New research may shed light on the enduring mystery of multiple sclerosis and its suspected cause, the Epstein-Barr virus. Scientists in Sweden have found that some patients with multiple sclerosis produce antibodies that block the virus and appear to mistakenly target a protein in the brain and spinal cord. The findings provide further evidence that the Epstein-Barr virus causes multiple sclerosis, the study authors said, and help explain why some patients experience more severe disease than others.

Sclerosis, or MS, is caused by an overactive immune system attacking our nervous system’s myelin sheath – the protective coating that surrounds nerve cells. Losing myelin not only makes neurons 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 experience many symptoms that are mild at first, but often eventually develop more severe symptoms that do not go away.

Viral infections have long been suspected to be a key trigger for MS, with the leading suspect being the Epstein-Barr virus, or EBV. A big study last year It is close. The strongest evidence for this relationship so far. Military personnel newly infected with EBV have been shown to be more likely to develop MS than those who clear the infection.

At the same time, many questions remain about this link. Most people get EBV at some point in their lives. Some people may become temporarily ill from the infection (EBV is the main cause of mono). But only a few –Less than 1% The People’s-Later MS. So something else must be helping to fuel the process that starts with EBV infection and ends with multiple sclerosis.

One leading theory of how EBV may cause MS is related to a concept called molecular mimicry. Simply put, an EBV or fragment (also known as an antigen) can closely resemble proteins or other molecules naturally found in the body. As our immune system tries to fight off 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 at the Karolinska Institute in Sweden and elsewhere provide evidence that this chain of events occurs in at least some EBV patients.

The authors studied blood samples collected from more than 700 MS patients and compared them with samples from similar controls. Based on previous research, they decided to focus on a specific protein found in the brain and body, which is mistakenly called EBV. Criab Among other functions, CRYAB is thought to help prevent certain proteins from forming into potentially harmful aggregates.

They found that MS patients were more likely to produce Antibodies On CRYAB. They also showed that these antibodies could. Responding to a specific viral antigen—previous research has linked it to the development of MS. Finally, they found some evidence that this counter-reaction may also occur in T cells, another part of the immune system.

“We identified that the immune response to EBV can target proteins in humans that are normally supposed to control infection,” Karolinska Institutet researcher Olivia Thomas told Gizmodo. That is, we found that responses to alpha crystallin B and EBNA1 from EBV are more common in people with MS.

The findings, while important, cannot explain every case of MS. For example, only 23 percent of MS patients seem to have these antibodies to CRYAB. But the authors say there may be many other native molecules that can be mistaken for EBV by the immune system and cause MS. This may explain why no two MS patients experience the disease in the same way.

The researchers went on to show that faulty T cells are responsible for MS. Elsewhere, drug companies have begun testing treatments aimed at eradicating chronic EBV, hoping to halt or slow the progression of MS. Some of them They have already shown promise.

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