New research could provide clues to a lingering mystery surrounding multiple sclerosis and the common germ believed to be its primary cause, the Epstein-Barr virus. Swedish scientists have found that some MS patients produce antibodies against the virus that also appear to mistakenly target a protein found in the brain and spinal cord. The results provide more evidence that the Epstein-Barr virus can cause multiple sclerosis, the study authors say, and could help explain why some patients have more severe disease than others.
Multiple sclerosis, or MS, is caused by an overzealous immune system attacking our nervous system’s myelin sheath, a protective coating around nerve cells. The loss of myelin not only makes nerve cells more vulnerable, but also hinders their ability to communicate with each other. As a result, people with MS may experience a variety of neurological symptoms, including numbness, muscle weakness, pain, and difficulty walking. MS patients tend to experience episodes of disease that fade and recur at first, but they will often eventually develop symptoms that worsen and do not go away.
Viral infections have long been suspected as a key trigger for MS, with the main suspect being the Epstein-Barr virus, or EBV. Last year, a large study provided the strongest evidence to date of this connection. He found that service members newly infected with EBV were significantly more likely to develop MS than those who had avoided infection.
At the same time, there are still many questions about this link. Almost everyone will get EBV at some point in their life. Some people may become temporarily ill from the infection (EBV is a major cause of mono). But only a few—Less than 1% of the population – will later develop MS. So something else must help fuel the process that begins with EBV infection and ends with multiple sclerosis.
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One of the main theories for how EBV can cause MS relates to a concept called molecular mimicry. Simply put, it’s the idea that EBV or a part of it (also known as an antigen) can closely resemble proteins or other molecules that occur naturally in the body. When our immune system tries to mount a defense against infection, it can sometimes learn to target both EBV and these friendly bystanders, leading to MS.
In a study published In Science Advances on Wednesday, researchers from the Karolinska Institute in Sweden and elsewhere present evidence that this chain of events occurs in at least some patients with EBV.
The authors studied blood samples taken from more than 700 MS patients and compared them to samples from similarly matched controls. Based on previous research, they decided to focus on a particular protein found in the brain and body that could be confused with EBV, called CRYAB. Among other functions, CRYAB is believed to help prevent certain proteins from forming into potentially harmful clumps.
Jhey found that MS patients were more likely to produce autoantibodies against CRYAB. They also showed that these antibodies could cross reaction to a virus-specific antigen, an antigen that their previous research has linked to the development of MS. Finally, they found evidence that this cross-reaction can also occur in T cells, another key part of the immune system.
“We have identified that the immune response to EBV – which would normally control the infection – instead has the ability to target human proteins, which may be involved in the development or progression of multiple sclerosis,” said the author of the study, Olivia Thomas, a researcher at the Karolinska Institute. Gizmodo said. “This is further evidence that EBV infection can cause the immune system to mistakenly attack body tissues, and we found that these antibody responses, namely to alpha crystallin B and EBNA1 of EBV, are more common in people with MS.”
The results, while important, are not likely to explain all cases of MS. For example, only about 23% of MS patients appeared to have these cross-reacting antibodies against CRYAB. But it is possible that several other native molecules could be mistaken for EBV by the immune system and thus could trigger MS, according to the authors. This could also explain why no two MS patients experience the disease in the same way.
The researchers next plan to take a closer look at how miscalibrated T cells may contribute to MS. Elsewhere, pharmaceutical companies are beginning to conduct human trials of treatments intended to eradicate chronic EBV, in hopes of halting or slowing the progression of MS, some of which have already shown promise.