TABLE 2.

Impact of EBV latent antigens on B-cell transformation and subsequent lymphoma development

EBV latent protein	Function related to B-cell lymphomagenesis
EBNA1	Regulates viral DNA replication and transcription of a number of viral and cellular genes; facilitates p53 degradation and thereby promotes overall oncogenesis
EBNA2	One of the key viral transcription factors; in association with EBNALP, EBNA2 regulates transcription of several viral and cellular gene expression levels; essential for B-cell transformation
EBNALP	Transcriptional coactivator of EBNA2-mediated transcription of both viral and cellular genes; bypasses cell innate immune response; essential for B-cell transformation
EBNA3A	Along with EBNA3C, represses BIM and p14, p15, p16, and p18 gene transcription through epigenetic regulation; inhibits B-cell-to-plasma cell differentiation; essential for B-cell transformation
EBAN3B	Virus-encoded tumor suppressor protein
EBNA3C	Along with EBNA3A, represses BIM and p14, p15, p16, and p18 gene transcription through epigenetic regulation; facilitates G1-S and G2-M transitions of cell cycle; hijacks ubiquitin-proteasome pathway; inhibits p53-, E3F1-, and Bim-mediated apoptosis; activates autophagy; essential for B-cell transformation
LMP1	Functionally mimics CD40 signaling pathway; one of the major transcriptional regulators; constitutively activates NF-kB, JAK/STAT, ERK MAPK, IRF, and Wnt signaling pathways; stimulates bcl-2 and a20 expression to block apoptosis; essential for B-cell transformation
LMP2A	Functionally mimics BCR signaling pathway; blocks apoptosis; EBV latency regulation
LMP2B	Regulates LMP2A functions
EBERs	Most abundant noncoding viral RNAs present in all form of latency programs; affects innate immune response and gene expression; blocks PKR-dependent apoptosis
miRNAs	Transcribed from BART and BHRF1 loci; maintains latently infected B cells through blocking cellular apoptosis