Anti-human immunoglobulin (Ig) antibodies with single-chain specificities induced Epstein-Barr virus (EBV) in various Burkitt lymphoma lines when the corresponding Ig chain was expressed on the cell surface. The F(ab')2 fragments of IgG antibody were as potent as intact Ig, while the Fab and Fc fragments gave no induction, indicating that cross-linking of surface Ig was required for the induction. Simultaneously with EBV induction, anti-Ig inhibited the uptake of 3H-thymidine. This inhibition was also seen in EBV-genome-negative Burkitt lymphoma lines. In contrast, no effect on virus induction and cell growth was noted in lymphoblastoid lines of non-neoplastic origin. The possible relationship between cell differentiation and latency of EBV-carrier state is discussed.