A cancer-associated Epstein-Barr virus BZLF1 promoter variant enhances lytic infection
Fig 6
LMP2A, a BCR mimic, activates the Zp-V3 via the NFAT and ZIIIA binding sites.
(A) EBV-negative BJAB cells were transfected with the Zp-P or Zp-V3 luciferase vector with or without a plasmid expressing LMP2A. The fold increase in luciferase activity induced by co-transfection with the LMP2A vector for each promoter construct (relative to the untreated vector control, set as 1) is shown. Error bars indicate standard deviation. (B) BJAB cells were transfected with wildtype Zp-V3 luciferase vector, the Zp-V3-141A, or the Zp-V3 ZIIIA mutant promoter luciferase constructs, with or without a plasmid expressing LMP2A (in the presence or absence of cyclosporine A treatment) as indicated. The fold increase in luciferase activity induced by co-transfection with the LMP2A vector for each promoter construct (relative to the untreated vector control, set as 1) is shown.