Evidence map›Paper›PMID 16040995›Full record

ArticleInfection and immunity2005

Slow genetic divergence of Helicobacter pylori strains during long-term colonization.

Annelie Lundin, Britta Björkholm, Ilya Kupershmidt, Magnus Unemo, Peter Nilsson, Dan I Andersson, Lars Engstrand

Abstract read
In one paragraph

Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Diversification of theFrontiers in microbiology · 2016
    Article
  5. Identifying strains that contribute to complex diseases through the study of microbial inheritance.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  6. Genomic evolution and transmission of Helicobacter pylori in two South African families.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  7. Article
  8. Article
  9. Helicobacter pylori genome evolution during human infection.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  10. Article
  11. Article
  12. Article
  13. Evidence of intra-familial transmission of Helicobacter pylori by PCR-based RAPD fingerprinting in Bangladesh.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2009
    Article
  14. Article
  15. Article
  16. Article
  17. An enzymatic ruler modulates Lewis antigen glycosylation of Helicobacter pylori LPS during persistent infection.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Annelie LundinDepartment of Bacteriology, Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden.
Britta Björkholm
Ilya Kupershmidt
Magnus Unemo
Peter Nilsson
Dan I Andersson
Lars Engstrand

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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 ( approximately 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.

Indexed as

Biological EvolutionGenetic VariationAdultAnti-Infective AgentsBacterial ProteinsCarrier ProteinsDrug Resistance, BacterialGastric MucosaHelicobacter pyloriHumansLipoproteinsMetronidazoleMolecular Sequence DataMutationPolymerase Chain ReactionRepetitive Sequences, Nucleic AcidAnti-Infective AgentsBacterial ProteinsCarrier ProteinsLipoproteinsMetronidazole

Identifiers

PMID16040995
PMCPMC1201226

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.