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
Right arrow Citation Map
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ASM journals
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 Barbour, A. G.
Right arrow Articles by Sohaskey, C. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barbour, A. G.
Right arrow Articles by Sohaskey, C. D.

 Previous Article  |  Next Article 

Infection and Immunity, December 2000, p. 7114-7121, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Surface Protein Variation by Expression Site Switching in the Relapsing Fever Agent Borrelia hermsii

Alan G. Barbour,1,* Carol J. Carter,2 and Charles D. Sohaskey1,dagger

Departments of Microbiology & Molecular Genetics and Medicine, University of California---Irvine, Irvine, California 92697,1 and Department of Microbiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 782842

Received 9 May 2000/Returned for modification 28 June 2000/Accepted 22 September 2000

Borrelia hermsii, an agent of relapsing fever, undergoes antigenic variation of serotype-specifying membrane proteins during mammalian infections. When B. hermsii is cultivated in broth medium, one serotype, 33, eventually predominates in the population. Serotype 33 has also been found to be dominant in ticks but not in mammalian hosts. We investigated the biology and genetics of two independently derived clonal populations of serotype 33 of B. hermsii. Both isolates infected immunodeficient mice, but serotype 33 cells were limited in number and were only transiently present in the blood. Probes for vsp33, which encodes the serotype-specifying Vsp33 outer membrane protein, revealed that the gene was located on a 53-kb linear plasmid and that there was only one locus for the gene in serotype 33. The vsp33 probe and probes for other variable membrane protein genes showed that expression of Vsp33 was determined at the level of transcription and that when the vsp33 expression site was active, an expression site for other variable proteins was silent. The study confirmed that serotype 33 is distinct from other serotypes of B. hermsii in its biology and demonstrated that B. hermsii can change its major surface protein through switching between two expression sites.

* Corresponding author. Mailing address: Department of Microbiology & Molecular Genetics, B240 Med Sci I, University of California---Irvine, Irvine, CA 92697-4025. Phone: (949) 824-5626. Fax: (949) 824-8598. E-mail: abarbour{at}uci.edu.

dagger Present address: Tuberculosis Research Laboratory, Veterans Administration Medical Center, Long Beach, CA 90822.

Infection and Immunity, December 2000, p. 7114-7121, Vol. 68, No. 12
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Thein, M., Bunikis, I., Denker, K., Larsson, C., Cutler, S., Drancourt, M., Schwan, T. G., Mentele, R., Lottspeich, F., Bergstrom, S., Benz, R. (2008). Oms38 Is the First Identified Pore-Forming Protein in the Outer Membrane of Relapsing Fever Spirochetes. J. Bacteriol. 190: 7035-7042 [Abstract] [Full Text]  
  • Hermann, C. (2007). Review: Variability of host pathogen interaction. Innate Immunity 13: 199-218 [Abstract]  
  • Meri, T., Cutler, S. J., Blom, A. M., Meri, S., Jokiranta, T. S. (2006). Relapsing Fever Spirochetes Borrelia recurrentis and B. duttonii Acquire Complement Regulators C4b-Binding Protein and Factor H. Infect. Immun. 74: 4157-4163 [Abstract] [Full Text]  
  • Porcella, S. F., Raffel, S. J., Anderson, D. E. Jr., Gilk, S. D., Bono, J. L., Schrumpf, M. E., Schwan, T. G. (2005). Variable Tick Protein in Two Genomic Groups of the Relapsing Fever Spirochete Borrelia hermsii in Western North America. Infect. Immun. 73: 6647-6658 [Abstract] [Full Text]  
  • Belperron, A. A., Dailey, C. M., Bockenstedt, L. K. (2005). Infection-Induced Marginal Zone B Cell Production of Borrelia hermsii-Specific Antibody Is Impaired in the Absence of CD1d. J. Immunol. 174: 5681-5686 [Abstract] [Full Text]  
  • Barbour, A. G., Bundoc, V. (2001). In Vitro and In Vivo Neutralization of the Relapsing Fever Agent Borrelia hermsii with Serotype-Specific Immunoglobulin M Antibodies. Infect. Immun. 69: 1009-1015 [Abstract] [Full Text]  
  • Rich, S. M., Sawyer, S. A., Barbour, A. G. (2001). Antigen polymorphism in Borrelia hermsii, a clonal pathogenic bacterium. Proc. Natl. Acad. Sci. USA 98: 15038-15043 [Abstract] [Full Text]  


Copyright © 2010 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»