Acute infectious mononucleosis stimulates the selective expression/expansion of V beta 6.1-3 and V beta 7 T cells

Abstract

Abstract Acute infectious mononucleosis (AIM) is caused by the Epstein-Barr virus (EBV) and is characterized by a proliferation of atypical lymphocytes, predominantly CD8+ T cells. Various diseases associated with T-cell activation have been shown to stimulate the selective expansion of certain V beta (variable region of the T-cell receptor beta chain) expressing T-cell populations. The purpose of this investigation was to determine if the proliferation of T cells accompanying AIM is associated with selective expression/expansion of distinct populations of V beta T cells. We determined V beta expression in eight patients with clinical and laboratory evidence of AIM, including an atypical lymphocytosis. Gel electrophoresis and quantitative analysis were performed on cDNA amplified by the polymerase chain reaction (PCR) using different V beta region primers. Gel electrophoresis analysis showed prominent V beta 6.1–3 and V beta 7 bands in all eight patients with AIM but not in the controls. Quantitative PCR analysis showed that the V beta 6.1–3 and V beta 7 mean PCR ratios increased, respectively, from 163.0 +/- 22.5 and 142.3 +/- 5.5 in controls to 339.9 +/- 38.8 (P < .03) and 396.1 +/- 45.6 (P < .01) in the eight patients with AIM. Two of the eight patients who had increased V beta 6.1–3 and V beta 7 expression were retested after clinical resolution of AIM and no longer had evidence of increased V beta 6.1–3 and V beta 7 T-cell expression. AIM is associated with a selective increased expression of V beta 6.1–3 and V beta 7 T cells present at the time of initial clinical symptoms and atypical lymphocytosis. This increased expression resolves following recovery from AIM. This V beta-specific selective expression resembles the super- antigen response seen after staphylococcal toxin stimulation and may be caused by EBV triggering of selective expansion of V beta 6.1–3 and V beta 7 T-cell subsets.