HTLV-III infection of EBV-genome-positive B-lymphoid cells with or without detectable T4 antigens.

The infection of a number of new and established B-cell lines by human T-cell lymphotropic virus III (HTLV-III) was investigated. The B lymphocytes differed in their expression of T4 antigens detected by specific monoclonal antibodies (MAbs) and the presence of Epstein Barr virus (EBV)-DNA or antigens. The presence of the EBV genome was the only requirement for infection of B-lymphocytes by HTLV-III, although its presence did not ensure infection. Two EBV genome and T4 antigen-positive B-cell lines, lacking EBV early antigens (EA) and viral capsid antigens (VCA), could be productively infected with no induction of known EBV antigens. Two other EBV genome-positive cell lines, lacking T4, EA, and VCA could also be infected. Another genome-positive cell line (P3HR-I) that was EBV-EA, VCA-positive and produced non-transforming EBV, could also be infected by HTLV-III. However, 3 EBV genome- and T4 antigen-negative B-cell lines could only be infected with HTLV-III after successful conversion to an EBV-genome-positive state by pre-infection with EBV. Five other EBV-genome-positive B-cell lines lacking T4 antigens were not infectible with HTLV-III even after super-infection with EBV. Incomplete inhibition of the HTLV-III infection of a T4-positive (LDV-7) and a T4-negative (Craig) was obtained by preadsorption with specific MAb to T4 (OKT4A and Leu 3A). From these observations, it is not clear whether the presence of T4 antigen on the cell surface is needed for the infection of B lymphoblastoid cells; however, successful infection does depend upon the presence of the EBV genome. The mechanism of interaction of HTLV-III and EBV-infected B-cell lines permitting this infection is not fully understood. Although the clinical implications of these observations remain to be determined, it is possible that infection of EBV-positive B-cells may contribute to aberrant humoral responses and/or increased frequency of B-cell malignancies observed in HTLV-III-infected individuals.