Evidence map›Paper›PMID 25786000›Full record

ArticlePLoS pathogens2015

A Plasmodium phospholipase is involved in disruption of the liver stage parasitophorous vacuole membrane.

Paul-Christian Burda, Matthias A Roelli, Marco Schaffner, Shahid M Khan, Chris J Janse, Volker T Heussler

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
9.9field-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

63 citing papers in PubMed, 104 citations in OpenAlex.

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  10. Killing ofMicroorganisms · 2024
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  20. The role of cholesterol in invasion and growth of malaria parasites.Frontiers in cellular and infection microbiology · 2022
    Review

3 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

6 authors at 2 institutions in 2 countries.

Paul-Christian BurdaInstitute of Cell Biology, University of Bern, Bern, Switzerland; Graduate School of Cellular Biology, University of Bern, Bern, Switzerland.
Matthias A RoelliInstitute of Cell Biology, University of Bern, Bern, Switzerland.
Marco SchaffnerInstitute of Cell Biology, University of Bern, Bern, Switzerland.
Shahid M KhanLeiden Malaria Research Group, Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands.
Chris J JanseLeiden Malaria Research Group, Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands.
Volker T HeusslerInstitute of Cell Biology, University of Bern, Bern, Switzerland.
University of Bern · CHLeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The coordinated exit of intracellular pathogens from host cells is a process critical to the success and spread of an infection. While phospholipases have been shown to play important roles in bacteria host cell egress and virulence, their role in the release of intracellular eukaryotic parasites is largely unknown. We examined a malaria parasite protein with phospholipase activity and found it to be involved in hepatocyte egress. In hepatocytes, Plasmodium parasites are surrounded by a parasitophorous vacuole membrane (PVM), which must be disrupted before parasites are released into the blood. However, on a molecular basis, little is known about how the PVM is ruptured. We show that Plasmodium berghei phospholipase, PbPL, localizes to the PVM in infected hepatocytes. We provide evidence that parasites lacking PbPL undergo completely normal liver stage development until merozoites are produced but have a defect in egress from host hepatocytes. To investigate this further, we established a live-cell imaging-based assay, which enabled us to study the temporal dynamics of PVM rupture on a quantitative basis. Using this assay we could show that PbPL-deficient parasites exhibit impaired PVM rupture, resulting in delayed parasite egress. A wild-type phenotype could be re-established by gene complementation, demonstrating the specificity of the PbPL deletion phenotype. In conclusion, we have identified for the first time a Plasmodium phospholipase that is important for PVM rupture and in turn for parasite exit from the infected hepatocyte and therefore established a key role of a parasite phospholipase in egress.

Indexed as

AnimalsDisease Models, AnimalFluorescent Antibody TechniqueHepatocytesMalariaMicePhospholipasesPlasmodium bergheiProtozoan ProteinsReverse Transcriptase Polymerase Chain ReactionTranscriptomeVacuolesPhospholipasesProtozoan Proteins

Identifiers

PMID25786000
PMCPMC4364735
OpenAlexW2018643054

What OpenQuestion holds

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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.