Scientists link 22 genes to deadly risks from common virus

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Scientists have identified 22 genes that explain why one common virus leaves many people unharmed but puts others at risk of chronic and sometimes lethal diseases.

An international research team from the pharmaceutical company AstraZeneca and US academic institutions discovered the traits, which make it harder for people to control levels of the Epstein-Barr virus (EBV).

The revelation offers the potential to help sufferers of illnesses linked to EBV, including lupus, heart disease and some tumours.

“EBV has long posed a paradox: nearly everyone encounters it, yet only some go on to develop serious, long-term illness,” said Slavé Petrovski, vice-president of AstraZeneca’s Centre for Genomics Research. “This genetic lens explains the uneven burden of EBV-related disease and points to practical paths for earlier risk identification and, ultimately, targeted interventions.”

EBV, which is from the herpesvirus family, is transmitted primarily via saliva. It is thought to infect 90 per cent or more of people globally during their lifetimes and then lie dormant in their bodies, making it one of the world’s most common viruses. Most cases are asymptomatic or mild.

In some people it causes mononucleosis with symptoms including fever, malaise and lymph node swelling — known as glandular fever.

If the virus persists at elevated levels, it is thought to contribute to many conditions including cancers, neurological disorders and autoimmune diseases — in which the body’s defence mechanisms turn against it.

Scientists from AstraZeneca, Memorial Sloan Kettering Cancer Center and Baylor College of Medicine reviewed genetic and health data from about 750,000 people in the UK and US. They discovered that people with higher levels of EBV had specific variants of the 22 genes, many of which related to the immune system, according to a paper published in Nature on Wednesday.

People with elevated EBV levels were almost twice as likely to have chronic obstructive pulmonary disease, which causes breathing problems, mucus coughing and wheezing, the researchers found. They were about 50 per cent more likely to have rheumatoid arthritis, which causes painful inflammation in joints and other body parts.

The paper’s authors acknowledge that some of the chronic conditions identified may occur because of a “general state” of suppression of the body’s immune system, rather than EBV’s direct action. More research will be needed to show the apparent effects of the virus are causal rather than correlational, they and other scientists said.

The latest research is part of a broader effort to unlock the puzzle of EBV’s wide-ranging impact, including as a possible contributor to multiple sclerosis and long Covid. The endeavour has been boosted by advances such as large genetic databases and improved techniques to analyse the human body’s cells.

In November, scientists unveiled how EBV could infect and reprogramme immune cells to trigger the disease lupus, which causes skin rashes and inflammation of other organs.

The Nature paper shows a potential pathway to investigate why other viruses, including Covid-19, appear to cause debilitating long-term effects in some people but not others, scientists said.

The study “highlights the power of large-scale genomic analysis and its ability to provide novel insights” into the impact of common viruses on chronic diseases, said Lawrence Young, a virologist and emeritus professor of molecular oncology at the University of Warwick.