Evidence map›Paper›PMID 26150654›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2015

The within-host dynamics of African trypanosome infections.

Keith R Matthews, Richard McCulloch, Liam J Morrison

Abstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Coenzyme QJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2023
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Variable Surface Glycoprotein fromPathogens (Basel, Switzerland) · 2019
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Variant antigen repertoires inGenome research · 2018
    Article
  17. Article
  18. Article
  19. Review
  20. 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

3 authors.

Keith R MatthewsCentre for Immunity, Infection and Evolution, Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, UK keith.matthews@ed.ac.uk.
Richard McCullochWellcome Trust Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Sir Graeme Davies Building, 120 University Place, Glasgow G12 8TA, UK.
Liam J MorrisonRoslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK.

Funding

Biotechnology and Biological Sciences Research Council BB/L019035/1Biotechnology and Biological Sciences Research Council BB/M028909/1Wellcome Trust 085349Wellcome Trust 095831Wellcome Trust 103740Wellcome Trust 103740/Z/14/ZWellcome Trust 104111Wellcome Trust WT088293Wellcome Trust WT089172
6 · The paper itself

Abstract

African trypanosomes are single-celled protozoan parasites that are capable of long-term survival while living extracellularly in the bloodstream and tissues of mammalian hosts. Prolonged infections are possible because trypanosomes undergo antigenic variation-the expression of a large repertoire of antigenically distinct surface coats, which allows the parasite population to evade antibody-mediated elimination. The mechanisms by which antigen genes become activated influence their order of expression, most likely by influencing the frequency of productive antigen switching, which in turn is likely to contribute to infection chronicity. Superimposed upon antigen switching as a contributor to trypanosome infection dynamics is the density-dependent production of cell-cycle arrested parasite transmission stages, which limit the infection while ensuring parasite spread to new hosts via the bite of blood-feeding tsetse flies. Neither antigen switching nor developmental progression to transmission stages is driven by the host. However, the host can contribute to the infection dynamic through the selection of distinct antigen types, the influence of genetic susceptibility or trypanotolerance and the potential influence of host-dependent effects on parasite virulence, development of transmission stages and pathogenicity. In a zoonotic infection cycle where trypanosomes circulate within a range of host animal populations, and in some cases humans, there is considerable scope for a complex interplay between parasite immune evasion, transmission potential and host factors to govern the profile and outcome of infection.

Indexed as

Host-Parasite InteractionsAnimalsAntigenic VariationAntigens, ProtozoanCoinfectionGene ConversionGenes, ProtozoanGenetic Predisposition to DiseaseHumansImmune EvasionTrypanosomaTrypanosomiasis, AfricanVariant Surface Glycoproteins, TrypanosomaVirulenceZoonosesAntigens, ProtozoanVariant Surface Glycoproteins, Trypanosomaantigenic variationquorum sensingtransmissionTrypanosomatrypanosomewithin-host dynamics

Identifiers

PMID26150654
PMCPMC4528486

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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.