betadex and Burkitt-Lymphoma

Epstein-Barr virus (EBV) infection is a multi-step process, first requiring virus binding to the host cell, followed by fusion of the viral envelope with the host cell plasma membrane. Efficient EBV entry into B cells requires, at the minimum, the interaction of the EBV-encoded glycoproteins gp350 with cellular CD21 and gp42 with MHC class II proteins. In this study, use of the cholesterol-binding drugs methyl-beta-cyclodextrin and nystatin efficiently inhibited EBV infection of target Burkitt's lymphoma B-cell lines, indicating an important role for cholesterol and suggesting the involvement of lipid rafts in EBV infection.

Topics: beta-Cyclodextrins; Burkitt Lymphoma; Cholesterol; Cyclodextrins; Herpesvirus 4, Human; Humans; Membrane Glycoproteins; Membrane Microdomains; Nystatin; Signal Transduction; Tumor Cells, Cultured; Viral Envelope Proteins