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. Author manuscript; available in PMC: 2016 Jun 16.
Published in final edited form as: Adv Virus Res. 2014;88:279–313. doi: 10.1016/B978-0-12-800098-4.00006-4

Figure 3. EBV latency mRNAs are expressed as alternative isoforms and distinct transcripts.

Figure 3

At the top is a schematized EBV linear genome showing the positions of latency gene exons in black boxes and BamHI fragment names listed below (not to scale). Also shown on the genome are the terminal repeats (open boxes), the C promoter (Cp, green boxes), the W promoter (Wp, yellow box), the Q promoter (Qp, blue box), the bi-directional Latent Membrane Protein promoter (LMPp, purple boxes), the LMP2A-specific promoter (purple box), and the canonical EBNA poly-adenylation sites (pA, arrow). The ORF-containing exon of the lytic gene BHRF1 is shown as an orange box. All coding exons are shown as full height boxes while non-coding exons are half-height. Early after infection latency transcripts are initiated primarily from the W promoter, as shown in yellow. The special instance of alternative splicing between the upstream Wp or Cp splice donor and the W1 or W1′ exon that leads to inclusion of an ATG start codon and EBNA-LP protein production is shown (Inset). After EBNA2 and EBNA-LP production reach a significant level early after infection, the C promoter is activated and transcribes the rest of the EBNAs, as shown in green. Later in infection, the LMP promoters are active and LMP1, LMP2A, and LMP2B and transcribed and spliced as shown in purple. In Latency I only the Q promoter is active to transcribe EBNA1.