Evidence map›Paper›PMID 30541481›Full record

ArticleBMC infectious diseases2018

Motility of human renal cells is disturbed by infection with pathogenic hantaviruses.

Stefan Hägele, Alexander Müller, Christian Nusshag, Jochen Reiser, Martin Zeier, Ellen Krautkrämer

Open access · goldAbstract read
In one paragraph

Article in BMC infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  9. Article
  10. Review
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  12. Soluble Urokinase Receptor (SuPAR) in COVID-19-Related AKI.Journal of the American Society of Nephrology : JASN · 2020
    Observational
  13. Article
  14. Orthohantavirus Pathogenesis and Cell Tropism.Frontiers in cellular and infection microbiology · 2020
    Review
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.

Stefan HägeleDepartment of Nephrology, University of Heidelberg, Im Neuenheimer Feld 162, 69120, Heidelberg, Germany.
Alexander MüllerDepartment of Nephrology, University of Heidelberg, Im Neuenheimer Feld 162, 69120, Heidelberg, Germany.
Christian NusshagDepartment of Medicine I and Clinical Chemistry/Department of Nephrology, University of Heidelberg, Heidelberg, Germany.
Jochen ReiserDepartment of Internal Medicine, Rush University Medical Center, Chicago, IL, USA.
Martin ZeierDepartment of Nephrology, University of Heidelberg, Im Neuenheimer Feld 162, 69120, Heidelberg, Germany.
Ellen KrautkrämerDepartment of Nephrology, University of Heidelberg, Im Neuenheimer Feld 162, 69120, Heidelberg, Germany. ellen.krautkraemer@med.uni-heidelberg.de.
Heidelberg University · DERush University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHemorrhagic fever with renal syndrome (HFRS) caused by pathogenic hantaviruses in Europe and Asia is often characterized by acute kidney injury (AKI) with massive proteinuria. Renal filtration depends on the integrity of epithelial and endothelial monolayers in the tubular and glomerular apparatus. Tubular and glomerular cells represent target cells of hantavirus infection. However, the detailed mechanisms of renal impairment induced by hantaviruses are not well understood.

methodsWe analyzed the cellular consequences of hantavirus infection by measuring adhesion and migration capacity of human renal cells infected with Puumala (PUUV) or Hantaan (HTNV) virus. The impact of hantaviral nucleocapsid proteins (N proteins) on motility was examined by transfection of podocytes.

resultsInfection of kidney cells with hantavirus species PUUV and HTNV causes a significant reduction of migration capacity. The impaired motility depends on viral replication and transfection of podocytes with N protein of PUUV or HTNV reveals that the expression of N protein alone is sufficient to deteriorate podocyte function. The cellular effects are more pronounced for the more pathogenic HTNV than for PUUV that causes a milder form of HFRS.

conclusionsThe direct impairment of migration capacity of renal cells by hantaviral N proteins may contribute substantially to proteinuria observed in the clinical picture of hantavirus infection.

Indexed as

AnimalsCell MovementCells, CulturedChlorocebus aethiopsEpithelial CellsHantavirus InfectionsHumansKidneyKidney GlomerulusKidney TubulesOrthohantavirusPodocytesPuumala virusVero CellsVirus ReplicationGlomerulusHantavirusKidneyPodocytesProteinuriaTubular epithelium

Identifiers

PMID30541481
PMCPMC6292036
OpenAlexW2905151395

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.