Evidence map›Paper›PMID 22123959›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Fy(a)/Fy(b) antigen polymorphism in human erythrocyte Duffy antigen affects susceptibility to Plasmodium vivax malaria.

Christopher L King, John H Adams, Jia Xianli, Brian T Grimberg, Amy M McHenry, Lior J Greenberg, Asim Siddiqui, Rosalind E Howes, Monica da Silva-Nunes, Marcelo U Ferreira and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 2% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Pooled it
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  14. Blood group antigens and malaria susceptibility.Frontiers in cellular and infection microbiology · 2025
    Review
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  19. Article
  20. Vaccination withScience translational medicine · 2023
    Article

28 more citing papers are in PubMed but not listed here.

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

11 authors at 5 institutions in 4 countries.

Christopher L KingCenter for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106, USA. cxk21@case.edu
John H Adams
Jia Xianli
Brian T Grimberg
Amy M McHenry
Lior J Greenberg
Asim Siddiqui
Rosalind E Howes
Monica da Silva-Nunes
Marcelo U Ferreira
Peter A Zimmerman
Case Western Reserve University · USCenter for Global Health · USUniversidade de São Paulo · BRUniversity of South Florida · USUniversity of Oxford · GB

Funding

Immunological characterization of the P. vivax DBPR01AI064478 · NIAID · UNIVERSITY OF SOUTH FLORIDA · PI ADAMS, JOHN H · 2006 to 2023
$9.6M
NIAID NIH HHS R01 AI064478
6 · The paper itself

Abstract

Plasmodium vivax (Pv) is a major cause of human malaria and is increasing in public health importance compared with falciparum malaria. Pv is unique among human malarias in that invasion of erythrocytes is almost solely dependent on the red cell's surface receptor, known as the Duffy blood-group antigen (Fy). Fy is an important minor blood-group antigen that has two immunologically distinct alleles, referred to as Fy(a) or Fy(b), resulting from a single-point mutation. This mutation occurs within the binding domain of the parasite's red cell invasion ligand. Whether this polymorphism affects susceptibility to clinical vivax malaria is unknown. Here we show that Fy(a), compared with Fy(b), significantly diminishes binding of Pv Duffy binding protein (PvDBP) at the erythrocyte surface, and is associated with a reduced risk of clinical Pv in humans. Erythrocytes expressing Fy(a) had 41-50% lower binding compared with Fy(b) cells and showed an increased ability of naturally occurring or artificially induced antibodies to block binding of PvDBP to their surface. Individuals with the Fy(a+b-) phenotype demonstrated a 30-80% reduced risk of clinical vivax, but not falciparum malaria in a prospective cohort study in the Brazilian Amazon. The Fy(a+b-) phenotype, predominant in Southeast Asian and many American populations, would confer a selective advantage against vivax malaria. Our results also suggest that efficacy of a PvDBP-based vaccine may differ among populations with different Fy phenotypes.

Indexed as

Genetic Predisposition to DiseasePolymorphism, GeneticAntibodies, BlockingAntibodies, ProtozoanAntigens, ProtozoanArylsulfatasesDuffy Blood-Group SystemErythrocytesGene FrequencyGeographyHumansMalaria, VivaxPlasmodium vivaxProtein BindingProtozoan ProteinsReceptors, Cell SurfaceACKR1 protein, humanAntibodies, BlockingAntibodies, ProtozoanAntigens, ProtozoanArylsulfatasesDuffy antigen binding protein, PlasmodiumDuffy Blood-Group SystemProtozoan ProteinsReceptors, Cell Surface

Identifiers

PMID22123959
PMCPMC3250126
OpenAlexW2084029545

What OpenQuestion holds

Textmetadata
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.