Abstract
Epstein–Barr Virus (EBV) can transform B cells and contributes to the development of Burkitt lymphoma and other cancers. Through decades of study, we now recognize that many of the viral genes required to transform cells are not expressed in EBV-positive Burkitt lymphoma (BL) tumors, likely due to the immune pressure exerted on infected cells. This recognition has led to the hypothesis that the loss of expression of these viral genes must be compensated through some mechanisms. Recent progress in genome-wide mutational analysis of tumors provides a wealth of data about the cellular mutations found in EBV-positive BLs. Here, we review common cellular mutations found in these tumors and consider how they may compensate for the viral genes that are no longer expressed. Understanding these mutations and how they may substitute for EBV’s genes and contribute to lymphomagenesis can serve as a launchpad for more mechanistic studies, which will help us navigate the sea of genomic data available today, and direct the discoveries necessary to improve the treatment of EBV-positive BLs.
Highlights
Infectious agents cause approximately 2.2 million cases of cancer each year (de Martel et al, 2020), about 15% of all human cancers worldwide (Parkin, 2006; de Martel et al, 2012; Plummer et al, 2016; de Martel et al, 2020)
We hypothesize that Epstein-Barr Virus (EBV)-positive tumor cells must have acquired cellular mutations to compensate for the loss of expression of viral genes
One controversial question is: Are some tumors found to be EBV-negative formerly EBV-positive having evolved to be independent of the virus? It has been observed that some Burkitt lymphoma (BL) spontaneously lose EBV in culture (Akata, MutuI, and Daudi) (Shimizu et al, 1994; Kitagawa et al, 2000; Nanbo et al, 2002)
Summary
Infectious agents cause approximately 2.2 million cases of cancer each year (de Martel et al, 2020), about 15% of all human cancers worldwide (Parkin, 2006; de Martel et al, 2012; Plummer et al, 2016; de Martel et al, 2020). For EBV to transform a cell it infects, the virus must express certain viral genes. We consider how EBV-transformed B cells evolve as BLs to shut off the expression of some viral genes necessary for transformation and substitute for their functions through cellular mutations.
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