There is a link between childhood viral infections and the development of multiple sclerosis in adulthood, say Swiss researchers.
Multiple sclerosis is considered an autoimmune disease whose severity and evolution are very different from one person to another. It attacks the central nervous system by targeting myelin, which is in a way the protective envelope of nerve fibers.
The deterioration of this substance causes inflammation, which in turn causes interruptions in the propagation of nerve impulses.
When the myelin is slightly deteriorated, the impulse is transmitted without too many interruptions, but when this deterioration increases, the nerve fibers are altered and become incapable of communicating.
So far, the causes of multiple sclerosis remain mysterious, and there is no cure for it.
Researchers associate its triggering with genetic and environmental components, but which exactly?
- On average, 1 in 1,000 people have multiple sclerosis;
- the disease is usually diagnosed in people aged 20 to 40 years;
- northern countries are more affected than countries close to the equator;
- Canada has the highest rate of multiple sclerosis in the world (about 1 in 400 cases).
The viral track
Prof. Doron Merkler and his colleagues from the Faculty of Medicine at the University of Geneva have studied in mice the potential link between transient cerebral viral infections that occurred in early childhood and the appearance of an autoimmune disease. cerebral immune later in life.
We wondered whether early childhood viral infections were among the possible causes.
Transient brain infections can be rapidly controlled by the immune system, even without the child’s noticing.
“But such a transient infection may, under certain circumstances, leave a local imprint in the brain, which could be characterized by inflammatory signature,” says Prof. Merkler.
Swiss scientists are therefore interested in this type of impression in young brains and the appearance of the disease years later.
They caused a transient viral infection in a group of adult mice and a group of mice that cleared the infection within a week, showing a similar antiviral response.
Then they let the two groups of rodents age and then transfer immune cells to brain structures called self-reactive cells that are found in a patient with multiple sclerosis.
Such cells may also be present in humans, without necessarily being associated with a disease, as they are controlled by different mechanisms and do not have access to the brain.
Karin Steinbach, Faculty of Medicine, University of Geneva
Their results show that :
in the group of mice infected with the virus in adulthood, autoreactive cells did not induce brain lesions;
in infected mice when young, self-reactive cells migrated to the brain at the precise location of infection and began to destroy their structures.
According to the researchers, the brain area struck in childhood undergoes a tissue modification that leads, years later, the immune system to turn against itself in this specific place, triggering autoimmune lesions.
T lymphocytes give the signal
When analyzing the tissues of the virus-infected area in the mice group, the researchers observed an accumulation of immune cells, memory-resident T cells in the brain tissue.
Normally, these are distributed throughout the brain, ready to protect it in case of viral attack. But here, these cells accumulate in excess in the precise place of the infant infection, changing the structure of the tissue.
They also found that this cellular accumulation produces a molecule that attracts self-reactive cells, opening them access to the brain.
They then start destroying their structures, causing multiple sclerosis.
In order to verify this observation, we blocked the autoreactive cell receptor that perceives the signal produced by the accumulation of memory T cells resident in the brain, and indeed, the mice have been protected from brain damage!
“We then looked at whether, in people with multiple sclerosis, we found this accumulation of memory T-cells residing in the brain tissue that produces the call signal to self-reactive cells, and that’s the case! Adds Karin Steinbach.
Scientists believe that such a mechanism could exist in humans. However, other work is needed to establish it.
We are continuing our research in this direction, particularly to understand why T cells accumulate in a child’s brain as a result of infection and do not occur in an adult.
The details of this work are published in the journal Science Translational Medicine.
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