EBV Genome Mutations and Malignant Proliferations

Abstract

The Epstein-Barr virus (EBV) is a DNA virus with a relatively stable genome. Indeed, genomic variability is reported to be around 0.002%. However, some regions are more variable such as those carrying latency genes and specially EBNA1,-2,-LP, and LMP1. Tegument genes, particularly BNRF1, BPLF1, and BKRF3, are also quite mutated. For a long time, it has been considered for this ubiquitous virus, which infects a very large part of the population, that particular strains could be the cause of certain diseases. However, the mutations found, in some cases, are more geographically restricted rather than associated with proliferation. In other cases, they appear to be involved in oncogenesis. The objective of this chapter is to provide an update on changes in viral genome sequences in malignancies associated with EBV. We focused on describing the structure and function of the proteins corresponding to the genes mentioned above in order to understand how certain mutations of these proteins could increase the tumorigenic character of this virus. Mutations described in the literature for these proteins were identified by reporting viral and/or cellular functional changes as they were described.

The Pathologic and Genetic Characteristics of Extranodal NK/T-Cell Lymphoma

“…HEA is characterized by the mutation of epigenetic modifiers with the activation of the NF-kB pathway and TCR signaling pathway. HEA presents a latency II pattern and a higher level of the lytic gene BNRF1, which is important for the establishment of latency and cell immortalization [142]. When considering these data, the TSIM molecular subgroup appears to represent the prototype of ENKTL, which is typically of the NK lineage, having deletions or mutations of many tumor-suppressor genes and having mutations of genes in the JAK/STAT pathway, as well as a high expression of PDL1 in tumor tissue.…”