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.