A common childhood virus could be an important trigger for multiple sclerosis (MS) in later life, research has suggested.
The finding, which could be a platform for the development of new treatments for the condition, has been published in the journal Science Advances.
The research, led by Dr Olivia Thomas of Sweden’s Karolinska Institute, has suggested the body’s immune response to the Epstein-Barr virus (EBV), a normally harmless infection, can misfire and mistakenly target a crucial protein in the brain and spinal cord.
EBV infects most people early in life and then remains in the body, usually without causing symptoms. The link between EBV and MS was discovered many years ago and has long puzzled researchers.
The latest research builds on two papers published in the journals Science and Nature last year. These suggested EBV infection could precede MS and that antibodies against the virus could be involved. Those infected with EBV were 32 times more likely to develop MS, they concluded. However, the molecular mechanisms appeared to vary between patients and remained largely unknown.
Multiple sclerosis
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“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 Dr Thomas, postdoctoral researcher in the institute’s Department of Clinical Neuroscience.
“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.”
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, called 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% of MS patients yet only 7% 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 Dr Thomas. “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.”
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The researchers also found that there is likely a similar cross-reactivity among T cells of the immune system.
“We are now expanding our research to investigate how T cells fight EBV infection and how these immune cells may damage the nervous system in multiple sclerosis and contribute to disease progression,” said Mattias Bronge, affiliated researcher at the institute’s Department of Clinical Neuroscience.
