While the world debates the shocking allegations and criminal details in the ‘Epstein files’, the medical research community has shed new light on a highly contagious virus that also bears the Epstein name. The Epstein-Barr virus (EBV) is named after two scientists—Michael Anthony Epstein and Yvonne Barr—who discovered the tiny herpes-family viral particles in 1964 while studying a rare African childhood cancer called Burkitt lymphoma. EBV—the first virus linked to human cancer—is also one of the most common human viruses and spreads through body fluids, primarily saliva. Most people are infected at some point in their lives, usually in childhood, and experience no symptoms. In that sense, EBV behaves like a long-buried story: it can remain unnoticed for years, only revealing itself when conditions allow it to reactivate.
Interestingly, Epstein identified the virus only three years after obtaining the biopsy samples he suspected might contain it, and largely by accident. In 1961, after attending surgeon Denis Burkitt’s lecture on a mysterious “jaw tumour” common in equatorial Africa, he suspected a viral cause and secured tumour samples, but found no viral particles.
The breakthrough came in late 1963 when a flight carrying a sample from Uganda was delayed, extending the transit time. By the time it arrived, the specimen looked cloudy and nearly contaminated and was close to being discarded. Instead, Epstein examined it and found free-floating tumour cells that had loosened during the long journey and began growing in culture. Working with Barr and pathologist Bert Achong, he used electron microscopy on these cultured cells and, in 1964, observed the EBV for the first time.
Those with weakened immune systems are more prone to EBV reactivation. When that happens, symptoms can vary in severity, ranging from sore throat and fatigue to skin rashes, swollen lymph nodes and an enlarged spleen or liver. If viral genes begin altering the growth cycle of infected cells, they can also contribute to cancer.
Recently, a landmark study by AstraZeneca and Memorial Sloan Kettering Cancer Center, published in Nature, identified 22 genetic variants that influence how effectively the immune system controls persistent EBV levels in the blood. Using large genomic and health-data libraries alongside innovative computational methods, the researchers measured EBV levels across hundreds of thousands of individuals and found that certain genetic differences—many in immune-related genes—make it harder for the body to keep the virus in check. People carrying these variants are more likely to have higher viral loads, which are linked to increased rates of chronic disease.
This latest finding, too, echoed the virus’s own accidental discovery. Because the team analysed fragments of genome-sequence data that are usually discarded in routine human genetic studies and turned them into meaningful insights at an unprecedented scale. After publication, Caleb Lareau, principal investigator at Memorial Sloan Kettering Cancer Center, described the approach as turning “trash into treasure”.