Evidence map›Paper›PMID 28850598›Full record

ArticlePloS one2017

Association of TLR variants with susceptibility to Plasmodium vivax malaria and parasitemia in the Amazon region of Brazil.

Allyson Guimarães Costa, Rajendranath Ramasawmy, Hiochelson Najibe Santos Ibiapina, Vanderson Souza Sampaio, Lilyane Amorim Xábregas, Larissa Wanderley Brasil, Andréa Monteiro Tarragô, Anne Cristine Gomes Almeida, Andrea Kuehn, Sheila Vitor-Silva and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Infection and drug resistance · 2022
    Article
  9. Review
  10. Plasma Eicosanoid Profile inFrontiers in immunology · 2019
    Article
  11. Article
  12. 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

15 authors at 3 institutions in 2 countries.

Allyson Guimarães CostaPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.ORCID http://orcid.org/0000-0002-7312-6822
Rajendranath RamasawmyPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
Hiochelson Najibe Santos IbiapinaPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
Vanderson Souza SampaioPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
Lilyane Amorim XábregasDiretoria de Ensino e Pesquisa, Fundação de Medicina Tropical Dr. Heitor Vieira Dourado (FMT-HVD), Manaus, AM, Brazil.
Larissa Wanderley BrasilPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
Andréa Monteiro TarragôLaboratório de Genômica, Fundação Hospitalar de Hematologia e Hemoterapia do Amazonas (HEMOAM), Manaus, AM, Brazil.
Anne Cristine Gomes AlmeidaPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
Andrea KuehnDiretoria de Ensino e Pesquisa, Fundação de Medicina Tropical Dr. Heitor Vieira Dourado (FMT-HVD), Manaus, AM, Brazil.
Sheila Vitor-SilvaDiretoria de Ensino e Pesquisa, Fundação de Medicina Tropical Dr. Heitor Vieira Dourado (FMT-HVD), Manaus, AM, Brazil.
Gisely Cardoso MeloPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
André Machado SiqueiraPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
Wuelton Marcelo MonteiroPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
Marcus Vinicius Guimarães LacerdaPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
Adriana MalheiroPrograma de Pós-Graduação em Medicina Tropical, Universidade do Estado do Amazonas (UEA), Manaus, AM, Brazil.
Fundação de Medicina Tropical · BRUniversidade do Estado do Amazonas · BRFundação Hospitalar de Hematologia e Hemoterapia do Amazonas · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlasmodium vivax malaria (Pv-malaria) is still considered a neglected disease despite an alarming number of individuals being infected annually. Malaria pathogenesis occurs with the onset of the vector-parasite-host interaction through the binding of pathogen-associated molecular patterns (PAMPs) and receptors of innate immunity, such as toll-like receptors (TLRs). The triggering of the signaling cascade produces an elevated inflammatory response. Genetic polymorphisms in TLRs are involved in susceptibility or resistance to infection, and the identification of genes involved with Pv-malaria response is important to elucidate the pathogenesis of the disease and may contribute to the formulation of control and elimination tools. METHODOLOGY/PRINCIPAL

findingsA retrospective case-control study was conducted in an intense transmission area of Pv-malaria in the state of Amazonas, Brazil. Genetic polymorphisms (SNPs) in different TLRs, TIRAP, and CD14 were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis in 325 patients infected with P. vivax and 274 healthy individuals without malaria history in the prior 12 months from the same endemic area. Parasite load was determined by qPCR. Simple and multiple logistic/linear regressions were performed to investigate association between the polymorphisms and the occurrence of Pv-malaria and parasitemia. The C/T (TLR5 R392StopCodon) and T/T (TLR9 -1486C/T) genotypes appear to be risk factors for infection by P. vivax (TLR5: C/C vs. C/T [OR: 2.116, 95% CI: 1.054-4.452, p = 0.031]; TLR9: C/C vs. T/T [OR: 1.919, 95% CI: 1.159-3.177, p = 0.010]; respectively). Fever (COEF = 7599.46, 95% CI = 3063.80-12135.12, p = 0.001) and the C/C genotype of TLR9 -1237C/T (COEF = 17006.63, 95% CI = 3472.83-30540.44, p = 0.014) were independently associated with increased parasitemia in patients with Pv-malaria.

conclusionsVariants of TLRs may predispose individuals to infection by P. vivax. The TLR5 R392StopCodon and TLR9 -1486C/T variants are associated with susceptibility to Pv-malaria. Furthermore, the TLR9 variant -1237C/C correlates with high parasitemia.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdultAllelesBrazilCase-Control StudiesFemaleGenetic Association StudiesGenotypeHumansLipopolysaccharide ReceptorsMalaria, VivaxMaleMembrane GlycoproteinsMiddle AgedParasitemiaLipopolysaccharide ReceptorsMembrane GlycoproteinsReceptors, Interleukin-1TIRAP protein, humanTLR5 protein, humanToll-Like Receptor 5Toll-Like Receptor 9

Identifiers

PMID28850598
PMCPMC5574562
OpenAlexW2752567914

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.