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. 2019 Mar 12;24(5):997. doi: 10.3390/molecules24050997

Figure 2.

Figure 2

(a) Patterns of gene expression during EBV latency. The majority of the endemic BL presents a latency I type and carry a wild-type transformation-competent EBV genome and express only the Epstein–Barr nuclear antigen 1 (EBNA1) from the EBNA1-specific latent promoter Qp, non-coding EBERs (Epstein–Barr virus-encoded small RNAs) and several microRNAs (miRNAs). Around 15% of BL endemic tumors, the so called Wp-restricted BLs, carry an EBNA2 gene-deleted genome and express EBNA1, -3A, -3B, and-3C and the viral Bcl2 homologue BHRF1 from the Wp latent promoter [2,6]. * The EBNA-LP gene is partially deleted in the Wp-restricted latency. A major type of latency in EBV-associated malignancies is latency II, in which the latent membrane proteins LMP1, LMP2A, and LMP2B are expressed in addition to the Latency I genes. The entire EBV latency gene complex, which consists of several EBNA proteins, LMP1, LMP2A, LMP2B, EBERs, and miRNAs are expressed in the type III latency. (b) The cellular genetic alterations and/or co-infections are known to occur in the different types of EBV-associated malignancies. PEL: primary effusion lymphoma; HL: Hodgkin lymphoma; BL: Burkitt lymphoma; NHL: non-Hodgkin lymphoma; PTLD: post-transplant lymphoproliferative disorder; NPC: nasopharyngeal carcinoma; GC: gastric carcinoma.