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Infection and Immunity, August 2005, p. 4818-4822, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4818-4822.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Slow Genetic Divergence of Helicobacter pylori Strains during Long-Term Colonization

Annelie Lundin,1,2 Britta Björkholm,1,2 Ilya Kupershmidt,3,4 Magnus Unemo,5 Peter Nilsson,3 Dan I. Andersson,1,2 and Lars Engstrand1,2*

Department of Bacteriology, Swedish Institute for Infectious Disease Control, Solna, Sweden,1 Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden,2 Department of Biotechnology, KTH-Royal Institute of Technology, Stockholm, Sweden,3 Agilent Technologies, Redwood City, California,4 Department of Clinical Microbiology, Örebro University Hospital, Örebro, Sweden5

Received 17 September 2004/ Returned for modification 2 November 2004/ Accepted 4 April 2005

The genetic variability of Helicobacter pylori is known to be high compared to that of many other bacterial species. H. pylori is adapted to the human stomach, where it persists for decades, and adaptation to each host results in every individual harboring a distinctive bacterial population. Although clonal variants may exist within such a population, all isolates are generally genetically related and thus derived from a common ancestor. We sought to determine the rate of genetic change of H. pylori over 9 years in two asymptomatic adult patients. Arbitrary primed PCR confirmed the relatedness of individual subclones within a patient. Furthermore, sequencing of 10 loci (~6,000 bp) in three subclones per time and patient revealed only two base pair changes among the subclones from patient I. All sequences were identical among the patient II subclones. However, PCR amplification of the highly divergent gene amiA revealed great variation in the size of the gene between the subclones within each patient. Thus, both patients harbored a single strain with clonal variants at both times. We also studied genetic changes in culture- and mouse-passaged strains, and under both conditions no genetic divergence was found. These results suggest that previous estimates of the rate of genetic change in H. pylori within an individual might be overestimates.

* Corresponding author. Mailing address: Department of Bacteriology, Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden. Phone: 46 8 457 2415. Fax: 46 8 30 17 97. E-mail: Lars.Engstrand{at}smi.ki.se.

Editor: J. B. Bliska

Infection and Immunity, August 2005, p. 4818-4822, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4818-4822.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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