Researchers from Baylor College of Medicine, AstraZeneca, and Memorial Sloan Kettering Cancer Center have identified 22 genes that increase the risk of developing chronic conditions after infection with Epstein-Barr Virus (EBV). The study, published in Nature, analyzed genetic and health data from about 750,000 people in the UK and US.
EBV infects around 90% of people worldwide but usually remains inactive. For some individuals, however, EBV can persist at higher levels and is linked to chronic illnesses such as lupus, chronic lung disease, heart disease, and certain cancers. The reasons for these long-term effects have not been fully understood.
The research team used large-scale genomic and health data along with new computational methods to measure EBV levels across hundreds of thousands of individuals. They found that specific genetic differences—many related to immune system function—make it harder for some people to control EBV. Those with these gene variants are more likely to have higher viral levels in their blood, which correlates with a greater risk of chronic diseases.
Dr. Ryan Dhindsa, assistant professor at Baylor College of Medicine and principal investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital said: “This research adds a missing piece to the puzzle of chronic disease. We show that genetic variation influences how well EBV is controlled, and that poorer viral control is associated with several long-term illnesses. These findings suggest that health outcomes reflect a complex interaction between our genes, lifestyle, and viral history. While further work is needed to determine which of these links are causal, the results point to new ways to identify risk and guide future efforts to prevent and treat chronic disease.”
Slavé Petrovski from AstraZeneca stated: “Identifying the roles of these 22 genes that are a significant factor in EBV control offers a profound leap forward. We found that people with higher EBV levels are about 50% more likely to have rheumatoid arthritis and nearly twice as likely to have COPD compared to those with lower levels. Insight into the genetic drivers behind this not only helps us understand who is at greater risk of longer-term disease burden but also informs the next wave of research into therapeutic and potentially early intervention strategies.”
Caleb Lareau from Memorial Sloan Kettering Cancer Center added: “Using innovative computational methods, we took pieces of genome sequence data that are typically discarded in routine human genetic studies and transformed them into valuable new insights at a scale previously unimaginable; turning trash into treasure. Our approach can be extended beyond EBV, enabling the detection and analysis of other viruses hidden within large genome sequence datasets.”
Baylor College of Medicine operates independently while collaborating on clinical partnerships focused on advancing education across its schools as well as promoting biomedical research and patient care. The institution has played an important role in community service since relocating its main activities from Dallas to Houston’s Texas Medical Center in 1943 and continues its mission as an independent health sciences university.
The findings contribute to growing evidence linking EBV with various chronic illnesses by uncovering how gene-virus interactions may influence lifelong health risks.
