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Infection and Immunity, April 2007, p. 1973-1983, Vol. 75, No. 4
0019-9567/07/$08.00+0 doi:10.1128/IAI.01815-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Microbiology and Immunology, University of Maryland School of Medicine, 660 West Redwood St., HH Room 324, Baltimore, Maryland 21201,1 Virginia Bioinformatics Institute (0477), Bioinformatics Facility, Virginia Tech, Washington St., Blacksburg, Virginia 240612
Received 15 November 2006/ Returned for modification 21 December 2006/ Accepted 21 January 2007
Recent studies aimed at elucidating the rickettsia-tick interaction have discovered that the spotted fever group rickettsia Rickettsia montanensis, a relative of R. rickettsii, the etiologic agent of Rocky Mountain spotted fever, induces differential gene expression patterns in the ovaries of the hard tick Dermacentor variabilis. Here we describe a new defensin isoform, defensin-2, and the expression patterns of genes for three antimicrobials, defensin-1 (vsnA1), defensin-2, and lysozyme, in the midguts and fat bodies of D. variabilis ticks that were challenged with R. montanensis. Bioinformatic and phylogenetic analyses of the primary structure of defensin-2 support its role as an antimicrobial. The tissue distributions of the three antimicrobials, especially the two D. variabilis defensin isoforms, are markedly different, illustrating the immunocompetence of the many tissues that R. montanensis presumably invades once acquired by the tick. Antimicrobial gene expression patterns in R. montanensis-challenged ticks suggest that antimicrobial genes play a role during the acquisition-invasion stages in the tick.
Published ahead of print on 29 January 2007.
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