T-cell receptor heterogeneity among Epstein-Barr virus-stimulated T-cell populations.

The mechanism by which Epstein-Barr Virus (EBV) escapes T-cell activity during latency in immunocompetent individuals has long been debated. In order to identify potential weaknesses in the EBV-specific immune response, a study of T-cell receptors (TCR) within virus stimulated T-cell populations was performed. Membrane staining techniques and the polymerase chain reaction were used to address two questions: (1) Does EBV behave as a superantigen, thus stimulating, and possibly eliminating, T-cell subsets based on TCR V beta expression?, and (2) Are T-cells dependent on a predominant TCR V beta segment for effective cytotoxic function towards EBV? In search for superantigen effects, V beta repertoires among PBL from seropositive and seronegative individuals were compared both before and after short term in vitro exposure to EBV. In order to characterize functional TCR, the V beta usage among CD8+ EBV-specific cytotoxic T-cell clones was determined. Taken together, results illustrated the strengths rather than weaknesses of the EBV-specific T-cell immune response. T-cells did not respond to EBV in a manner typifying potent superantigen activity, nor did T-cells rely on the expression of a single V beta gene segment for efficient, EBV-specific cytotoxic function.