| Abstract: | The P3HR-1 substrain of Epstein-Barr virus does not transform B cells. This defect is known to be determined by the loss of the coding sequence for the nuclear antigen EBNA-2. The virus can attach to and enter resting B cells. The initial events after EBV infection are reminiscent of those induced by polyclonal B cell activators. Similar to the effect of these, P3HR-1 virus lowers membrane IgD expression on B cells and abrogates the transient elevation of activation markers BB-1 and LB-1 induced by the culture conditions. An important event of B cell activation is the acquisition of competence to respond to specific growth factors produced by T cells. This was induced by the P3HR-1 virus. The infected B cells had elevated 3H]thymidine incorporation when exposed to the supernatant of PHA-treated T cells. The EBV receptor is identical with the complement receptor CR2. Ligand binding to CR2 has been shown both with mouse and human B cells to deliver certain activation signals. Therefore, it is possible that the early step of activation by EBV is initiated through the binding to the receptor and is thus a cell surface event. |
