A common childhood virus appears to be the cause of the autoimmune disease lupus, according to groundbreaking research.
The study suggests that the Epstein-Barr Virus (EBV), which for most people is harmless, can cause the immune system to “go to the immune system” and mistakenly attack its own tissues. The team behind the work says that the discovery of the cause of lupus can change treatments.
“We think it applies to 100% of cases of Lupus,” said Prof William Robinson, a professor of immunology and rheumatology at Stanford University and the senior author of the study. “I think this sets the stage for a new generation of therapies that may benefit lupus patients.”
Lupus, which affects around 69,000 people in the UK, is a chronic autoimmune condition in which the immune system creates antibodies that attack its own tissues. The causes are still unknown and there is no known cure for the condition, which can cause joint and muscle pain, extreme fatigue and skin and skin rashes.
Epidemiological surveys were previously initiated on a link between EBV and lupus, an idea that gained traction after a recent outbreak confirmed the Link between EBV and Multiple sclerosisanother autoimmune disease. The latest work helps unravel, at a cellular level, how EBV appears to cause lupus by sending immunity into a tailspin.
“This study solves a year-long mystery,” said Shady Inis, an immunologist at Stanford and first author of the paper.
EBV is usually a mild disease that causes a sore throat, fever and tonsillitis. By adulthood, about 19 out of 20 people are infected and – because the virus sheds its DNA genetic material – carry the dormant virus in their cells.
“The reason why it’s so strange is because it’s a common virus that most of us got from our sibling at the kitchen table when we were teenagers,” Robinson said. “The only practical way to prevent EBV housing is in a bubble.”
Among the cell types in which EBV takes up permanent residence are the cells, part of the immune system. These cells specialize in binding to proteins on the surface of viruses, known as antigens. About 20% of b cells have the potential to bind to parts of the body’s own cells, but in healthy individuals cells “Autooractive” cells “Autooractive” remain inactive.
For the first time, scientists used high-precision genetic engineering to identify differences in the number and type of lesions in 10 Lupus patients compared to 10 healthy controls.
In the control group, fewer than 1 in 10,000 B Cells hosted EBV, compared to about 1 in 400 cells for the Lupus group – a 25-fold difference. EBV is also predominantly found in autoreactive B cells
The presence of dormant virus indicates that these cells are in a hyperactive state where they not only target antigens inside the body, including killer cells, including killer cells, to participate in the attack.
“We think this is the critical discovery: that EBV … then activates the b cells to drive the autoimmune response that is Lupus,” Robinson said.
There are other well-known risk factors that feed easily to a person, beyond EBV. For example, lupus is more prevalent in women, which may be due to hormones such as estrogen increasing B-cell activity, Robinson said. People with an African, Caribbean or Asian background are also at a higher risk
Gorochoch of Prof Gorochov, a professor of medicine at the Sorbonne University said that the work is “impressive”.
“Not the last paper about lupus, but they did a lot and developed an interesting concept,” he said.
If confirmed, the findings will add impetus to clinical trials for the EBV vaccine, which are already underway. There are also several teams exploring repurposing cancer treatments designed to wipe out b cells for severe cases of lupus.
The findings were published in the journal Science Writing Medicine.