Childhood viral infections that
reach the brain may prime it for the development of autoimmune conditions, such
as multiple sclerosis, later in life — this is what a recent study that
scientists conducted in mice seems to suggest.
Recent research has shown
that multiple
sclerosis (MS) is the most common neurological autoimmune
condition among young adults worldwide, with 2,221,188 prevalent cases of MS in 2016
alone.
This condition can cause
problems with movement, balance, coordination, and even vision, alongside fatigue and
other symptoms.
Despite the fact that MS can
be debilitating, and that it affects such a large number of people worldwide,
scientists are still unsure what causes it.
Now, a team of researchers
from the University of Geneva (UNIGE) and the Geneva University Hospitals in
Switzerland are proposing a new theory that viral infections during childhood
could reach the brain and render the development of an autoimmune condition
more likely later in life.
The researchers support this
theory through evidence from a study of mouse models of MS, and they report
their findings in the journal Science Translational Medicine.
"We asked ourselves
whether brain viral infections that could be contracted in early childhood were
among the possible causes," explains study co-author Doron Merkler, who is
an associate professor in the Department of Pathology and Immunology at UNIGE's
Faculty of Medicine.
"But these transient
infections may, under certain circumstances, leave a local footprint, an
inflammatory signature, in the brain," he adds, pointing out that this
"mark" might be a factor in MS.
Brain lesions after a viral
infection
In the current study,
Merkler and team first induced a transient viral infection (an attenuated
strain of the lymphocytic choriomenigitis virus) in two groups of mice — one of
adult rodents, and another of very young ones.
"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," notes study co-author Karin
Steinbach, Ph.D.
For the second step of the
research, the investigators allowed all the mice to age. Then, they transferred
self-reactive cells to the mice. This type of cell, the researchers explain,
can impact brain structure, and some scientists also believe that they contribute
to MS.
"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," Steinbach explains.
This was certainly true for
the mice that had had the viral infection in adulthood. In these rodents, the
transferred self-reactive cells did not reach the brain.
However,
the mice that had had a viral infection early in their life developed brain
lesions — in their case, the self-reactive cells managed to infiltrate the
brain and affect it. Moreover, when they entered the brain, they went straight
to the area where the viral infection had been present.
When they studied the brains
of the mice that had had the viral infection as pups, the investigators found
that an abnormal number of brain-resident memory T cells, which are a certain
type of immune cells, had accumulated in the cortex.
"Under normal
circumstances, these cells are distributed throughout the brain, ready to
protect it in case of a viral attack. But here, the cells accumulate in surplus
at the exact spot of the infantile infection in the brain," notes Merkler.
In the mice, brain-resident
memory T cells produced a molecule that attracted self-reactive cells, which
helped them to gain access to the brain, causing lesions.
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