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Review
. 2015 Mar 19;11(3):e1004656.
doi: 10.1371/journal.ppat.1004656. eCollection 2015 Mar.

To be or not IIb: a multi-step process for Epstein-Barr virus latency establishment and consequences for B cell tumorigenesis

Alexander M Price  1 , Micah A Luftig  1
Affiliations
Review

To be or not IIb: a multi-step process for Epstein-Barr virus latency establishment and consequences for B cell tumorigenesis

Alexander M Price et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. EBV latency gene expression in different latency states.
This figure depicts, from left to right, the theoretical progression of EBV latency gene expression from initial infection to true latency. The EBV genome is shown in episomal form closed at the terminal repeats (TR). Promoters are shown as white boxes and include the EBNA promoters Cp, Wp, and Qp as well as the bidirectional LMPp. Primary mRNA transcripts are shown as dotted lines, while coding regions have been simplified as colored boxes. An expanded list of viral genes expressed in each latency state is listed directly underneath the representative schematic.
Fig 2
Fig 2. EBV latency types found in EBV-driven malignancies.
Cell morphology (including cellular size and classic Reed–Sternberg-like nuclear morphology in the case of Latency IIa cells) that is associated with various EBV latency types is depicted. In heterogeneous malignancies, the relative percentage of cells displaying each latency type as shown by tumor cross-sections and immunohistochemistry are shown below (Relevant citations: Day 7 post infection [14], Post-Transplant Lymphoproliferative Disease (PTLD) [26,27], HIV-Lymphoma [26], IM [28], all others [2]). *Of note, approximately 15% of Burkitt lymphomas carry a mutant EBV genome containing a deleted EBNA2 gene, resulting in expression of the EBNA3s and Wp-BHRF1 (vBcl2), as well as EBNA1.
See this image and copyright information in PMC

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