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Infection and Immunity, March 2003, p. 1200-1208, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1200-1208.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Polymorphic Membrane Protein H Has Evolved in Parallel with the Three Disease-Causing Groups of Chlamydia trachomatis

Diane R. Stothard,* Gregory A. Toth, and Byron E. Batteiger

The Department of Medicine, Division of Infectious Diseases, Indiana University School of Medicine, Indianapolis, Indiana 46202

Received 2 July 2002/ Returned for modification 26 September 2002/ Accepted 2 December 2002

Chlamydia trachomatis is a human pathogen causing trachoma, urogenital disease, and lymphogranuloma venereum (LGV). A family of nine polymorphic membrane protein genes (pmpA to pmpI), resembling autotransporter proteins, has recently been discovered in C. trachomatis. pmp genes are large and predicted to be outer membrane proteins. We hypothesized that they would contain useful nucleotide sequence variability for epidemiologic studies. Since sequence information is available only for serovars D and L2, we sought to determine the amount of diversity within an individual pmp gene among serovars. We used restriction fragment length polymorphism (RFLP) analysis as a primary screen to assess the amount of sequence divergence among the pmp genes for serovars A to L3 of C. trachomatis. RFLP analysis showed little variation for some of the genes, such as pmpA, but substantial variation in others, such as pmpI. pmpH and pmpE yielded RFLP patterns that clustered the 15 serovars into ocular, urogenital, and LGV groups, and both proteins have been localized to the outer membrane. Therefore, we chose to sequence pmpE, pmpH, and pmpI from each of the 15 serovars. Evolutionary analysis showed three distinct divergence patterns. PmpI was least variable, resulting in an ambiguous evolutionary pattern. PmpE showed a high degree of diversity in the ocular strains compared to the other strains. Finally, the evolution of PmpH shows three groups that reflect disease groups, suggesting this protein may play a role in pathogenesis.


* Corresponding author. Mailing address: Department of Medicine, Division of Infectious Diseases, Indiana University School of Medicine, 435 Emerson Hall, 545 Barnhill Dr., Indianapolis, IN 46202. Phone: (317) 278-1791. Fax: (317) 274-1587. E-mail: dstothar{at}iupui.edu.

Editor: J. T. Barbieri


Infection and Immunity, March 2003, p. 1200-1208, Vol. 71, No. 3
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.3.1200-1208.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




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