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Infection and Immunity, May 2005, p. 3096-3103, Vol. 73, No. 5
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.5.3096-3103.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Structural and Genetic Diversity of Group B Streptococcus Capsular Polysaccharides

Michael J. Cieslewicz,1,2,{dagger} Donald Chaffin,3,{dagger} Gustavo Glusman,4,{dagger} Dennis Kasper,1,2,5 Anup Madan,4 Stephani Rodrigues,4 Jessica Fahey,4 Michael R. Wessels,1,2,6 and Craig E. Rubens3*

Channing Laboratory, Department of Medicine, Brigham and Women's Hospital,1 Division of Infectious Diseases, Children's Hospital Boston,6 Department of Microbiology and Molecular Genetics,5 Harvard Medical School, Boston, Massachusetts,2 Institute for Systems Biology,4 Division of Infectious Diseases, Children's Hospital, University of Washington, Seattle, Washington3

Received 20 August 2004/ Returned for modification 16 November 2004/ Accepted 24 December 2004

Group B Streptococcus (GBS) is an important pathogen of neonates, pregnant women, and immunocompromised individuals. GBS isolates associated with human infection produce one of nine antigenically distinct capsular polysaccharides which are thought to play a key role in virulence. A comparison of GBS polysaccharide structures of all nine known GBS serotypes together with the predicted amino acid sequences of the proteins that direct their synthesis suggests that the evolution of serotype-specific capsular polysaccharides has proceeded through en bloc replacement of individual glycosyltransferase genes with DNA sequences that encode enzymes with new linkage specificities. We found striking heterogeneity in amino acid sequences of synthetic enzymes with very similar functions, an observation that supports horizontal gene transfer rather than stepwise mutagenesis as a mechanism for capsule variation. Eight of the nine serotypes appear to be closely related both structurally and genetically, whereas serotype VIII is more distantly related. This similarity in polysaccharide structure strongly suggests that the evolutionary pressure toward antigenic variation exerted by acquired immunity is counterbalanced by a survival advantage conferred by conserved structural motifs of the GBS polysaccharides.

* Corresponding author. Mailing address: Division of Infectious Diseases, Children's Hospital, University of Washington, Seattle, WA 98109. Phone: (206) 987-2073. Fax: (206) 987-7311. E-mail: craig.rubens{at}seattlechildrens.org.

Editor: V. J. DiRita

{dagger} M.J.C., D.C., and G.G. contributed equally to this work.

Infection and Immunity, May 2005, p. 3096-3103, Vol. 73, No. 5
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.5.3096-3103.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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