November 22, 2024

How Can a Common Virus Cause Multiple Sclerosis? New Study Explains

The Epstein-Barr Virus (EBV), a type of herpesvirus, is one of the most frequently found viruses in human beings. In young adults, EBV frequently leads to contagious mononucleosis, colloquially known as glandular fever or the kissing disease.
Researchers from the Karolinska Institute in Sweden have actually discovered additional evidence concerning the Epstein-Barr viruss role in initiating or intensifying numerous sclerosis. The study, released in Science Advances, indicates that particular people have antibodies versus this virus that accidentally target a protein located in the brain and spinal cable.
The Epstein-Barr virus (EBV) usually infects individuals throughout early life, staying within the body forever without setting off visible signs. The link in between EBV and the neurological illness numerous sclerosis (MS) was discovered many years ago and has actually puzzled researchers since.
Increasing proof, including 2 papers published in Science and Nature in 2015, recommends that EBV infection precedes MS and that antibodies against the infection might be involved. However, the molecular mechanisms appear to differ in between clients and stay largely unknown.

The Epstein-Barr Virus (EBV), a type of herpesvirus, is one of the most frequently found viruses in people. Its estimated that over 90% of individuals internationally are carriers of EBV, keeping a normally symptom-free and latent infection throughout their lives. In young grownups, EBV often leads to transmittable mononucleosis, colloquially understood as glandular fever or the kissing disease.
They found that antibodies that bind to a particular protein in the Epstein-Barr virus, EBNA1, can also bind to a comparable protein in the brain and spine cord called CRYAB, whose function is to prevent protein aggregation throughout conditions of cellular stress such as swelling.” This shows that, whilst these antibody reactions are not needed for disease development, they may be included in disease in up to a quarter of MS clients,” says Olivia Thomas.

” MS is an incredibly complicated disease, however our research study provides an essential piece in the puzzle and might describe why some individuals establish the illness,” says Olivia Thomas, a postdoctoral scientist at the Department of Clinical Neuroscience, Karolinska Institutet and shared very first author of the paper. “We have actually found that certain antibodies versus the Epstein-Barr virus, which would typically fight the infection, can mistakenly target the brain and spine and cause damage.”
Misdirected antibodies
They found that antibodies that bind to a certain protein in the Epstein-Barr infection, EBNA1, can likewise bind to a similar protein in the brain and spinal cord called CRYAB, whose role is to avoid protein aggregation throughout conditions of cellular stress such as inflammation. The antibodies were present in about 23 percent of MS clients and 7 percent of control people.
” This reveals that, whilst these antibody responses are not needed for illness advancement, they might be included in disease in as much as a quarter of MS clients,” says Olivia Thomas. “This likewise demonstrates the high variation between clients, highlighting the need for tailored therapies. Present treatments work at reducing relapses in MS however sadly, none can prevent illness progression.”
T cells may likewise be included
The researchers also found that there is likely a similar cross-reactivity among T cells of the body immune system.
” We are now broadening our research to investigate how T cells battle EBV infection and how these immune cells might damage the nerve system in several sclerosis and add to illness progression,” states Mattias Bronge, associated researcher at the Department of Clinical Neuroscience, Karolinska Institutet and shared first author of the paper.
Reference: “Cross-reactive EBNA1 resistance targets alpha-crystallin B and is associated with several sclerosis” by Olivia G. Thomas, Mattias Bronge, Katarina Tengvall, Birce Akpinar, Ola B. Nilsson, Erik Holmgren, Tara Hessa, Guro Gafvelin, Mohsen Khademi, Lars Alfredsson, Roland Martin, André Ortlieb Guerreiro-Cacais, Hans Grönlund, Tomas Olsson and Ingrid Kockum, 17 May 2023, Science Advances.DOI: 10.1126/ sciadv.adg3032.
The study was funded by Swedens development firm Vinnova, the Swedish Research Council, the Swedish Brain Foundation, Karolinska Institutet, MS Forskningsfonden, Neuro, and Region Stockholm. Birce Akpinar, Ola B. Nilsson, Erik Holmgren and Guro Gafvelin hold positions at NEOGAP Therapeutics AB. Roland Martin is a co-founder, co-owner and a staff member of Cellerys, a spin-out from the University of Zürich, and is a coinventor and patent holder for several patents.