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Infection and Immunity, September 2007, p. 4237-4244, Vol. 75, No. 9
0019-9567/07/$08.00+0     doi:10.1128/IAI.00632-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Role of Outer Surface Protein D in the Borrelia burgdorferi Life Cycle{triangledown}

Xin Li,1,{dagger} Girish Neelakanta,1,{dagger} Xianzhong Liu,1,{dagger} Deborah S. Beck,1 Fred S. Kantor,2 Durland Fish,3 John F. Anderson,4 and Erol Fikrig1,3*

Sections of Rheumatology,1 Allergy and Immunology, Department of Internal Medicine,2 Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut 06520-8031,3 Department of Entomology, Connecticut Agricultural Experiment Station, New Haven, Connecticut 06504-11064

Received 4 May 2007/ Returned for modification 5 June 2007/ Accepted 25 June 2007

Borrelia burgdorferi preferentially induces selected genes in mice or ticks, and studies suggest that ospD is down-regulated in response to host-specific signals. We now directly show that ospD expression is generally elevated within Ixodes scapularis compared with mice. We then assessed the importance of OspD throughout the spirochete life cycle by generating OspD-deficient B. burgdorferi and examining the mutant in the murine model of tick-transmitted Lyme borreliosis. The lack of OspD did not influence B. burgdorferi infectivity in mice or the acquisition of spirochetes by I. scapularis. OspD adhered to tick gut extracts in vitro, and the OspD-deficient B. burgdorferi strain had a threefold decrease in colonization of the tick gut in vivo. This decrease, however, did not alter subsequent spirochete transmission during a second blood meal. These data suggest that B. burgdorferi can compensate for the lack of OspD in both ticks and mice and that OspD may have a nonessential, secondary, role in B. burgdorferi persistence within I. scapularis.

* Corresponding author. Mailing address: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520-8031. Phone: (203) 785-2453. Fax: (203) 785-7053. E-mail: erol.fikrig{at}yale.edu

{triangledown} Published ahead of print on 9 July 2007.

Editor: D. L. Burns

{dagger} X. Li., G.N., and X. Liu contributed equally to this work.

Infection and Immunity, September 2007, p. 4237-4244, Vol. 75, No. 9
0019-9567/07/$08.00+0     doi:10.1128/IAI.00632-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • 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]  
  • Stewart, P. E., Bestor, A., Cullen, J. N., Rosa, P. A. (2008). A Tightly Regulated Surface Protein of Borrelia burgdorferi Is Not Essential to the Mouse-Tick Infectious Cycle. Infect. Immun. 76: 1970-1978 [Abstract] [Full Text]  


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