Immune hematology

The researches find that the the potential link between transient cerebral viral infections in early childhood and the development of this cerebral autoimmune disease later in life. Indeed, the brain area affected by viral infection during childhood undergoes a change that can call, a long time later; on the immune system to turn against itself at this precise location; triggering autoimmune lesions.  These results; which are publish in the journal Science Translational Medicine; provide a first step in answering one of the possible environmental causes of this serious disease.

Cerebral viral infections

Multiple sclerosis affects one in 1,000 people in Switzerlane; two-thirds of whom are women. It is the most common auto-immune disease affecting the brain. Up to date; there is still neither a cure available, nor a clear understanding of the factors that trigger this disease at around 30 years of age.

“They asked ourselves whether brain viral infections that could be contract in early childhood are among the possible causes;” says Doron Merkler; a professor in the Department of Pathology and Immunology in UNIGE’s Faculty of Medicine and senior consultant in the Clinical Pathology Service of the HUG.

Pathology and Immunology

Such transient brain infections  control quickly by the immune system; without the affected individual even noticing any symptoms. “But these transient infections may, under certain circumstances; leave a local footprint, an inflammatory signature; in the brain;” continues the researcher.

The scientists induced a transient viral infection in a group of adult mice and in a group of mice at a very young age in order to test this hypothesis. Karin Steinbach, a researcher in the same department, explains: In both cases, the mice showed no signs of the disease and eliminated the infection within a week with a similar anti-viral immune response.”

Brain in adulthood

The scientists then allowed the two groups of mice to grow older before they are transfer with self-reactive cells, which can target the normal brain structure and are also thought to contribute to the illness of patients with multiple sclerosis. “These self-reactive cells are present in most of us; but do not necessarily induce a disease; since they are controlled by different regulatory mechanisms and usually don’t have access to the brain,” explains Karin Steinbach.

Indeed, in the group of mice infected with the virus in adulthood; the transferred self-reactive cells did not gain access to the brain and no brain lesions were observed. However, in those mice that had been infected at a very young age, the self-reactive cells gained access to the brain in adulthood, and migrated to the precise location where the infection had previously occurred.