A team of researchers at the University of California San Diego has unraveled a crucial mechanism that explains how the Epstein-Barr virus (EBV), also known as human herpes virus 4, can trigger the development of various types of cancer. Although this virus is extremely common in humans and is latently harbored by most people, its association with disease has been a cause for concern.
The study, recently published in the prestigious journal “Nature”, focused on an EBV-encoded viral protein called EBNA1. The scientists discovered that this protein has the ability to bind to a fragile region of human chromosome 11 and cause it to break. The presence of EBNA1 at sufficiently high levels is necessary for this phenomenon to occur, indicating a dose dependence.
Of particular interest is the close location of two genes relevant to cancer: the ATM gene, a tumor suppressor that is often altered in certain tumors, and the MLL gene, a regulator of expression that is often involved in chromosomal rearrangements in different types of leukemia.
The research team also examined samples of human tumors and found that those positive for the presence of the Epstein-Barr virus had a higher frequency of structural alterations in chromosome 11. In addition, cases of tumors negative for the virus were even detected that showed alterations in said chromosome, suggesting that the action of EBNA1 may occur without direct detection of the virus.
Advances in Knowledge of the Epstein-Barr Virus
The findings of this study provide a better understanding of the mechanisms by which Epstein-Barr virus may promote tumor development. Specifically, they show how the virus can induce chromosomal changes that have the potential to affect cancer-related genes.
The clinical relevance of this discovery is significant. On the one hand, it offers the possibility of identifying the individual risk of developing diseases associated with Epstein-Barr virus infection, based on specific characteristics of chromosome 11. On the other hand, it opens up new opportunities for the development of therapies that block the binding of EBNA1 to chromosome 11, which could prevent chromosome instability and associated disease processes.
Dr. Julia Li, lead author of the study and a researcher at the University of California, San Diego, noted: “This finding suggests that the susceptibility of chromosome 11 to EBNA1-induced fragmentation depends on controlled levels of EBNA1 in latent infection.” , as well as genetic variability in the number of Epstein-Barr virus-like sequences present on chromosome 11 in each individual.”