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. 2020 Oct 28;12(11):1222. doi: 10.3390/v12111222

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Methylation induction following Epstein-Barr virus (EBV) infection of epithelial cells. (A) Subtypes of genes that are unmethylated prior to EBV infection. Methylation occurs at and around the transcriptional start site (TSS). Genes can become methylated, remain unmethylated or appear to be methylation resistant, suggesting protection from silencing. (B) Pathways by which EBV latency proteins LMP1 and LMP2A can drive methylation. LMP2A can phosphorylate STAT3 which binds to the promoter region and activates transcription of DNMT1. Additionally, LMP1 can activate DNMT1 through c-Jun/JNK signaling. LMP1 can also drive transcription of DNMT3A and DNMT3B through NFκB signaling. All DNMT proteins then methylate gene promoters, including TSGs such as PTEN.