Evidence map›Paper›PMID 31221984›Full record

ArticleScientific reports2019

Complement Receptor 1 availability on red blood cell surface modulates Plasmodium vivax invasion of human reticulocytes.

Surendra Kumar Prajapati, Céline Borlon, Eduard Rovira-Vallbona, Jakub Gruszczyk, Sebastien Menant, Wai-Hong Tham, Johanna Helena Kattenberg, Elizabeth Villasis, Katlijn De Meulenaere, Dionicia Gamboa and 10 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Blood group antigens and malaria susceptibility.Frontiers in cellular and infection microbiology · 2025
    Review
  5. Complement receptor 1 is the human erythrocyte receptor forProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Structural biology of complement receptors.Frontiers in immunology · 2023
    Review
  10. Review
  11. Band 3-mediatedFrontiers in cellular and infection microbiology · 2022
    Article
  12. Article
  13. Identification of the RecombinantFrontiers in cell and developmental biology · 2021
    Article
  14. Review
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

20 authors at 11 institutions in 8 countries.

Surendra Kumar PrajapatiDepartment of Biomedical Sciences, Institute of Tropical Medicine, Antwerp, Belgium.ORCID http://orcid.org/0000-0003-1188-668X
Céline BorlonDepartment of Biomedical Sciences, Institute of Tropical Medicine, Antwerp, Belgium.
Eduard Rovira-VallbonaDepartment of Biomedical Sciences, Institute of Tropical Medicine, Antwerp, Belgium.
Jakub GruszczykThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.ORCID http://orcid.org/0000-0003-4536-2964
Sebastien MenantThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.ORCID http://orcid.org/0000-0003-1979-0367
Wai-Hong ThamThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.ORCID http://orcid.org/0000-0001-7950-8699
Johanna Helena KattenbergDepartment of Biomedical Sciences, Institute of Tropical Medicine, Antwerp, Belgium.
Elizabeth VillasisDepartamento de Ciencias Celulares y Moleculares, Universidad Peruana Cayetano Heredia, Lima, Peru.
Katlijn De MeulenaereDepartment of Biomedical Sciences, Institute of Tropical Medicine, Antwerp, Belgium.
Dionicia GamboaDepartamento de Ciencias Celulares y Moleculares, Universidad Peruana Cayetano Heredia, Lima, Peru.
Joseph VinetzDepartamento de Ciencias Celulares y Moleculares, Universidad Peruana Cayetano Heredia, Lima, Peru.
Ricardo FujitaCentro de Genética y Biología Molecular, Universidad de San Martín de Porres, Lima, Peru.
Xa Nguyen XuanNational Institute of Malariology, Parasitology and Entomology, Hanoi, Vietnam.
Marcelo Urbano FerreiraDepartamento de Parasitologia, Universidade de São Paulo, São Paulo, Brazil.
Carlos H NiñoMolecular Biology and Immunology Department, Fundación Instituto de Inmunología de Colombia (FIDIC), Bogotá, Colombia.
Manuel A PatarroyoMolecular Biology and Immunology Department, Fundación Instituto de Inmunología de Colombia (FIDIC), Bogotá, Colombia.ORCID http://orcid.org/0000-0002-4751-2500
Gregory SpanakosHellenic Centre for Diseases Control and Prevention, Maroussi, Greece.
Luc KestensDepartment of Biomedical Sciences, Institute of Tropical Medicine, Antwerp, Belgium.
Jan Van Den AbbeeleDepartment of Biomedical Sciences, Institute of Tropical Medicine, Antwerp, Belgium.
Anna Rosanas-UrgellDepartment of Biomedical Sciences, Institute of Tropical Medicine, Antwerp, Belgium. arosanas@itg.be.
Instituut voor Tropische Geneeskunde · BEUniversidad Peruana Cayetano Heredia · PEFundación Instituto de Inmunología de Colombia · COWalter and Eliza Hall Institute of Medical Research · AUHellenic Center for Disease Control & Prevention · GRNational Institute of Malariology, Parasitology and Entomology · VNThe University of Melbourne · AUUniformed Services University of the Health Sciences · USUniversidad de San Martín de Porres · PEUniversidade de São Paulo · BRUniversity of Antwerp · BE

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
NCATS NIH HHS UL1 TR001863Wellcome Trust 208693/Z/17/Z
6 · The paper itself

Abstract

Plasmodium vivax parasites preferentially invade reticulocyte cells in a multistep process that is still poorly understood. In this study, we used ex vivo invasion assays and population genetic analyses to investigate the involvement of complement receptor 1 (CR1) in P. vivax invasion. First, we observed that P. vivax invasion of reticulocytes was consistently reduced when CR1 surface expression was reduced through enzymatic cleavage, in the presence of naturally low-CR1-expressing cells compared with high-CR1-expressing cells, and with the addition of soluble CR1, a known inhibitor of P. falciparum invasion. Immuno-precipitation experiments with P. vivax Reticulocyte Binding Proteins showed no evidence of complex formation. In addition, analysis of CR1 genetic data for worldwide human populations with different exposure to malaria parasites show significantly higher frequency of CR1 alleles associated with low receptor expression on the surface of RBCs and higher linkage disequilibrium in human populations exposed to P. vivax malaria compared with unexposed populations. These results are consistent with a positive selection of low-CR1-expressing alleles in vivax-endemic areas. Collectively, our findings demonstrate that CR1 availability on the surface of RBCs modulates P. vivax invasion. The identification of new molecular interactions is crucial to guiding the rational development of new therapeutic interventions against vivax malaria.

Indexed as

Erythrocyte MembraneGene FrequencyHumansLinkage DisequilibriumMalaria, VivaxPlasmodium vivaxReceptors, ComplementReticulocytesReceptors, Complement

Identifiers

PMID31221984
PMCPMC6586822
OpenAlexW2951237226

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.