Evidence map›Paper›PMID 26910229›Full record

ArticlePloS one2016

De Novo Genome Assembly Shows Genome Wide Similarity between Trypanosoma brucei brucei and Trypanosoma brucei rhodesiense.

Mark Sistrom, Benjamin Evans, Joshua Benoit, Oliver Balmer, Serap Aksoy, Adalgisa Caccone

Abstract readComparative Study
In one paragraph

Article in PloS one, 2016. 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.

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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

6 authors.

Mark SistromSchool of Natural Sciences, University of California, Merced, 5200 N. Lake Rd, Merced, CA, 95343, United States of America.
Benjamin EvansDepartment of Ecology and Evolutionary Biology, Yale University, 21 Sachem Street New Haven, CT 06520, United States of America.
Joshua BenoitDepartment of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT 06520, United States of America.
Oliver BalmerSwiss Tropical and Public Health Institute, Socinstrasse 57, 4051 Basel, Switzerland.
Serap AksoyDepartment of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT 06520, United States of America.
Adalgisa CacconeDepartment of Ecology and Evolutionary Biology, Yale University, 21 Sachem Street New Haven, CT 06520, United States of America.

Funding

Evolutionary Genetics of Tsetse and Its SymbiontsR01AI068932 · NIAID · YALE UNIVERSITY · PI AKSOY, SERAP, CACCONE, ADALGISA · 2008 to 2018
$7.0M
Training in Parasitology and Vector BiologyT32AI007404 · NIAID · YALE UNIVERSITY · PI TSCHUDI, CHRISTIAN · 1991 to 2017
$3.8M
Next generation sequencing of East African trypanosomes to expand the molecular eR21AI094615 · NIAID · YALE UNIVERSITY · PI AKSOY, SERAP, CACCONE, ADALGISA · 2011 to 2012
$459k
Tsetse-Trypanosome InteractionsR21AI076879 · NIAID · YALE UNIVERSITY · PI AKSOY, SERAP · 2008 to 2009
$454k
NIAID NIH HHS R01 AI068932NIAID NIH HHS R21 AI076879NIAID NIH HHS R21 AI094615NIAID NIH HHS R21 AI094615-01NIAID NIH HHS T32 AI007404
6 · The paper itself

Abstract

backgroundTrypanosoma brucei is a eukaryotic pathogen which causes African trypanosomiasis. It is notable for its variant surface glycoprotein (VSG) coat, which undergoes antigenic variation enabled by a large suite of VSG pseudogenes, allowing for persistent evasion of host adaptive immunity. While Trypanosoma brucei rhodesiense (Tbr) and T. b gambiense (Tbg) are human infective, related T. b. brucei (Tbb) is cleared by human sera. A single gene, the Serum Resistance Associated (SRA) gene, confers Tbr its human infectivity phenotype. Potential genetic recombination of this gene between Tbr and non-human infective Tbb strains has significant epidemiological consequences for Human African Trypanosomiasis outbreaks.

resultsUsing long and short read whole genome sequencing, we generated a hybrid de novo assembly of a Tbr strain, producing 4,210 scaffolds totaling approximately 38.8 megabases, which comprise a significant proportion of the Tbr genome, and thus represents a valuable tool for a comparative genomics analyses among human and non-human infective T. brucei and future complete genome assembly. We detected 5,970 putative genes, of which two, an alcohol oxidoreductase and a pentatricopeptide repeat-containing protein, were members of gene families common to all T. brucei subspecies, but variants specific to the Tbr strain sequenced in this study. Our findings confirmed the extremely high level of genomic similarity between the two parasite subspecies found in other studies.

conclusionsWe confirm at the whole genome level high similarity between the two Tbb and Tbr strains studied. The discovery of extremely minor genomic differentiation between Tbb and Tbr suggests that the transference of the SRA gene via genetic recombination could potentially result in novel human infective strains, thus all genetic backgrounds of T. brucei should be considered potentially human infective in regions where Tbr is prevalent.

Indexed as

GenomicsEvolution, MolecularGene Transfer, HorizontalHumansMembrane GlycoproteinsProtozoan ProteinsSequence AnalysisTrypanosoma brucei bruceiTrypanosoma brucei rhodesienseTrypanosomiasis, AfricanMembrane GlycoproteinsProtozoan Proteinsserum resistance associated protein, Trypanosoma brucei

Identifiers

PMID26910229
PMCPMC4766357

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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.