Scientists have found that a particularly strong reaction to the Epstein-Barr virus could trigger multiple sclerosis, a finding that may lead to new approaches to treat the condition.

Results of the study, which was in part funded by the Howard Hughes Medical Institute, will appear in the June 2006 issue of the journal Brain.

Susceptibility to multiple sclerosis (MS) is inherited, so not everyone who is infected with Epstein-Barr develops the disease.

The virus has long been suspected to play a role in triggering MS, but until now researchers understood little about how it was involved.

“Epstein-Barr virus does not cause MS, but the immune response to this virus is different in MS patients, and our hypothesis is that the altered immune response contributes to the development and progression of the disease,” said Jan Lünemann, a neurologist and immunologist at RockefellerUniversity in New York.

Tysabri Implications

In essence, MS is a chronic inflammatory disease where immune system cells attack the insulating covering of nerve cells. At the end of February 2005, the drug companies Biogen Idec and Elan withdrew their MS drug, Tysabri, from the market after three people taking it developed a fatal infection called progressive multifocal leucoencephalopathy (PML).

The U.S. FDA has reviewed the drug and decided to allow patients previously taking it to resume their treatment (see FDA Mulls Tysabri’s Return).

On April 28, European regulators also recommended that Tysabri be made available again to some MS patients, but a final decision will likely be taken in the summer.

The scientists investigating the Epstein-Barr virus found that a viral protein called EBNA1 is critically important in separating those with the virus who do not go on to develop MS, from those who contract the disease.

A group of T cells, which form part of the immune system, specifically respond to EBNA1. Patients with MS had significantly more of these cells in a more active form.

“The broadened response of the T cells could lead them to recognize and attack cells they aren’t supposed to, like brain cells,” said Christian Münz, a RockefellerUniversity researcher.

The researchers also checked for differences in the T-cell responses of MS patients and healthy volunteers to other proteins associated with the Epstein-Barr virus, as well as proteins produced when people are infected with flu virus or a virus called cytomegalovirus (a type of herpes virus). Only EBNA1 seemed to be involved.

Next the researchers need to find out exactly why the T cells are so responsive to EBNA1 in some people, and how these cells go on to attack the body’s own nerve cells.