A new study has discovered an essential insight of the infection caused by the Epstein-Barr virus (EBV) – that it is linked to various kinds of cancer. The research, conducted by the University of California San Diego, UC San Diego Moores Cancer Center and Ludwig Cancer Research at UC San Diego, was published in the journal Nature.
The EBV is considered to be one of the most widespread viruses in the world, with more than 90% of the global population having it at some point during childhood. Although the infection is usually mild and short-lived, some cases may remain latent, causing cancer and inflammatory diseases.
The study found that EBV induces chromosomal breaks on human chromosome 11. This results in a cascade of genomic weaknesses, which can activate cancer-causing oncogene and disable important tumor suppressors. To prove this, the researchers observed 2,439 different cancers from 38 tumor types, focusing on those with detectable EBV levels. It was revealed that 100% of cases of head and neck cancer had higher levels of abnormalities on chromosome 11.
The main cause of EBV transmission is through saliva when people kiss or have the same utensils when eating. To make matters worse, the virus suppresses the body’s natural ability to inhibit tumor growth. This means that individuals who are infected with the virus are at higher risk of cancer.
Study co-author Don Cleveland, PhD, a distinguished professor at the University of California San Diego School of Medicine, has encouraged individuals to be aware of the dangers of the virus and to practice good hygiene habits. He further stressed the importance of understanding how the virus can cause genetic instability and its related effects.
“Ludwig Cancer Research at UC San Diego” is an organization which works tirelessly to comprehend the complexities of tumour existence and derive from that knowledge to improve the lives of cancer patients. Founded in 1967, the organization has made significant contributions to the field with its world-renowned research program. Today, the organization carries out toil in the field of cancer biology, treatment development and more.
Julia Li, PhD, the first author of the paper and post-doctoral fellow in Cleveland’s lab, focused on understanding how the virus was able to induce a “fragile DNA” site, an area which is more prone to producing breaks and gaps in the DNA when replicating. The researchers also shed light on EBNA1, a viral protein which is present in infected cells, and how it can impair an important gene called p53, which is intended to manage cell division and death. If p53 is found to be impaired, cancer growth can be initiated.
