‘Because Everyone Has Herpes’: Researchers explore link between Epstein-Barr virus and Alzheimer’s disease

Posted on February 24, 2020

Ana Tognosali
Ana Tognasoli is a PhD student in the Adamson Lab who first became interested in the connection between EBV and neurological diseases.

Researchers in UNC Greensboro’s Adamson Lab are exploring whether Epstein-Barr virus—a strain of herpes that infects 95 percent of American adults—can trigger neurological diseases like Alzheimer’s and Parkinson’s later in life.

Never heard of Epstein-Barr virus (EBV)? Well, you probably have it.

EBV is associated with mononucleosis, more commonly known as “mono” or “the kissing disease.” Most people are infected with EBV without realizing it. That’s why the Adamson Lab uses the hashtag #BecauseEveryoneHasHerpes on their Twitter page: to stress the … proliferation of their research subject.

“Epstein-Barr is so common, and most of us are A-OK with it,” said Dr. Amy Adamson, director of the molecular biology lab. “But like all herpes viruses, it stays with you forever. So chances are it’s causing changes in your cells that we just don’t know about. We want to find out what those are.”

There is already ample research linking EBV to cancer, particularly in Africa and China, where the virus and other compounding factors cause cancers like Burkitt’s lymphoma, an aggressive disease primarily affecting children.

Yet the connection between EBV and neurological diseases is relatively unexplored. Ana Tognasoli, a PhD student in the Adamson lab, decided to study this connection because of research she read tying EBV to Multiple Sclerosis, another disease affecting neurons.

“We know that this virus infects B-cells, immune cells that travel throughout your entire body. So if there is inflammation in the brain, the EBV-infected cells can go in,” said Tognasoli.

Ana Tognasoli is a PhD student in the Adamson Lab who first became interested in the connection between EBV and neurological diseases.

Even though Alzheimer’s disease is the sixth leading cause of death in the U.S., the root cause is still unknown. A key hallmark of the disease are large clusters of proteins that build up in the cells of neurons. The protein clusters form because cells have stopped the mechanism known as autophagy, a process during which the cell “cleans house” and disposes of bad proteins.

“When you look at people who have passed away from Alzheimer’s disease, they have these big clusters of proteins in their neurons that won’t break down, and it is associated with cell death,” said Adamson.

Though drugs have been developed to destroy these protein clusters, they aren’t working to stop the development of Alzheimer’s or Parkinson’s diseases.

That’s what is leading researchers to believe there may be something unexpected at play within the nervous system: a virus, perhaps.

“Just in the last few months, people are starting to think that the cause of these cells dying might be something infectious,” said Adamson. “The protein accumulation may be a viral side effect.”

We’ll have to wait and see where the research leads. Yet the implications would be huge.

“If you find out it’s something infectious, you may be able to develop a vaccine,” said Adamson. “Not everyone who is EBV-infected is going to develop Alzheimer’s, but under certain circumstances, maybe they have a genetic predisposition as well, it could be a trigger. And if we can stop the virus before it gets that far, then you can hopefully reduce the chance of developing these neurodegenerative diseases.”

accumulation of protein in nerve cells
Arrow points to an accumulation of protein in a neuronal cell in the brain of a patient who died with Alzheimer’s disease. Photo credit: Tulemo

Currently, no vaccine exists for Epstein-Barr virus. That’s because in the U.S.—one of the biggest drivers of vaccine production—the virus is still considered minor. Yet if EBV is found to have a close connection to Alzheimer’s and Parkinson’s diseases, that perception just might change.

“By 2030 we’re going to have 72 million Americans over age 65,” said Tognasoli. “To maintain quality of life and independent living, we’re going to need to find out how to stop neurodegenerative diseases.”

Could the key to finding out be a virus lying dormant inside us?

Story and lab photos by Elizabeth Keri, UNCG’s College of Arts & Sciences

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