Evidence map›Paper›PMID 27619017›Full record

ArticleBMC genomics2016

Recombination-driven generation of the largest pathogen repository of antigen variants in the protozoan Trypanosoma cruzi.

D Brent Weatherly, Duo Peng, Rick L Tarleton

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  11. AssessingPathogens (Basel, Switzerland) · 2021
    Article
  12. Article
  13. Review
  14. Repeat-Driven Generation of Antigenic Diversity in a Major Human Pathogen,Frontiers in cellular and infection microbiology · 2021
    Article
  15. Unpicking the Roles of DNA Damage Protein Kinases in Trypanosomatids.Frontiers in cell and developmental biology · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. DNA lesions and repair in trypanosomatids infection.Genetics and molecular biology · 2020
    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 at 1 institution in 1 country.

D Brent WeatherlyCenter for Tropical and Emerging Global Diseases, Institute of Bioinformatics and Department of Cellular Biology, University of Georgia, Athens, GA, 30602, USA.
Duo PengCenter for Tropical and Emerging Global Diseases, Institute of Bioinformatics and Department of Cellular Biology, University of Georgia, Athens, GA, 30602, USA.
Rick L TarletonCenter for Tropical and Emerging Global Diseases, Institute of Bioinformatics and Department of Cellular Biology, University of Georgia, Athens, GA, 30602, USA. tarleton@uga.edu.
University of Georgia · US

Funding

VACCINE DISCOVERY FOR TRYPANOSOMA CRUZIP01AI044979 · NIAID · UNIVERSITY OF GEORGIA (UGA) · PI TARLETON, RICK L · 1999 to 2008
$7.5M
Transmission-blocking live vaccine for Chagas diseaseR01AI089952 · NIAID · UNIVERSITY OF GEORGIA · PI TARLETON, RICK L · 2012 to 2016
$1.8M
NIAID NIH HHS P01 AI044979NIAID NIH HHS R01 AI089952
6 · The paper itself

Abstract

backgroundThe protozoan parasite Trypanosoma cruzi, causative agent of Chagas disease, depends upon a cell surface-expressed trans-sialidase (ts) to avoid activation of complement-mediated lysis and to enhance intracellular invasion. However these functions alone fail to account for the size of this gene family in T. cruzi, especially considering that most of these genes encode proteins lacking ts enzyme activity. Previous whole genome sequencing of the CL Brener clone of T. cruzi identified ~1400 ts variants, but left many partially assembled sequences unannotated.

resultsIn the current study we reevaluated the trans-sialidase-like sequences in this reference strain, identifying an additional 1779 full-length and partial ts genes with their important features annotated, and confirming the expression of previously annotated "pseudogenes" and newly annotated ts family members. Multiple EM for Motif Elicitation (MEME) analysis allowed us to generate a model T. cruzi ts (TcTS) based upon the most conserved motif patterns and demonstrated that a common motif order is highly conserved among ts family members. Using a newly developed pipeline for the analysis of recombination within large gene families, we further demonstrate that TcTS family members are undergoing frequent recombination, generating new variants from the thousands of functional and non-functional ts gene segments but retaining the overall structure of the core TcTS family members.

conclusionsThe number and variety as well as high recombination frequency of TcTS family members supports strong evolutionary pressure, probably exerted by immune selection, for continued variation in ts sequences in T. cruzi, and thus for a unique immune evasion mechanism for the large ts gene family.

Indexed as

Recombination, GeneticAntigens, ProtozoanBase SequenceChagas DiseaseGenes, ProtozoanHumansModels, MolecularMultigene FamilyOpen Reading FramesPhylogenyProtein ConformationProtozoan ProteinsTrypanosoma cruziAntigens, ProtozoanProtozoan ProteinsAntigen variantsChagas diseaseImmune evasionRecombinationTrans-sialidaseTrypanosoma cruzi

Identifiers

PMID27619017
PMCPMC5020489
OpenAlexW2519839019

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.