Evidence map›Paper›PMID 26195724›Full record

ArticleThe Journal of experimental medicine2015

Basigin is a druggable target for host-oriented antimalarial interventions.

Zenon A Zenonos, Sara K Dummler, Nicole Müller-Sienerth, Jianzhu Chen, Peter R Preiser, Julian C Rayner, Gavin J Wright

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
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  19. CD209L/L-SIGN and CD209/DC-SIGN act as receptors for SARS-CoV-2.bioRxiv : the preprint server for biology · 2021
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Zenon A ZenonosCell Surface Signalling Laboratory and Malaria Program, Wellcome Trust Sanger Institute, Cambridge CB10 2DP, England, UK Cell Surface Signalling Laboratory and Malaria Program, Wellcome Trust Sanger Institute, Cambridge CB10 2DP, England, UK.
Sara K DummlerSMART Singapore-MIT-Alliance for Research and Technology, Infectious Disease IRG, Singapore 138602, Singapore.
Nicole Müller-SienerthCell Surface Signalling Laboratory and Malaria Program, Wellcome Trust Sanger Institute, Cambridge CB10 2DP, England, UK.
Jianzhu ChenSMART Singapore-MIT-Alliance for Research and Technology, Infectious Disease IRG, Singapore 138602, Singapore Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02420.
Peter R PreiserSMART Singapore-MIT-Alliance for Research and Technology, Infectious Disease IRG, Singapore 138602, Singapore Nanyang Technological University, School of Biological Sciences, Singapore 637551, Singapore.
Julian C RaynerCell Surface Signalling Laboratory and Malaria Program, Wellcome Trust Sanger Institute, Cambridge CB10 2DP, England, UK.
Gavin J WrightCell Surface Signalling Laboratory and Malaria Program, Wellcome Trust Sanger Institute, Cambridge CB10 2DP, England, UK Cell Surface Signalling Laboratory and Malaria Program, Wellcome Trust Sanger Institute, Cambridge CB10 2DP, England, UK gw2@sanger.ac.uk.
Wellcome Sanger Institute · GBMassachusetts Institute of Technology · USNanyang Technological University · SGSingapore-MIT Alliance for Research and Technology · SG

Funding

PHS HHS 098051Wellcome Trust
6 · The paper itself

Abstract

Plasmodium falciparum is the parasite responsible for the most lethal form of malaria, an infectious disease that causes a large proportion of childhood deaths and poses a significant barrier to socioeconomic development in many countries. Although antimalarial drugs exist, the repeated emergence and spread of drug-resistant parasites limit their useful lifespan. An alternative strategy that could limit the evolution of drug-resistant parasites is to target host factors that are essential and universally required for parasite growth. Host-targeted therapeutics have been successfully applied in other infectious diseases but have never been attempted for malaria. Here, we report the development of a recombinant chimeric antibody (Ab-1) against basigin, an erythrocyte receptor necessary for parasite invasion as a putative antimalarial therapeutic. Ab-1 inhibited the PfRH5-basigin interaction and potently blocked erythrocyte invasion by all parasite strains tested. Importantly, Ab-1 rapidly cleared an established P. falciparum blood-stage infection with no overt toxicity in an in vivo infection model. Collectively, our data demonstrate that antibodies or other therapeutics targeting host basigin could be an effective treatment for patients infected with multi-drug resistant P. falciparum.

Indexed as

AnimalsAntibodiesBase SequenceBasiginCarrier ProteinsCloning, MolecularErythrocytesIntegration Host FactorsMalariaMiceMolecular Sequence DataPlasmodium falciparumRecombinant Fusion ProteinsSequence Analysis, DNASurface Plasmon ResonanceAntibodiesBasiginCarrier ProteinsIntegration Host FactorsRecombinant Fusion ProteinsRH5 protein, Plasmodium falciparum

Identifiers

PMID26195724
PMCPMC4516795
OpenAlexW2119363076

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.