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Infection and Immunity, November 2008, p. 5274-5284, Vol. 76, No. 11
0019-9567/08/$08.00+0     doi:10.1128/IAI.00803-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Deletion of BBA64, BBA65, and BBA66 Loci Does Not Alter the Infectivity of Borrelia burgdorferi in the Murine Model of Lyme Disease{triangledown}

Mahulena Maruskova and J. Seshu*

South Texas Center for Emerging Infectious Diseases and Department of Biology, The University of Texas at San Antonio, San Antonio, Texas 78249

Received 27 June 2008/ Returned for modification 2 August 2008/ Accepted 22 August 2008

Borrelia burgdorferi, the causative agent of Lyme disease, alters its gene expression in response to highly disparate environmental signals encountered in its tick vector versus vertebrate hosts. Whole-genome transcriptional profile analysis of B. burgdorferi, propagated in vitro under mammalian-host-specific conditions, revealed significant upregulation of several linear plasmid 54 (lp54)-encoded open reading frames (ORFs). Among these ORFs, BBA64, BBA65, and BBA66 have been shown to be upregulated in response to multiple mammalian-host-specific signals. Recently, we determined that there was no significant difference in the ability of BBA64– mutant to infect C3H/HeN mice compared to its isogenic control strains, suggesting that B. burgdorferi might utilize multiple, functionally related determinants to establish infection. We further generated BBA65– and BBA66– single mutants in a noninfectious, lp25– clonal isolate of B. burgdorferi strain B31 (ML23) and complemented them with the minimal region of lp25 (BBE22) required for restoring the infectivity. In addition, we generated a BBA64– BBA65– BBA66– triple mutant using an infectious, clonal isolate of B. burgdorferi strain B31 (5A11) that has all of the infection-associated plasmids. There were no significant differences in the ability to isolate viable spirochetes from different tissues of C3H/HeN mice infected via intradermal needle inoculation with either the individual single mutants or the triple mutant compared to their respective isogenic parental strains at days 21 and 62 postinfection. These observations suggest that B. burgdorferi can establish infection in the absence of expression of BBA64, BBA65, and BBA66 in the murine model of Lyme disease.

* Corresponding author. Mailing address: BSE3.230, Department of Biology, The University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249. Phone: (210) 458-6578. Fax: (210) 458-5658. E-mail: j.seshu{at}utsa.edu

{triangledown} Published ahead of print on 2 September 2008.

Editor: A. J. Bäumler

Infection and Immunity, November 2008, p. 5274-5284, Vol. 76, No. 11
0019-9567/08/$08.00+0     doi:10.1128/IAI.00803-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Sanjuan, E., Esteve-Gassent, M. D., Maruskova, M., Seshu, J. (2009). Overexpression of CsrA (BB0184) Alters the Morphology and Antigen Profiles of Borrelia burgdorferi. Infect. Immun. 77: 5149-5162 [Abstract] [Full Text]  


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