| Infections
early in life with viruses that cross-react with central nervous
system epitopes seem to prime individuals for development of
multiple sclerosis, Dr. Robert Fujinami reported here at the
General Meeting of the American Society for Microbiology.
Dr. Fujinami,
of the University of Utah in Salt Lake City, told Reuters
Health, "We hypothesize that if a virus encodes a cross-reacting
determinant with self central nervous system protein, that
would increase the numbers of autoreactive T cells, which
would be maintained below a threshold level. A later immunologic
trigger would lead to activation of those cells and CNS autoimmune
disease."
Dr. Fujinami and
his associates injected mice with carrier DNA encoding myelin
proteolipid protein, to mimic virus infections that cross-react
with proteolipid protein in the CNS. No evidence of central
nervous system disease was detected at that time. However,
inflammation of the CNS was triggered by a later challenge
with an unrelated virus that did not cross-react with the
host CNS proteins.
These findings
help explain why viral infections have been implicated in
the development and exacerbation of MS, yet no one virus has
been identified as the MS agent, Dr. Fujinami said.
Previous research
has suggested that viruses associated with MS attacks induce
the body to produce interleukin-12, Dr. Fujinami noted. His
group plans to compare viral infections that induce interleukin-12
with those that induce type 1 interferons.
"It might be that
certain kinds of infections may actually be beneficial if
they produce a lot of type 1 interferon, which downregulate
interleukin-12," Dr. Fujinami said.
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