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Article

Epstein-Barr Virus Binding to CD21 Activates the Initial Viral Promoter via NF-B Induction

From the Scripps Research Institute, Department of Immunology, La Jolla, California 92037

Epstein-Barr virus (EBV), an oncogenic human herpesvirus, binds to and infects normal human B lymphocytes via CD21, the CR2 complement receptor. Studies of the mechanisms that enable EBV to infect nonactivated, noncycling B cells provide compelling evidence for a sequence of events in which EBV binding to CD21 on purified resting human B cells rapidly activates the NF-B transcription factor, which, in turn, binds to and mediates transcriptional activation of Wp, the initial viral latent gene promoter. Thus, EBV binding to its cellular receptor on resting B cells triggers an NF-B–dependent intracellular signaling pathway which is required for infection.

¹ Abbreviations used in this paper: CAT, chloramphenicol acetyltransferase; EBNA, Epstein-Barr virus nuclear antigen; EMSA, electrophoretic mobility shift assay; LTR, long-terminal repeat; PKC, protein kinase C; rpL32, ribosomal protein L32; RT, reverse transcriptase.

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