymphomas in AIDS patients, we attempted to investigate infection and replication of HTLV-III in B-cells. We found that only (but not all) EBV genome-positive cells could be infected by HTLV-III, whether or not they possessed T4 receptors. Two EBV-positive lines became chronically infected with HTLV-III. Three EBV genome-negative cell lines (lacking T4 receptors) could not be infected with HTLV-III until they were converted to EBV positivity. Even after infection, however, the latter remained negative for T4 receptors, suggesting that the mechanism of infection of B-cells by HTLV-III does not involve T4 antigens. Alternatively, EBV may induce a receptor that may be required for HTLV-III infection. Results suggest the interaction of EBV and HTLV-III in B-cell lymphomas associated with AIDS. The specific role of megakaryocytes is not fully known except that they are involved in platelet formation. Three human megakaryocyte cell lines were found to contain the EBV genome. One of these lines also possessed approximately 3% EBV virus capsid antigens (VCA). This was the first report of the ability of megakaryocytes to replicate EBV, suggesting that this cell type possesses EBV receptors. Like the EBV genome-positive B-cells, the megakaryocyte lines were infectible with HTLV-III, further supporting the role of EBV in HTLV-III infection and adding another cell type for HTLV-III replication.
