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Contracting mono as a child raises autoimmune disease risks later on

The mono virus – commonly known as the ‘kissing disease’ – raise the risks of at least seven diseases, by sticking to human DNA, according to new breakthrough research 

Between 80 and 95 percent of Americans get mono over their lifetime, which may raise their risks for immune-related diseases like lupus, multiple sclerosis, arthritis, diabetes, celiac disease and inflammatory bowel disease. 

Of those who got lupus in childhood, nearly 100 percent had had mono when they were young, according previous work by the Cincinnati Children’s Hospital researchers 

Typically, the virus only sickens people once, but the new research sheds light on how its lingering effects on the genome may help give rise to chronic diseases later in life.

Mono is marked by swollen glands and typically dismissed as a common childhood illness, but new research suggests the virus can raise risks of seven diseases for some who get it young

Modern medical research has unveiled risk factors and mechanisms that underlie many of the major chronic diseases that sicken and strike people down over the course of their lives.

But an incomplete understanding of what happens to make some vulnerable to these illnesses remains a roadblock to the development effective treatments and preventative measures.

Categorically, autoimmune diseases – which cause the body to attack itself – are particularly mysterious, and, as it becomes more common, scientists are continuously digging deeper to discover what genetic and environmental factors might underlie the disease.

Now, it appears that a common virus may trigger some instances of lupus – and alter DNA in a way that facilitates the onset of other diseases as well.

The mono virus – or glandular fever, an illness caused by the Epstein-Barr virus (EBV) – is exceedingly common and can cause extreme fatigue, achiness, a sore throat and headache and is most classically identifiable by swollen lymph nodes and sometimes by a rash.

Many who get the virus will never show any signs or symptoms, and those that do get ill will probably only feel the virus’s effects once in their lives.

But regardless, once the virus enters someone’s symptoms – typically through saliva, hence its nickname – EBV is there for life.

In previous research, the new study’s lead author, Dr John Harley, had found that the vast majority of people who had developed lupus during childhood had had mono early in life too.

Of all people who carry the mono virus in the US, more than 90 percent get it before age 20, when contracting the virus carries the greatest risk of instigating other illnesses. 

He and his team knew that lupus is most likely caused by a combination of environmental and genetic factors, like a number of other immune system-related diseases, including multiple sclerosis and diabetes.

They also knew that each of these diseases had been linked to particular variations at about 100 locations on the human genome. But what was missing was the link between the two – genetic and environmental – links. 

So he and his multi-disciplinary team decided to examine how the mono virus might interact with those genes. 

They discovered that EBV burrows into the very immune cells – called B cells – that are meant to build antibodies against it. But EBV actually corrupts and reprograms these cells.  

It appears to do so by messing with proteins called transcription factors, so traces of EBV’s activity are visible on these. 

In the new study, the researchers found that the seven disease, which share no obvious common links or symptoms, were all marked by the altered transcription factors – and therefore, by the mono virus. 

This told the Cincinnati Children’s Hospital researchers that those with particular genetic variants are vulnerable targets for an environmental disease risk factor: the virus. 

‘We were looking for the link between genetics and environment,’ said study co-author Dr Leah Kottyan, and now it appears they may have found it. 

There are currently no vaccines against mono on the market, and research to develop any has been slow to take off.  

Now that they have a well-described link between the mono virus and potentially lethal diseases, Dr Kottyan and her team hopes that the US might throw more weight behind research into vaccines against it. 

‘Hopefully we can come to a societal agreement that funding for a mono vaccine might really be a good idea,’ she said.  

Furthermore, ‘this discovery is probably fundamental enough that it will spur many other scientists around the world to reconsider this virus in these disorders,’ speculated lead study author Dr Harley. 

The study, which was funded by the National Institutes of Health, has already garnered attention for its success in describing a new and significant relationship between environmental and genetic factors of disease. 

‘Many cases of autoimmune illness are difficult to treat and can result in debilitating symptoms,’ said Dr Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases. 

‘Studies like this are allowing us to untangle environmental and genetic factors that may cause the body’s immune system to attack its own tissues. A better understanding of the complex causes of autoimmunity promises to lead to better treatment and prevention options,’ he concluded.