Objectives: To understand the mechanism for the refractoriness of B- chronic lymphocyte leukemia (B-CLL) cells for EBV-induced immortalization. Study Design/Methods: Cells from four B-CLL patients were infected with Epstein-Barr virus (EBV). Noninfected and infected aliquots were exposed to CD40L. Five days later, the cultures were analyzed for cell survival, activation, DNA synthesis, and expression of EBV-encoded and of cellular regulatory proteins retinoblastoma (Rb), p53, recombinant sequence binding protein (RBP)Jk, and PU.1. The proteins were detected by immunoblotting and by immunofluorescence. Results: A proportion of the cells were activated and ex- pressed Epstein-Barr nuclear antigens (EBNAs) and elevated Rb level but not latent membrane protein (LMP)-1 and p53. They did not enter the cell cycle. Exposure to CD40L induced DNA synthesis but it did not modify the expression of the EBNAs. Conclusions: The virus could activate CLL cells, but the full course of the early events that leads to immortalization - as seen in normal B cells - did not proceed beyond a certain point. Compared to B lymphocytes, the critical point is between activation and initiation of the cell cycle. (C) Lippincott Williams and Wilkins, Inc.
|Number of pages||12|
|Journal||Journal of Human Virology|
|Publication status||Published - May 1 2000|
- CD40 ligand
ASJC Scopus subject areas