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Infection and Immunity, May 2001, p. 3507-3509, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.3507-3509.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Dissociation of Infectivity and Pathogenicity in Borrelia burgdorferi

Venetta Thomas,1 Juan Anguita,1 Swapna Samanta,1 Patricia A. Rosa,2 Philip Stewart,2 Stephen W. Barthold,3 and Erol Fikrig1,*

Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 065201; Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 598402; and Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 956163

Received 12 October 2000/Returned for modification 18 December 2000/Accepted 21 February 2001

Clonal Borrelia burgdorferi N40 (cN40) passaged 75 times in vitro (N40-75) infects mice but does not cause disease. N40-75 passaged 45 times further in vitro (N40-120) was no longer infectious and lacked genes encoded on linear plasmids 38 and 28-1, among other differences. These data suggest that B. burgdorferi cN40, N40-75, and N40-120 have distinct phenotypes that can be used to dissect the genetic elements responsible for pathogenicity and infectivity.

* Corresponding author. Mailing address: Yale University School of Medicine, Section of Rheumatology, Department of Internal Medicine, 608 Laboratory of Clinical Investigation, P.O. Box 208031, New Haven, CT 06520-8031. Phone: (203) 785-2453. Fax: (203) 785-7053. E-mail: erol.fikrig{at}yale.edu.

Infection and Immunity, May 2001, p. 3507-3509, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.3507-3509.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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