ArticleBlood2014
Glycophorin C (CD236R) mediates vivax malaria parasite rosetting to normocytes.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Clinical impact of vivax malaria: A collection review.PLoS medicine · 2022Pooled it
- IGFBP7 induces phenotypic shift from platelet-mediated autoagglutination to rosetting ofVirulence · 2026Article
- Transcriptomics of Plasmodium vivax rosettingMemorias do Instituto Oswaldo Cruz · 2026Article
- Effect of periostin (OSF-2) on phagocytosis ofFrontiers in microbiology · 2025Article
- The role of periostin (OSF-2) in the cytoadherence phenomena mediated by malaria parasites.Frontiers in cellular and infection microbiology · 2025Article
- Exploring the naturally acquired response to Pvs47 gametocyte antigen.Frontiers in immunology · 2024Article
- Review
- Rosette formation byFrontiers in cellular and infection microbiology · 2023Article
- Ultrastructural characterization of host-parasite interactions ofParasitology · 2022Article
- Biophysical Tools and Concepts Enable Understanding of Asexual Blood Stage Malaria.Frontiers in cellular and infection microbiology · 2022Review
- Article
- Plasmodium vivax binds host CD98hc (SLC3A2) to enter immature red blood cells.Nature microbiology · 2021Article
- Cytoadherence Properties ofFrontiers in microbiology · 2021Article
- Rosettes integrity protects Plasmodium vivax of being phagocytized.Scientific reports · 2020Article
- In vitro selection for adhesion of Plasmodium falciparum-infected erythrocytes to ABO antigens does not affect PfEMP1 and RIFIN expression.Scientific reports · 2020Article
- Microscopy-based Methods for Rosetting Assay in Malaria Research.Bio-protocol · 2020Article
- Genetic diversity and neutral selection in Plasmodium vivax erythrocyte binding protein correlates with patient antigenicity.PLoS neglected tropical diseases · 2020Article
- Article
- Rosetting revisited: a critical look at the evidence for host erythrocyte receptors inParasitology · 2020Review
- Robust continuous in vitro culture of the Plasmodium cynomolgi erythrocytic stages.Nature communications · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 8 institutions in 5 countries.
Funding
Abstract
Rosetting phenomenon has been linked to malaria pathogenesis. Although rosetting occurs in all causes of human malaria, most data on this subject has been derived from Plasmodium falciparum. Here, we investigate the function and factors affecting rosette formation in Plasmodium vivax. To achieve this, we used a range of novel ex vivo protocols to study fresh and cryopreserved P vivax (n = 135) and P falciparum (n = 77) isolates from Thailand. Rosetting is more common in vivax than falciparum malaria, both in terms of incidence in patient samples and percentage of infected erythrocytes forming rosettes. Rosetting to P vivax asexual and sexual stages was evident 20 hours postreticulocyte invasion, reaching a plateau after 30 hours. Host ABO blood group, reticulocyte count, and parasitemia were not correlated with P vivax rosetting. Importantly, mature erythrocytes (normocytes), rather than reticulocytes, preferentially form rosetting complexes, indicating that this process is unlikely to directly facilitate merozoite invasion. Although antibodies against host erythrocyte receptors CD235a and CD35 had no effect, Ag-binding fragment against the BRIC 4 region of CD236R significantly inhibited rosette formation. Rosetting assays using CD236R knockdown normocytes derived from hematopoietic stem cells further supports the role of glycophorin C as a receptor in P vivax rosette formation.
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What OpenQuestion holds
Registered trials
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.