This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lawrenz, M. B.
Right arrow Articles by Norris, S. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lawrenz, M. B.
Right arrow Articles by Norris, S. J.

 Previous Article  |  Next Article 

Infection and Immunity, November 2004, p. 6577-6585, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6577-6585.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Effects of vlsE Complementation on the Infectivity of Borrelia burgdorferi Lacking the Linear Plasmid lp28-1

Matthew B. Lawrenz,1,2,{dagger} R. Mark Wooten,3 and Steven J. Norris1,2*

Department of Pathology and Laboratory Medicine,1 Program in Microbiology and Molecular Genetics, Graduate School of Biomedical Sciences, University of Texas—Houston Health Science Center, Houston, Texas,2 Department of Microbiology and Immunology, Medical College of Ohio, Toledo, Ohio3

Received 6 April 2004/ Returned for modification 12 May 2004/ Accepted 10 August 2004

The loss of linear plasmid lp28-1, which contains the vls antigenic variation locus, is associated with reduced infectivity of Borrelia burgdorferi in immunocompetent mice. The recombinant shuttle vector pBBE22, which includes the virulence determinant BBE22 from lp25 and restores infectivity to readily transformable B. burgdorferi lacking lp25 and lp56, was used to determine the effect of trans expression of vlsE on virulence. Spirochetes lacking lp28-1 were complemented with the plasmid pBBE22:vlsE, containing both BBE22 and vlsE. VlsE protein produced by this construct was expressed and surface accessible in in vitro-cultured B. burgdorferi, as determined by surface proteolysis and immunoblot analysis. Clones lacking lp25 but containing lp28-1 and either pBBE22 or pBBE22:vlsE were reisolated consistently from immunocompetent mice 8 weeks after infection. In contrast, a clone lacking both lp25 and lp28-1 and complemented with pBBE22:vlsE was isolated from only a single tissue of one of six C3H/HeN mice 8 weeks postinfection. These results indicate that either an intact vls antigenic variation locus or another determinant on lp28-1 is required to restore complete infectivity. In addition, an isogenic clone that retained lp28-1 was complemented with the vlsE shuttle plasmid and was examined for vlsE sequence variation and infectivity. Sequence variation was not observed for the shuttle plasmid, indicating that the cis arrangement of vlsE and the vls silent cassettes in lp28-1 facilitate vlsE gene conversion. Lack of vlsE sequence variation on the shuttle plasmid thus did not result in clearance of the trans-complemented strain in immunocompetent mice under the conditions tested.

* Corresponding author. Mailing address: Department of Pathology and Laboratory Medicine, University of Texas Medical School at Houston, P.O. Box 20708, Houston, TX 77225-0708. Phone: (713) 500-5338. Fax: (713) 500-0738. E-mail: steven.j.norris{at}uth.tmc.edu.

Editor: D. L. Burns

{dagger} Present address: Department of Molecular Microbiology, Washington University, St. Louis, Mo.

Infection and Immunity, November 2004, p. 6577-6585, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6577-6585.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Chen, Q., Fischer, J. R., Benoit, V. M., Dufour, N. P., Youderian, P., Leong, J. M. (2008). In Vitro CpG Methylation Increases the Transformation Efficiency of Borrelia burgdorferi Strains Harboring the Endogenous Linear Plasmid lp56. J. Bacteriol. 190: 7885-7891 [Abstract] [Full Text]  
  • Xu, Q., McShan, K., Liang, F. T. (2008). Modification of Borrelia burgdorferi to overproduce OspA or VlsE alters its infectious behaviour. Microbiology 154: 3420-3429 [Abstract] [Full Text]  
  • Liveris, D., Mulay, V., Sandigursky, S., Schwartz, I. (2008). Borrelia burgdorferi vlsE Antigenic Variation Is Not Mediated by RecA. Infect. Immun. 76: 4009-4018 [Abstract] [Full Text]  
  • Embers, M. E., Alvarez, X., Ooms, T., Philipp, M. T. (2008). The Failure of Immune Response Evasion by Linear Plasmid 28-1-Deficient Borrelia burgdorferi Is Attributable to Persistent Expression of an Outer Surface Protein. Infect. Immun. 76: 3984-3991 [Abstract] [Full Text]  
  • Barbour, A. G., Dai, Q., Restrepo, B. I., Stoenner, H. G., Frank, S. A. (2006). Pathogen escape from host immunity by a genome program for antigenic variation. Proc. Natl. Acad. Sci. USA 103: 18290-18295 [Abstract] [Full Text]  
  • Tilly, K., Krum, J. G., Bestor, A., Jewett, M. W., Grimm, D., Bueschel, D., Byram, R., Dorward, D., VanRaden, M. J., Stewart, P., Rosa, P. (2006). Borrelia burgdorferi OspC Protein Required Exclusively in a Crucial Early Stage of Mammalian Infection.. Infect. Immun. 74: 3554-3564 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»