Common Herpes Virus Can Cause Multiple Sclerosis: Study

The study reveals that certain antibodies against the Epstein-Barr virus, which would normally fight the infection, can mistakenly target the brain and spinal cord and cause damage.

Image for representation

A team of Swedish researchers has found evidence for how the common herpes virus -- Epstein-Barr -- can trigger multiple sclerosis or drive disease progression of the neurological disease. The herpesvirus Epstein-Barr is one of the most widespread viruses in humans. It infects most people early in life and then remains in the body, usually without causing symptoms.

While the link between the Epstein-Barr virus and multiple sclerosis (MS) was discovered many years ago, the mechanism was not known. A study published in Science Advances shows that some individuals have antibodies against the virus that mistakenly attack a protein in the brain and spinal cord.

"MS is an incredibly complex disease, but our study provides an important piece in the puzzle and could explain why some people develop the disease," said Olivia Thomas, a postdoctoral researcher at the Department of Clinical Neuroscience, Karolinska Institutet in Sweden.

"We have discovered that certain antibodies against the Epstein-Barr virus, which would normally fight the infection, can mistakenly target the brain and spinal cord and cause damage," she added.

The researchers analysed blood samples from more than 700 patients with MS and 700 healthy individuals. They found that antibodies that bind to a certain protein in the Epstein-Barr virus, EBNA1, can also bind to a similar protein in the brain and spinal cord called CRYAB, whose role is to prevent protein aggregation during conditions of cellular stress such as inflammation.

These misdirected, cross-reactive antibodies may damage the nervous system and cause severe symptoms in MS patients, including problems with balance, mobility, and fatigue. The antibodies were present in about 23 percent of MS patients and 7 percent of control individuals.

"This shows that, whilst these antibody responses are not required for disease development, they may be involved in disease in up to a quarter of MS patients," said Olivia Thomas. The researchers also found that there is likely a similar cross-reactivity among T cells of the immune system.

This demonstrates the high variation between patients, highlighting the need for personalised therapies. Current therapies are effective at reducing relapses in MS but unfortunately, none can prevent disease progression, Thomas said.