Scientists inch closer to solving the ‘kissing disease’ mystery

NEW YORK – Scientists have identified 22 genes that increase the risk of conditions like lupus, stroke, and rheumatoid arthritis in patients who’ve caught the virus behind mono, an illness known as the “kissing disease”.

The research, published on Jan 28 in the journal Nature, tried to unravel why some people who contract the Epstein-Barr virus go on to experience other medical conditions later in life.

The hope is that by understanding who is most at risk, scientists might be able to better target treatments and turbo-charge research into vaccines for prevention. 

The pandemic sparked renewed interest in Epstein-Barr as experts probed its potential connection to long Covid. The latest study from researchers at Memorial Sloan Kettering Cancer Center, Baylor College of Medicine and drugmaker AstraZeneca Plc pointed to a likely relationship between the virus and chronic-fatigue syndrome, a condition that shares similarities with long Covid.

Epstein-Barr, or EBV, is a common virus that causes infectious mononucleosis, which is sometimes known as glandular fever or the “kissing disease” as it is spread through saliva. Most people get infected with the virus in their life, particularly in teenage-hood, but only some actually develop symptoms. After the infection, the virus sits silently in the body and can reactivate.

“I think 50 years from now, we’re going to look back and say, ‘how were we letting ourselves all get infected by EBV?’” said Dr Caleb Lareau, a principal investigator at Memorial Sloan Kettering and one of the paper’s authors.

“This is clearly a detriment to our health.” The research should be a further motivation for developing vaccines against EBV, he said. 

The researchers looked at whole genome sequencing and health-record data of about 750,000 people in two large databases – the UK Biobank and the US National Institutes of Health’s All of Us. 

Some viruses leave a bit of DNA behind, even after a patient has recovered. Dr Lareau described an “aha moment” when he and his colleagues realised that because EBV leaves a copy of itself in some white blood cells, the genome sequencing done on hundreds of thousands of people in Britain and US probably had left precious data behind.  

“We sort of joke internally that this was a project of churning trash into a treasure,” Dr Lareau said. 

The study results don’t indicate that the virus actually causes conditions such as lupus or rheumatoid arthritis – rather it shows a correlation between persistent EBV DNA and these illnesses. 

The findings should help researchers better understand the biology of patients who have common chronic diseases and understand “what part of their medical history might be most relevant towards their current clinical manifestation,” said Dr Slave Petrovski, vice-president of AstraZeneca’s Centre for Genomics Research. “That might then dictate what is the best course of treatment.” 

While earlier research has indicated EBV could play a role in multiple sclerosis, the new study did not show a strong link. That does not mean there is no association, rather that the design of the two studies differed, explained Baylor College of Medicine’s Ryan Dhindsa, who is an assistant professor of pathology and another author on the paper. 

“Everything that we’ve found is purely a statistical association,” Prof Dhindsa said. “So at this point we can’t really comment much on causality.” In addition to conditions like lupus, Prof Dhindsa and his colleagues found associations between EBV and chronic pulmonary disease as well as depressive episodes. BLOOMBERG