Evidence map›Paper›PMID 25656360›Full record

ReviewParasitology2015

A co-evolutionary arms race: trypanosomes shaping the human genome, humans shaping the trypanosome genome.

Paul Capewell, Anneli Cooper, Caroline Clucas, William Weir, Annette Macleod

Open access · hybridAbstract readReview
In one paragraph

Review in Parasitology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
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

31 citing papers in PubMed, 57 citations in OpenAlex.

  1. Wildlife surveys detectCurrent research in parasitology & vector-borne diseases · 2026
    Article
  2. Review
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  8. Fatty acid uptake inFrontiers in cellular and infection microbiology · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Comprehensive analysis of oral administration of Vitamin E on the early stage ofJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. Review
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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

5 authors at 3 institutions in 1 country.

Paul CapewellWellcome Trust Centre for Molecular Parasitology, College of Medical, Veterinary and Life Sciences,University of Glasgow,464 Bearsden Road, Glasgow G61 1QH,UK.
Anneli CooperWellcome Trust Centre for Molecular Parasitology, College of Medical, Veterinary and Life Sciences,University of Glasgow,464 Bearsden Road, Glasgow G61 1QH,UK.
Caroline ClucasWellcome Trust Centre for Molecular Parasitology, College of Medical, Veterinary and Life Sciences,University of Glasgow,464 Bearsden Road, Glasgow G61 1QH,UK.
William WeirWellcome Trust Centre for Molecular Parasitology, College of Medical, Veterinary and Life Sciences,University of Glasgow,464 Bearsden Road, Glasgow G61 1QH,UK.
Annette MacleodWellcome Trust Centre for Molecular Parasitology, College of Medical, Veterinary and Life Sciences,University of Glasgow,464 Bearsden Road, Glasgow G61 1QH,UK.
Wellcome Centre for Molecular Parasitology · GBUniversity of Glasgow · GBWellcome Trust · GB

Funding

Wellcome Trust 085349
6 · The paper itself

Abstract

Trypanosoma brucei is the causative agent of African sleeping sickness in humans and one of several pathogens that cause the related veterinary disease Nagana. A complex co-evolution has occurred between these parasites and primates that led to the emergence of trypanosome-specific defences and counter-measures. The first line of defence in humans and several other catarrhine primates is the trypanolytic protein apolipoprotein-L1 (APOL1) found within two serum protein complexes, trypanosome lytic factor 1 and 2 (TLF-1 and TLF-2). Two sub-species of T. brucei have evolved specific mechanisms to overcome this innate resistance, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense. In T. b. rhodesiense, the presence of the serum resistance associated (SRA) gene, a truncated variable surface glycoprotein (VSG), is sufficient to confer resistance to lysis. The resistance mechanism of T. b. gambiense is more complex, involving multiple components: reduction in binding affinity of a receptor for TLF, increased cysteine protease activity and the presence of the truncated VSG, T. b. gambiense-specific glycoprotein (TgsGP). In a striking example of co-evolution, evidence is emerging that primates are responding to challenge by T. b. gambiense and T. b. rhodesiense, with several populations of humans and primates displaying resistance to infection by these two sub-species.

Indexed as

AnimalsApolipoproteinsBiological EvolutionGenome, HumanGenome, ProtozoanHost-Parasite InteractionsHumansMembrane GlycoproteinsProtozoan ProteinsSerumTrypanosoma brucei bruceiTrypanosoma brucei gambienseTrypanosoma brucei rhodesienseTrypanosomiasis, AfricanApolipoproteinsMembrane GlycoproteinsProtozoan ProteinsTrypanosome

Identifiers

PMID25656360
PMCPMC4413828
OpenAlexW2198766301

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.