Evidence map›Paper›PMID 28520715›Full record

ArticlePloS one2017

Geographical distribution of complement receptor type 1 variants and their associated disease risk.

Thaisa Lucas Sandri, Selorme Adukpo, Dao Phuong Giang, Christian N Nguetse, Fabiana Antunes Andrade, Hoang van Tong, Nguyen Linh Toan, Le Huu Song, Preetham Elumalai, Kumarasamy Thangaraj and 6 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 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 43% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Learning from the past: Pandemics, genetics, and health disparities.Proceedings (Baylor University. Medical Center) · 2024
    Article
  3. Article
  4. Article
  5. 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

16 authors at 10 institutions in 6 countries.

Thaisa Lucas SandriInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Selorme AdukpoInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Dao Phuong Giang108 Military Central Hospital, Hanoi, Vietnam.
Christian N NguetseInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Fabiana Antunes AndradeLaboratory of Molecular Immunopathology, Federal University of Paraná, Curitiba, Brazil.
Hoang van TongInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Nguyen Linh ToanVietnamese - German Center for Medical Research, Hanoi, Vietnam.
Le Huu Song108 Military Central Hospital, Hanoi, Vietnam.
Preetham ElumalaiKerala University of Fisheries and Oceanic Studies, Kochi, India.
Kumarasamy ThangarajCSIR-Centre for Cellular and Molecular Biology, Hyderabad, India.
Vijaya Lakshmi ValluriLEPRA- Blue Peter Public Health and Research Center, Hyderabad, India.
Francine NtoumiFondation Congolaise pour la Recherche Médicale, Brazzaville, Republic of Congo.
Christian G MeyerInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Iara Jose de Messias ReasonLaboratory of Molecular Immunopathology, Federal University of Paraná, Curitiba, Brazil.
Peter G KremsnerInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Thirumalaisamy P VelavanInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.ORCID http://orcid.org/0000-0002-9809-9883
Universidade Federal do Paraná · BRVietnamese - German Center of Excellence in Medical Research · VNDuy Tan University · VNUniversity of Tübingen · DECentre for Cellular and Molecular Biology · INFondation Congolaise Pour La Recherche Médicale · CGKerala University of Fisheries and Ocean Studies · INLepra Society · INUniversity of Ghana · GHVietnam Military Medical University · VN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPathogens exert selective pressure which may lead to substantial changes in host immune responses. The human complement receptor type 1 (CR1) is an innate immune recognition glycoprotein that regulates the activation of the complement pathway and removes opsonized immune complexes. CR1 genetic variants in exon 29 have been associated with expression levels, C1q or C3b binding and increased susceptibility to several infectious diseases. Five distinct CR1 nucleotide substitutions determine the Knops blood group phenotypes, namely Kna/b, McCa/b, Sl1/Sl2, Sl4/Sl5 and KCAM+/-.

methodsCR1 variants were genotyped by direct sequencing in a cohort of 441 healthy individuals from Brazil, Vietnam, India, Republic of Congo and Ghana.

resultsThe distribution of the CR1 alleles, genotypes and haplotypes differed significantly among geographical settings (p≤0.001). CR1 variants rs17047660A/G (McCa/b) and rs17047661A/G (Sl1/Sl2) were exclusively observed to be polymorphic in African populations compared to the groups from Asia and South-America, strongly suggesting that these two SNPs may be subjected to selection. This is further substantiated by a high linkage disequilibrium between the two variants in the Congolese and Ghanaian populations. A total of nine CR1 haplotypes were observed. The CR1*AGAATA haplotype was found more frequently among the Brazilian and Vietnamese study groups; the CR1*AGAATG haplotype was frequent in the Indian and Vietnamese populations, while the CR1*AGAGTG haplotype was frequent among Congolese and Ghanaian individuals.

conclusionThe African populations included in this study might have a selective advantage conferred to immune genes involved in pathogen recognition and signaling, possibly contributing to disease susceptibility or resistance.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdolescentAdultBrazilExonsFemaleGene FrequencyGhanaHumansIndiaLinkage DisequilibriumMaleMiddle AgedRacial GroupsReceptors, Complement 3bCR1 protein, humanReceptors, Complement 3b

Identifiers

PMID28520715
PMCPMC5435133
OpenAlexW2616311661

What OpenQuestion holds

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LicenceCC BY
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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.