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. 2021 Jan 12;6:15. doi: 10.1038/s41392-020-00376-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Mitochondria play an important etiological and pathogenesis role in the EBV-associated cancers. EBV has a new function in remodeling of mitochondrial dynamics during latency and lytic infection. EBV-encoded latent oncogene BARF1 and EBNA1 suppress the apoptotic pathways by decreasing Bax translocation to mitochondria and activating casepase-9. The BZLF1 protein encoded during EBV lytic activation inhibits the replication and copy number of mtDNA