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.
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Katzman et al. (2003) studied this question.
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