PubMed:9271588 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/9271588","sourcedb":"PubMed","sourceid":"9271588","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/9271588","text":"Epstein-Barr virus binding to CD21 activates the initial viral promoter via NF-kappaB induction.\nEpstein-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-kappaB 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-kappaB-dependent intracellular signaling pathway which is required for 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