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Science

Science in Mind

Stealth, molecular trickery key to EEE’s deadly efficiency

They have become reluctant late-summer traditions: Stay indoors after dusk, apply mosquito repellent, and cancel outdoor events and sports practices to avoid possible exposure to Eastern equine encephalitis, the most deadly mosquito-borne illness in North America.

While the dangers posed by the virus are well known — a 35 percent to 75 percent chance of death — precisely why it is so severe and comes on so suddenly has remained a mystery. A new study by researchers at the University of Pittsburgh Center for Vaccine Research illuminates how the virus uses a molecular trick to avoid triggering immune system sentinel cells and causing warning symptoms before the infection is at its height.

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“You’re feeling OK, walking around, and on Friday you feel a little bit bad. Saturday, you go to the hospital. And Sunday, you have severe brain damage and you may die,” said William Klimstra, associate professor of microbiology and molecular genetics at the University of Pittsburgh, and senior author of the paper published Wednesday in Nature. “We found that Eastern [equine encephalitis] does not elicit an innate immune response,” which would give rise to that weak, sick, feverish feeling people get when they’re coming down with the flu.

One intriguing piece of evidence that may support the finding comes from the experience of physicians in Boston, who have found that children who are sick longer before the peak of the infection — with what are known as prodromal symptoms — tend to do better.

“There was a pretty clear cut difference. . . . Children that presented with no prodromal symptoms or short prodromal symptoms, up to two days, those children didn’t do as well. Whereas children that presented with more of a five-day illness, seem to do a lot better,” said Dr. Asim Ahmed, an instructor in the division of infectious diseases at Boston Children’s Hospital.

Ahmed, who has treated a half-dozen patients with Eastern equine encephalitis, said that more work needs to be done to understand whether the molecular mechanisms described in the paper explain the differences in the severity of the disease in patients, but that the new level of insight is exciting.

“Any time you can understand how a pathogen causes disease, that gives you a better chance at coming up with strategies to interfere,” Ahmed said.

Carolyn Y. Johnson can be reached at cjohnson@globe.com. Follow her on Twitter @carolynyjohnson.

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