Inhibition of Germinal Centre Apoptotic Programmes by Epstein-Barr Virus

Figure 1

Model of establishment of EBV latency in B cells. EBV infects naïve IgD-positive B cells and drives their proliferation by expression of the viral latency III genes, including the latent membrane proteins LMP1, LMP2A, and LMP2B, the EBV nuclear antigens EBNA1, 2, LP, 3A, 3B, and 3C and noncoding RNA species, the EBV-encoded RNAs (EBERS), and BamHI-A rightward transcripts (BARTs). In vitro, these blasts form continuously proliferating immortalised, lymphoblastoid cell lines (LCLs). EBV-infected cells participate in the GC reaction during which time the number of viral gene products expressed decreases due to the downregulation of the viral transcription factor EBNA-2. Following differentiation, long-lived memory B cells emerge as the site of persistent latent infection carrying viral episomal DNA and expressing few viral genes to avoid immune surveillance. *Transient lytic gene expression may occur but without virion production.