Epstein-Barr virus - the cause of infectious mononucleosis - is responsible for a range of illnesses, such as Hodgkin's lymphoma and Burkitt's lymphoma. But now, researchers have discovered how it takes over our cells' gene-regulating mechanisms to allow the virus to duplicate itself.
Commonly known as the "kissing disease" - because it can be passed from human to human through kissing - Epstein-Barr virus (EBV) is also known as human herpesvirus 4.
According to the Centers for Disease Control and Prevention (CDC), EBV is spread by saliva through kissing, sharing drinks and food, using the same cups or utensils, or having contact with toys children have drooled on.
The CDC say symptoms of the virus can include:
Once an individual gets an EBV infection, it becomes inactive in the body, but it may reactivate under certain circumstances, as in people with compromised immune systems.
Researchers from this latest study - led by Dr. James Omichinski of the University of Montreal in Canada and published in PLOS Pathogens - explain that viruses like EBV use complex strategies to "subvert" human cells during an infection.
Because viruses are unable to exist outside of human cells, they have found a way to imitate important elements of human cell function. As there is currently no cure for EBV, Dr. Omichinski explains that gaining knowledge of how the virus mimics these elements is vital:
"Unraveling the atomic level details of these interactions using structural biology allows us to understand how the virus tricks the human defense systems. Having this knowledge is the first step towards developing new therapeutic treatments for viral infections."
Findings provide potential targets for drug development
In the US, around 90% of adults have antibodies for EBV, a virus spread through saliva.
To investigate further, he and his team used innovative nuclear magnetic resonance (NMR) techniques to study how the EBNA2 protein of EBV binds to a protein of the TFIIH complex, which helps regulate a protein called RNA polymerase II.
RNA polymerase II, the researchers note, is a molecule responsible for controlling most of our genes.
Essentially, the team found that the virus begins when a viral protein contacts the molecules that control our genes, an interaction that could be used as a target for drug development.
Using NMR spectroscopy, the researchers labeled the EBNA2 protein and TFIIH with stable isotopes, and pinpointed the molecular structure of their communication.
They say if their findings do lead to the development of drug targets, they may one day be able to better treat not only EBV, but also the cancers caused by this virus.
According to the CDC, diagnosing EBV infection can be tricky since symptoms are so similar to other illnesses. However, the infection can be confirmed through a blood test that detects antibodies.
Around 90% of adults in the US have antibodies, showing they have a current or past EBV infection.