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1 January 2006

Volume 193, Number 1
The Journal of Infectious Diseases 2006;193:121–128
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2006/19301-0018$15.00
DOI: 10.1086/498574
MAJOR ARTICLE

Single‐Nucleotide Polymorphism–Based Population Genetic Analysis of Mycobacterium tuberculosis Strains from 4 Geographic Sites

Michaela M. Gutacker,1,a

Barun Mathema,2,3

Hanna Soini,5

Elena Shashkina,2

Barry N. Kreiswirth,2

Edward A. Graviss,4 and

James M. Musser1,4

1Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana; 2Public Health Research Institute Tuberculosis Center, Newark, New Jersey; 3Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York; 4Center for Human Infectious Diseases Research, Department of Pathology, Baylor College of Medicine, Houston, Texas; 5Mycobacterial Reference Laboratory, KTL National Public Health Institute, Turku, Finland

We studied genetic relationships among 5069 Mycobacterium tuberculosis strains recovered from patients enrolled in 4 population‐based studies in the United States and Europe, by analysis of 36 synonymous single‐nucleotide polymorphisms (SNPs). All strains were assigned to 1 of 9 major genetic clusters based on sSNP profile. The same 9 genetic clusters were revealed by analysis of 227 nonsynonymous SNPs, 121 intergenic SNPs, and concatenated profiles of 578 SNPs available for a subset of 48 representative strains. IS6110 profiles, spoligotypes, and mycobacterial interspersed repetitive unit patterns were nonrandomly associated with SNP‐based phylogenetic lineages, together indicating a strongly clonal population structure. Isolates of the 9 genetic clusters were not distributed with equal frequency in all localities, reflecting geographic subdivision. The SNP‐based phylogenetic framework provides new insight into the worldwide evolution of M. tuberculosis and a gateway for investigating genotype‐disease phenotype relationships in large samples of strains.

Received 19 May 2005; accepted 29 July 2005; electronically published 28 November 2005.

Reprints or correspondence: Dr. James M. Musser, Methodist Hospital Research Institute, 6565 Fannin St., Houston, TX 77030 ().

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  • Potential conflicts of interest: none reported.

    Financial support: Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health.

  • Present affiliation: Instituto Cantonale di Microbiologia, Bellinzona, Switzerland.

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