IAI Accepts, published online ahead of print on 8 September 2008

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Infect. Immun. doi:10.1128/IAI.00410-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Outer surface protein A protects Lyme disease spirochetes from acquired host immunity in the tick vector

James M. Battisti, James L. Bono, Patricia A. Rosa, Merry E. Schrumpf, Tom G. Schwan, and Paul F. Policastro^*

Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840 USA

^* To whom correspondence should be addressed. Email: ppolicastro{at}niaid.nih.gov.

The Lyme disease spirochete Borrelia burgdorferi alters expression of outer surface protein (osp) genes as the bacterium cycles between ticks and mammals. OspA is produced as borreliae enter the tick vector and remains a major surface antigen during midgut colonization. To elucidate its role in the vector, we created an insertional deletion of ospA in strain B31-A3. The ospA mutant infects mice when injected intradermally and is acquired by larval ticks fed on these mice, where it persists through the molt to nymphs. Survival in the vector was compared when artificially infected tick larvae were fed on naïve and immune mice. The ospA mutant proliferates in larvae if exposed to blood from naïve mice, but declines in density after larval feeding if the blood is from immune mice. When uninfected larvae are fed on B cell-deficient mice infected with the ospA mutant, larvae show borrelial densities and persistence significantly greater than those fed on infected, immunocompetent mice. We conclude that OspA serves a critical antibody shielding role during vector blood meal uptake from immune hosts, and is not required for persistence in the tick vector.

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