Researchers uncover trigger mechanism for onset of multiple sclerosis

Scientists have recently obtained additional evidence supporting the connection between the Epstein-Barr virus (EBV) and the development or progression of the neurological disease multiple sclerosis (MS).

EBV, a herpesvirus that is highly prevalent in humans, infects more than 90 per cent of the global population, remaining latent and typically asymptomatic throughout life.

While most individuals acquire the virus during childhood with mild or no symptoms, young adults often experience infectious mononucleosis caused by the virus, commonly known as glandular fever or the kissing disease.

The findings of this study conducted by the Karolinska Institutet in Sweden has been published in the journal Science Advances.

Previous studies have established a connection between EBV and MS indicating that EBV infection often precedes the development of MS and that antibodies against the virus may play a role.

However, the specific molecular mechanisms involved in this process have remained largely unknown and are believed to vary among patients.

In this recent study, researchers aimed to uncover and understand these molecular mechanisms, shedding light on the intricate relationship between EBV and MS.

“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,” said Olivia Thomas, postdoctoral researcher at the Department of Clinical Neuroscience, Karolinska Institutet and shared first author of the paper.

In a comprehensive analysis of blood samples taken from over 700 patients with multiple sclerosis and 700 healthy individuals, the researchers made a significant discovery.

They observed that antibodies targeting a specific protein in the EBV, known as EBNA1, can also bind to a similar protein found in the brain and spinal cord called CRYAB.

Normally, CRYAB functions to prevent protein aggregation under cellular stress conditions like inflammation. However, the researchers found that these antibodies, which mistakenly target CRYAB, could potentially cause damage to the nervous system.

This damage may contribute to the development of severe symptoms in MS patients, including difficulties with balance, mobility, and fatigue.

These antibodies were present in about 23 per cent of MS patients and 7 per cent 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.

“This also 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. “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 Thomas.

(PTI)