DNA research uncovers 22 genes that could put people at risk of long-term health conditions following common viral infection

Baylor College of Medicine researchers are part of a collaborative research group with AstraZeneca and Memorial Sloan Kettering Cancer Center that have identified 22 genes which increase the risk of developing a range of chronic conditions following a common viral infection.

Differences in these genes help explain why Epstein-Barr Virus (EBV) can have lasting health effects, in some people but not others. In a landmark study published in Nature, the team analysed genetic and health data from approximately 750,000 people in the UK and US.

EBV infects nearly everyone—around 90% of people—but typically remains silent in the body. For some, however, this common virus can persist at higher levels and can contribute to serious chronic illnesses, including lupus, chronic lung disease, heart disease and certain cancers later in life—a mystery that has long challenged scientists.

This breakthrough work uses existing libraries of genomic and health data alongside novel computational methods to quantify EBV levels across hundreds of thousands of individuals. The team discovered that certain genetic differences – many in immune system genes – could make it harder for the body to keep EBV under control. People with these variants are more likely to have higher levels of the virus in their blood, which is linked to increased rates of chronic disease.

While we cannot yet prevent EBV infection, this research points to how we can understand who may be most at risk for developing various chronic diseases, opening the door to earlier detection and intervention strategies.

“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,” said Dr. Ryan Dhindsa, assistant professor, pathology & immunology at Baylor and principal investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital. “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, VP, Centre for Genomics Research at AstraZeneca added, “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.”

“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,” said Caleb Lareau, assistant member, Computational and Systems Biology Program at Memorial Sloan Kettering Cancer Center and assistant professor, Computational Biology and Medicine, Weill Cornell Medicine. “Our approach can be extended beyond EBV, enabling the detection and analysis of other viruses hidden within large genome sequence datasets.”

These findings build on a recent rapidly growing body of research validating links between EBV and chronic illness. By uncovering the gene-virus connection, this study sets the stage for a new wave of scientific discovery that prioritizes risk management and early intervention and accounts for the imprint that viruses we meet during our lifetime leave within us.

For a list of all collaborators and funding, see publication.