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Infection and Immunity, January 2008, p. 391-402, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.01118-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role of the BBA64 Locus of Borrelia burgdorferi in Early Stages of Infectivity in a Murine Model of Lyme Disease{triangledown}

Mahulena Maruskova, M. Dolores Esteve-Gassent, Valerie L. Sexton, 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 10 August 2007/ Returned for modification 20 September 2007/ Accepted 25 October 2007

Borrelia burgdorferi, the causative agent of Lyme disease, undergoes rapid adaptive gene expression in response to environmental signals encountered during different stages of its life cycle in the arthropod vector or the mammalian host. Among all the plasmid-encoded genes of B. burgdorferi, several linear plasmid 54 (lp54)-encoded open reading frames (ORFs) exhibit the greatest differential expression in response to mammalian host-specific temperature, pH, and other uncharacterized signals. These ORFs include members of the paralogous gene family 54 (pgf 54), such as BBA64, BBA65, and BBA66, present on lp54. In an attempt to correlate transcriptional up-regulation of these pgf 54 members to their role in infectivity, we inactivated BBA64 and characterized the phenotype of this mutant both in vitro and in vivo. There were no major differences in the protein profiles between the BBA64 mutant and the control strains, while immunoblot analysis indicated that inactivation of BBA64 resulted in increased levels of BBA65. Moreover, there was no significant difference in the ability of the BBA64 mutant to infect C3H/HeN mice compared to that of its parental or complemented control strains as determined by culturing of viable spirochetes from infected tissues. However, enumeration of spirochetes using quantitative real-time PCR revealed tissue-specific differences, suggesting a minimal role for BBA64 in the survival of B. burgdorferi in select tissues. Infectivity analysis of the BBA64 mutant suggests that B. burgdorferi may utilize multiple determinants to establish infection in mammalian hosts.

* Corresponding author. Mailing address: The University of Texas at San Antonio, Department of Biology, BSE3.230, 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 5 November 2007.

Editor: A. J. Bäumler

Infection and Immunity, January 2008, p. 391-402, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.01118-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Weening, E. H., Parveen, N., Trzeciakowski, J. P., Leong, J. M., Hook, M., Skare, J. T. (2008). Borrelia burgdorferi Lacking DbpBA Exhibits an Early Survival Defect during Experimental Infection. Infect. Immun. 76: 5694-5705 [Abstract] [Full Text]  
  • Maruskova, M., Seshu, J. (2008). Deletion of BBA64, BBA65, and BBA66 Loci Does Not Alter the Infectivity of Borrelia burgdorferi in the Murine Model of Lyme Disease. Infect. Immun. 76: 5274-5284 [Abstract] [Full Text]  
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