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| Untersuchte Arbeit: Seite: 7, Zeilen: 6-31 |
Quelle: Wanken 2003 Seite(n): 13-14, Zeilen: 13:6-23-14:1ff. |
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| There is increasing evidence that recombination occurs between different H. pylori strains (Kraft et al., 2006; Kraft and Suerbaum, 2005; Suerbaum and Achtman, 2004). Simultaneous colonization of human stomachs with more than one strain of H. pylori is detectable in about 5-10% of patients in the United States (Fujimoto et al., 1994), and may occur even more commonly in other populations (Jorgensen et al., 1996). Mixed infections, even those that are transient, provide an opportunity for genetic exchange between strains. Analysis of single cell clones from a patient who was naturally infected with two different H. pylori strains, one of which was cag+ and the other cag-, revealed evidence for at least six different genetic exchanges. One of these exchanges resulted in the replacement of the entire cag PAI with DNA containing the empty site allele from the cag-negative strain. Several others involved a region encoding putative outer membrane proteins that could be involved in interactions with the host (Kersulyte et al., 1999). Genetic exchange may play an important role in the biology of H. pylori by generating new genotypes much more rapidly than is possible by mutation alone, therefore allowing cells to rapidly adapt to new sites in the gastric environment or to new hosts. For several genes, including flaA, flaB, and portions of vacA, phylogenetic analyses of orthologous sequences from different strains have yielded a bush-like rather than a tree-like pattern, indicating considerable interstrain recombination. Recombination is thought to occur more commonly in H. pylori than in any other bacterial species analyzed thus far (Suerbaum et al., 1998). Thus, the high level of allelic variation observed in H. pylori can be attributed to at least two factors. First, large populations of H. pylori have probably evolved within millions of individual human stomachs over thousands of years, resulting in considerable mutational diversity. Second, additional diversity has accumulated as a result of extensive intragenic recombination due to mixed infections (Kraft and Suerbaum, 2005).
Fujimoto, S., B. Marshall, and M. J. Blaser, PCR-based restriction fragment length polymorphism typing of Helicobacter pylori, J Clin Microbiol, 32, 331-334, 1994. Jorgensen, M., G. Daskalopoulos, V. Warburton, H. M. Mitchell, and S. L. Hazell, Multiple strain colonization and metronidazole resistance in Helicobacter pylori-infected patients: identification from sequential and multiple biopsy specimens, J Infect Dis, 174, 631-635, 1996. Kersulyte, D., H. Chalkauskas, and D. E. Berg, Emergence of recombinant strains of Helicobacter pylori during human infection, Mol Microbiol, 31, 31-43, 1999. Kraft, C., and S. Suerbaum, Mutation and recombination in Helicobacter pylori: mechanisms and role in generating strain diversity, Int J Med Microbiol, 295, 299-305, 2005. Kraft, C., A. Stack, C. Josenhans, E. Niehus, G. Dietrich, P. Correa, J. G. Fox, D. Falush, and S. Suerbaum, Genomic changes during chronic Helicobacter pylori infection, J Bacteriol, 188, 249-254, 2006. Suerbaum, S., and M. Achtman, Helicobacter pylori: recombination, population structure and human migrations, Int J Med Microbiol, 294, 133.139, 2004. Suerbaum, S., J. M. Smith, K. Bapumia, G. Morelli, N. H. Smith, E. Kunstmann, I. Dyrek, and M. Achtman, Free recombination within Helicobacter pylori, Proc Natl Acad Sci U S A, 95, 12,619-12,624, 1998. |
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There is increasing evidence that recombination occurs between different H. pylori strains (10, 58, 61). Simultaneous colonization of human stomachs with more than one strain of H. pylori is detectable in about 5-10% of patients in the United States (57), and may occur even more commonly in other populations (82). Mixed infections, even those that are transient, provide an opportunity for genetic exchange between strains. Analysis of single cell clones from a patient who was naturally infected with two different H. pylori strains, one of which was cag+ and the other cag-, revealed evidence for at least six different genetic exchanges. One of these exchanges resulted in the replacement of the entire cag PAI with DNA containing the “empty site allele” from the cag-negative strain. Several others involved a region encoding putative outer membrane proteins that could be involved in interactions with the host (86). Genetic exchange may play an important role in the biology of H. pylori by generating new genotypes much more rapidly than is possible by mutation alone, therefore allowing cells to rapidly adapt to new sites in the gastric environment or to new hosts. For several genes, including flaA, flaB, and portions of vacA, phylogenetic analyses of orthologous sequences from different strains have yielded a “bush”-like rather than a “tree”-like pattern, indicating considerable interstrain recombination. Recombination is thought to occur more commonly in H. pylori than in any other [Page 14] bacterial species analyzed thus far (153). Thus, the high level of allelic variation observed in H. pylori can be attributed to at least two factors. First, large populations of H. pylori have probably evolved within millions of individual human stomachs over thousands of years, resulting in considerable mutational diversity. Second, additional diversity has accumulated as a result of extensive intragenic recombination due to mixed infections (34). 10. Atherton, J. C., P. Cao, J. R. M. Peek, M. K. R. Tummuru, M. J. Blaser, and T. L. Cover. 1995. Mosaicism in vacuolating cytotoxin alleles of Helicobacter pylori. Association of specific vacA types with cytotoxin production and peptic ulceration. J. Biol. Chem. 270:17771-17777. 34. Cover, T. L., D. E. Berg, M. J. Blaser, and H. L. T. Mobley. 2001. H. pylori pathogenesis, p. 509-558. In E. A. Groisman (ed.), Principles of Bacterial Pathogenesis. Academic Press, San Diego. 57. Fujimoto, S., B. Marshall, and M. J. Blaser. 1994. PCR-based restriction fragment length polymorphism typing of Helicobacter pylori. J. Clin. Microbiol. 34:331-334. 58. Garner, J. A., and T. L. Cover. 1995. Analysis of genetic diversity in cytotoxin-producing and non-cytotoxin-producing Helicobacter pylori strains. J. Infect. Dis. 172:290-293. 61. Go, M. F., V. Kapur, D. Y. Graham, and J. M. Musser. 1996. Population genetic analysis of Helicobacter pylori by multilocus enzyme electrophoresis: Extensive allelic diversity and recombinational population structure. J. Bacteriol. 178:3934-3938. 82. Jorgensen, M., G. Daskalopoulos, V. Warburton, H. M. Mitchell, and S. L. Hazell. 1996. Multiple strain colonization and metronidazole resistance in Helicobacter pylori-infected patients: Identification from sequential and multiple biopsy specimens. J. Infect. Dis. 174:631-635. 86. Kersulyte, D., H. Chalkauskas, and D. E. Berg. 1999. Emergence of recombinant strains of Helicobacter pylori during human infection. Mol. Microbiol. 31:31-43. 153. Suerbaum, S., J. M. Smith, K. Bapumia, G. Morelli, N. H. Smith, E. Kunstmann, I. Dyrek, and M. Achtman. 1998. Free recombination within Helicobacter pylori. Proc. Natl. Acad. Sci. U.S.A. 95:12619-12624. |
Although identical, nothing has been marked as a citation; the source is not given. S. Suerbaum has been the advisor for this PhD-Thesis, thus the preference for literary references with him as author or co-author instead of the original references. |
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