Scientists have found more evidence of how the Epstein-Barr virus (EBV) triggers the neurological disease multiple sclerosis (MS) or controls the progression of the disease.
Herpesvirus EBV, one of the most common viruses in humans, has infected more than 90 percent of the world’s population, who carry the virus throughout their lives as a latent and 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 shown a link between EBV and MS, with growing evidence suggesting that EBV infection precedes MS and that antibodies to the virus may be involved.
This study revealed the molecular mechanisms involved, which differed between patients and remained largely unknown, the researchers said.
“We found 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, a postdoctoral researcher at the Department of Clinical Neuroscience, Karolinska Institutet and shared the first author of the article.
Analyzing blood samples from more than 700 MS patients and 700 healthy individuals, the researchers found that antibodies that bind to a particular Epstein-Barr virus protein, 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 these misdirected, cross-reacting antibodies can 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 percent of MS patients and 7 percent of controls. “This shows that although these antibody responses are not necessary for the development of the disease, they may be involved in the disease in up to a quarter of MS patients.
“This also demonstrates the wide variation between patients, highlighting the need for personalized therapies. Current therapies are effective in reducing MS relapses, but unfortunately none can prevent disease progression.”
“MS is an incredibly complex disease, but our study provides an important piece of the puzzle and may explain why some people develop the disease,” said Thomas.
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