Epstein-Barr Virus Promotes Lymphoma by Taking Control of 2 Key Genes, Study Finds

Epstein-Barr Virus Promotes Lymphoma by Taking Control of 2 Key Genes, Study Finds

Epstein-Barr virus, which causes mononucleosis, can also cause lymphoma by taking control of two genes involved in blood cancers and switching them on or off, a new study reported.

The study, “MYC activation and BCL2L11 silencing by a tumour virus through the large-scale reconfiguration of enhancer-promoter hubs,” may have solved a major puzzle in science — how the Epstein-Barr virus (EBV), long known to raise a person’s risk of lymphoma, actually went about promoting the cancer. The work, led by Professor Michelle West at the University of Sussex and published in the journal eLife, demonstrated that EBV can switch on the MYC gene, a key driver of lymphoma development, and switch off the BCL2L11 gene, which normally controls cell death to prevent lymphoma.

EBV is one of the most common viruses in humans, and most people are infected with it at some point in their lives. It can be responsible for mild illnesses and even go unnoticed, but it is implicated in severe diseases such as cancer.

Previous studies have shown that if the virus infects a specific subset of immune cells, the B-lymphocytes, it can induce the development of blood cancers, such as Burkitt’s and Hodgkin’s lymphoma.

Researchers in this study discovered that the virus could control the MYC and BCL2L11 genes by hijacking specific DNA regions, known as enhancers. These enhancers work as control centers, regulating the expression of genes via direct contact.

By changing how enhancers contact the MYC gene, the virus was found to switch on its expression. This is important as MYC is thought to be a driver gene for Burkitt’s lymphoma, with nearly 85 percent of patients having MYC activating mutations. The research team believes that these findings can help to explain how the virus causes the MYC gene changes found in Burkitt’s lymphoma.

EBV was also able to prevent these enhancers from contacting and switching on BCL2L11, a gene that normally triggers programmed cell death when malignancies arise. Importantly, this blocking effect could be reversed by a drug, a finding that could be paving the way for new lymphoma treatments.

“This is a key step towards uncovering how this common virus, which affects thousands of people every year, causes blood cancer,” West said in a press release. “It is now important to carry out further studies to determine how the Epstein-Barr virus controls other genes that are associated with lymphoma. This will tell us more about how the virus drives lymphoma development and will help to identify new ways of targeting Epstein-Barr virus-infected cancer cells with specific drugs.”

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