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Journal of Clinical Microbiology, December 2004, p. 5658-5663, Vol. 42, No. 12
0095-1137/04/$08.00+0 DOI: 10.1128/JCM.42.12.5658-5663.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Novel 180- and 480-Base-Pair Insertions in African and African-American Strains of Helicobacter pylori
Shannon L. McNulty ,1,
,
Beth M. Mole,1,,
Daiva Dailidiene,2
Issy Segal,3
Reid Ally,3
Rajesh Mistry,3
Ousman Secka,4
Richard A. Adegbola,4
Julian E. Thomas,5
Erik M. Lenarcic,1
Richard M. Peek Jr.,6,7
Douglas E. Berg,2* and
Mark H. Forsyth1
Department of Biology, College of William and Mary, Williamsburg, Virginia,1 Department of Molecular Microbiology, Washington University Medical School, St. Louis, Missouri,2 African Institute of Digestive Disease, Chris Hani Baragwanath Hospital, Soweto, Johannesburg, South Africa,3 Medical Research Council Laboratories, Fajara, The Gambia,4 Royal Victoria Infirmary, Newcastle upon Tyne, United Kingdom,5 Departments of Gastroenterology and Cancer Biology, Vanderbilt University Medical Center,6 Veterans Administration Medical Center, Nashville, Tennessee7
Received 19 July 2004/ Returned for modification 10 August 2004/ Accepted 30 August 2004
Helicobacter pylori is a genetically diverse bacterial species that chronically infects human stomachs and sometimes causes severe gastroduodenal disease. Studies of polymorphic DNA sequences can suggest geographic origins of individual strains. Here, we describe a 180-bp insertion (ins180), which is just after the translation stop of a gene of unknown function, near the promoter of jhp0152-jhp0151 two-component signal transduction genes in strain J99, and absent from this site in strain 26695. This ins180 insertion was found in 9 of 9 Gambian (West African), 9 of 20 (45%) South African, and 9 of 40 (23%) Spanish strains but in only 2 of 20 (10%) North American strains and none of 20 Lithuanian, 20 Indian, and 20 Japanese strains. Four South African isolates that lacked ins180 and that belonged to an unusual outlier group contained a 480-bp insertion at this site (ins480), whereas none of 181 other strains screened contained ins480. In further tests 56% (10 of 18) of strains from African Americans but only 17% (3 of 18) of strains from Caucasian Americans carried ins180 (P < 0.05). Thus, the H. pylori strains of modern African Americans seem to retain traces of African roots, despite the multiple generations since their ancestors were taken from West Africa. Fragmentary ins180-like sequences were found at numerous sites in H. pylori genomes, always between genes. Such sequences might affect regulation of transcription and could facilitate genome rearrangement by homologous recombination. Apparent differences between African-American and Caucasian-American H. pylori gene pools may bear on our understanding of H. pylori transmission and disease outcome.
* Corresponding author. Mailing address for Mark H. Forsyth: The College of William and Mary, Department of Biology, 214 Millington Hall, Landrum Drive, Williamsburg, VA 23187. Phone: (757) 221-2489. Fax: (757) 221-6483. E-mail: mhfors{at}wm.edu. Mailing address for Douglas E. Berg: Department of Molecular Microbiology, Campus Box 8230, Washington University Medical School, 4940 Parkview Place, St. Louis, MO 63110. Phone: (314) 362-2772. Fax: (314) 362-1232. E-mail: berg{at}borcim.wustl.edu.
S.L.M. and B.M.M. contributed equally to this work.
Present address: Department of Microbiology and Molecular Genetics, Emory University, Atlanta, Ga.
Present address: Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, N.C.
Journal of Clinical Microbiology, December 2004, p. 5658-5663, Vol. 42, No. 12
0095-1137/04/$08.00+0 DOI: 10.1128/JCM.42.12.5658-5663.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
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