Previous studies have established a link between EBV and MS, with increasing evidence suggesting that EBV infection precedes MS
Researchers have found further evidence for how the Epstein-Barr virus (EBV) triggers the neurological disease multiple sclerosis (MS) or drives disease progression.
The herpesvirus EBV, one of the most widespread viruses in humans, has infected over 90 per cent of the world’s population, who carry the virus for life as a latent and a usually asymptomatic infection.
Most people are infected as children with few or no symptoms but in young adults, the virus often causes infectious mononucleosis, also known as glandular fever or kissing disease.
This study from the Karolinska Institutet in Sweden is published in the journal Science Advances.
Previous studies have established a link between EBV and MS, with increasing evidence suggesting that EBV infection precedes MS and that antibodies against the virus may be involved.
This study uncovered the molecular mechanisms involved, which seemed to vary between patients and remained largely unknown, the researchers said.
“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.
Analysing blood samples from more than 700 patients with MS and 700 healthy individuals, the researchers 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.
They said that these misdirected, cross-reactive antibodies may damage the nervous system and cause severe symptoms in MS patients, including problems 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.
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