Schematic diagram of linear EBV genome (∼172 kb). (A) In proportion to their size, largely unique (U1-U5), internal repeat (IR1-IR4), and terminal repeat (TR) sequence domains are demonstrated. Ori P (indicated in red), the origin for latent infection EBV episome replication, has plasmid maintenance and DNA replication activity. Location of exons for latent EBV-induced membrane proteins and nuclear proteins and the size of each gene are shown. Of note, LMP1 transcription has an opposite direction to the other gene transcripts. LMP2 can only be transcribed when EBV exists as episome because the gene spans across the TR. LMP2A is transcribed from exon 1, whereas LMP2B is transcribed from exon 2. EBNAs are transcribed from differently spliced primary EBNA transcript. In latency III, EBNA1 transcription begins from Cp or Wp, whereas it starts from Qp in latency I or II. EBNA-LP has variable sizes due to variable numbers of repetitive exons.⁹⁸  (B) Schematic diagram of circular EBV genome. The U1-U5, IR1-IR4, TR, and Ori P sequence domains are indicated. Open reading frames for latent proteins are shown. Of note, the size of each open reading frame does not illustrate the size of each latent protein.⁹⁸  (C) Amino acid sequences of CTAR1 and CTAR2. TRAF-binding motif in CTAR1 and TRADD-binding motif are indicated with an underbar. Numbers on the right denote the order of the amino acid sequence.⁹⁹  Cp, C promoter; EBNA-LP, EBNA leader protein; LMP, latent membrane protein; TRAF, tumor necrosis factor receptor-associated factor; TRADD, tumor necrosis factor receptor type 1–associated DEATH domain; Qp, Q promoter; Wp, W promoter.