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Relapsing Fever Spirochete Switches Surface Proteins When It Changes Hosts

Scientists at the Rocky Mountain Laboratories (RML) report that the corkscrew-shaped bacterium that causes tick-borne relapsing fever switches surface proteins when it moves from a tick into a mammal or vice versa. Their finding, they say, could lead to an improved blood test for diagnosing the illness, one that might help clinicians distinguish relapsing fever from its better known relative, Lyme disease, in the Western United States where both diseases are endemic.

Tom G. Schwan, Ph.D., acting chief of the RML Laboratory of Microbial Structure and Function, and B. Joseph Hinnebusch, Ph.D., staff fellow in the lab, co-authored the report published July 19 in the journal Science. RML, based in Hamilton, Mont., is part of the National Institute of Allergy and Infectious Diseases (NIAID).

"A large number of proteins on the surface of the relapsing fever spirochete vary during infection in mammals," explains Dr. Schwan. In fact, it's the spontaneous changes in these proteins during human infection that allow the microbe to periodically escape immune detection, leading to a relapse of symptoms. "In our mouse studies," says Dr. Schwan, "we found that these proteins all get turned off during infection in the tick and a different stable type of protein gets produced in their place. But when the spirochete's transmitted back to a mammal, that tick-specific protein gets turned off again and the microbe again produces that very same variable membrane protein that was being produced when the tick ingested it."

Decreasing the temperature, the RML scientists discovered, can trigger the change. "One likely cue that promotes this switch is the drop in temperature that occurs when the spirochete moves from a warm-blooded animal to a tick," Dr. Schwan notes.

Their observations of Borrelia hermsii, the spirochete that causes relapsing fever, can be extended to other Borrelia species, says Dr. Schwan, including B. burgdorferi, the causative agent of Lyme dis
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Contact: Laurie K. Doepel
ldoepel@nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
18-Jun-1998


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