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.