New Discovery Could Lead to New Treatments for Cancers Linked to the Epstein-Barr Virus

According to an article from VCU Massey Center’s blog, a team of researchers from the VCU Massey Cancer Center have successfully discovered a pair of genes that could be essential for replicating the Epstein-Barr virus, which has been linked to the development of several rare and dangerous cancers. These findings have been published in Cell Reports and PLOS Pathogens.

The Epstein-Barr virus (EBV) is a very common infection, and nearly 95 percent of human adults on the planet carry it. Most people are first infected with the virus when they are relatively young and generally experience no symptoms, though infection can cause symptoms when a previously uninfected adult is exposed. Despite being relatively harmless most of the time, EBV has been cited as a potential cause of cancer, and it is estimated that the virus contributes to approximately 200,000 cancer cases per year and roughly 140,000 annual deaths from cancer.

EBV has been implicated in a wide variety of cancers, including certain types of stomach cancer, Hodgkin’s lymphoma, Burkitt’s lymphoma, and nasopharyngeal (head and neck) cancer. Researchers have identified the gene PIAS1 as essential for the prevention of EBV’s replication. Before the virus can infect cells, the virus must shut down the expression of the gene. In the study, scientists were able to shut down this process, which stopped EBV from replicating.

Another important gene is IRF8. This protein is critical for the normal development of blood cells. As part of EBV’s replication process, the protein plays a major role in reactivating the virus. In this instance, reducing the influence of IRF8 greatly reduced the ability of EBV to continue replicating. The study also found that the protein controls the activation of enzymes that can destroy KAP1, which is an additional gene that is capable of stopping the activity of EBV.

In cancer cells where the virus was present, IRF8 activity was shut down which allowed for an increase in KAP1. As a result, the viruses in the cancer cells were deactivated. This new information could offer a major path forward for developing a treatment that could potentially treat the wide array of cancer types that are associated with the presence of EBV. Hopefully, new therapeutic options developed from this new data will lead to a breakthrough in treating EBV related cancers.

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