Abstract
Abstract Epstein-Barr virus (EBV), a human herpesvirus that causes infectious mononucleosis in adolescence, has been implicated in various lymphoid and epithelial malignancies. Entry of EBV into primate cells requires interaction of several EBV glycoproteins and cell receptors. The gp85-gp25 complex has been suggested to play a crucial role in the infection of human epithelial cells and B cells. Moreover, Takada’s group found that gp25 is bound to epithelial cells rather than B cells, implying that EBV might infect epithelial cells with the assistance of this protein. The purpose of my study is to determine whether gp25 plays an active role in EBV infection of epithelial cells and B cells. By using DNA vaccination, immune response specific to EBV gp25 was elicited. The anti-serum was then used to determine its activity in neutralizing EBV infection. Two methods are proposed in this study to monitor the entry of EBV into cells. First, for the reporter cell assay, we constructed two EGFP-based reporter plasmids; each was driven by an EBV early gene promoter, BMRF1 or BALF2. The plasmids were stably transfected into the AGS cell and the expression of EGFP upon EBV infection was monitored. One of the transfected reporter cells, AGS (BM/EGFP), expressed EGFP after 24 hr of TPA treatment for virus induction. Second, we estimated the EBV genome copy numbers within infected cells with the Real-Time PCR. In summary, no significant difference in EBV genomic DNA copy number with or without the pretreatment of anti-gp25 antibodies was noted.