Relationship between epstein-barr virus (EBV)-production and the loss of the ebv receptor/complement receptor complex in a series of sublines derived from the same original burkitt's lymphoma

Abstract

Virus production, EBV (P3HR‐1 substrain) superinfectability, IdUrd inducibility, EBV receptor and complement (C3) receptor expression were assessed in two independently maintained Jijoye lines, the derived P3HR‐1 clone that releases a growth inhibitory and cytopathic, non‐transforming viral mutant, and in non‐producer sublines derived from the P3HR‐1 line by the spontaneous cessation of virus production. Both Jijoye lines were superinfectable, inducible, and carried EBV and C3 receptors. Virus‐producing P3HR‐1 cells and recently derived non‐producer sublines lacked EBV‐receptors and C3 receptors, could not be superinfected, but were IdUrd inducible. Two long‐passaged non‐producer sublines of P3HR‐1 reexpressed EBV and C3 receptors to an equal degree (different in the two sublines). EBV‐superinfectability became partially reestablished in the subline with the higher expression of EBV and C3 receptors. These findings support the hypothesis that the EBV‐receptor/C3 receptor negativity of the producer P3HR‐1 sublines and their recent non‐producer derivatives is due to negative selection by the growth‐inhibitory, cytopathic P3HR‐1 virus variant. The closely linked disappearance and reappearance of EBV‐receptors and complement receptors gives further support to the idea that these two receptors are either identical or closely linked constituents of the cell membrane.