Evidence map›Paper›PMID 41461753›Full record

ArticleScientific reports2025

Highly conserved Plasmodium vivax genomes in Duffy-negative individuals from Sudan.

Regan E Schroeder, Safaa Ahmed, Anthony Ford, Mohammed Elfaki, Samuel Omer Hamad, Tarig Mohamed Elfaki, Sumaia Mohamed, Emilia Manko, Taane G Clark, Susana Campino and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Regan E SchroederDepartment of Microbiology and Immunology, College of Medicine, Drexel University, Philadelphia, USA. rs3772@drexel.edu.
Safaa AhmedInstitute of Endemic Diseases, University of Khartoum, Khartoum, Sudan.
Anthony FordDepartment of Bioinformatics and Genomics, University of North Carolina, Charlotte, NC, USA.
Mohammed ElfakiInstitute of Endemic Diseases, University of Khartoum, Khartoum, Sudan.
Samuel Omer HamadInstitute of Endemic Diseases, University of Khartoum, Khartoum, Sudan.
Tarig Mohamed ElfakiInstitute of Endemic Diseases, University of Khartoum, Khartoum, Sudan.
Sumaia MohamedDepartment of Zoology, Faculty of Science, University of Khartoum, Khartoum, Sudan.
Emilia MankoDepartment of Infection Biology, London School of Hygiene and Tropical Medicine, Keppel Street, London, UK.
Taane G ClarkDepartment of Infection Biology, London School of Hygiene and Tropical Medicine, Keppel Street, London, UK.
Susana CampinoDepartment of Infection Biology, London School of Hygiene and Tropical Medicine, Keppel Street, London, UK.
Muzamil Mahdi Abdel HamidInstitute of Endemic Diseases, University of Khartoum, Khartoum, Sudan. mahdi@iend.org.
Eugenia LoDepartment of Microbiology and Immunology, College of Medicine, Drexel University, Philadelphia, USA. el855@drexel.edu.

Funding

Plasmodium vivax Erythrocyte Invasion Mechanisms and Humoral Immune Response in Duffy Negative AfricansR01AI162947 · NIAID · UNIVERSITY OF NORTH CAROLINA CHARLOTTE · PI Eugenia Lo · 2022 to 2026
$3.4M
National Institute of Allergy and Infectious Diseases R01AI162947NIAID NIH HHS R01 AI162947UK Research and Innovation BBSRC BB/X018156/1
6 · The paper itself

Abstract

Duffy-negatives were previously thought to be immune to Plasmodium vivax infections due to Duffy binding protein's (PvDBP1) inability to invade erythrocytes lacking Duffy antigen receptor for chemokines (DARC) expression. Nevertheless, reports of P. vivax cases are growing throughout Africa and among Duffy-negative people. Although there are alternative invasion mechanisms by P. vivax, the exact mechanisms in Duffy-negative individuals are unclear. Sudan, with a mixed Duffy-negative and Duffy-positive population, is ideal to study differences between these infections on epidemiological and genetic scales. The goal of this study was to compare Duffy-positive and Duffy-negative infections in Sudanese individuals on epidemiological and genomic scales. We collected epidemiological data and sequenced parasite genomes and found that Duffy-positive individuals had significantly higher parasitemia than Duffy-negatives. Furthermore, Duffy-positive infected P. vivax genomes were much more diverse than Duffy-negatives, across all 14 chromosomes and 44 specific erythrocyte binding gene candidates. Genes of the merozoite surface protein family account for much of the genetic diversity found. Many erythrocyte binding gene candidates are under selection pressure, both positive and negative. Finally, in DBP and RBP genes, as well as TRAg38, changes in amino acids in the binding regions to a structurally different residue could affect erythrocyte binding affinity and antigenic conformation.

Indexed as

Duffy Blood-Group SystemGenome, ProtozoanMalaria, VivaxPlasmodium vivaxReceptors, Cell SurfaceAntigens, ProtozoanErythrocytesHumansProtozoan ProteinsSudanACKR1 protein, humanAntigens, ProtozoanDuffy antigen binding protein, PlasmodiumDuffy Blood-Group SystemProtozoan ProteinsReceptors, Cell SurfaceDuffy blood groupEpidemiologyP. vivaxSingle nucleotide polymorphismSudanWhole genome sequencing

Identifiers

PMID41461753
PMCPMC12749326

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.