Evidence map›Paper›PMID 26676785›Full record

ArticleJournal of virology2015

Nipah Virus Matrix Protein Influences Fusogenicity and Is Essential for Particle Infectivity and Stability.

Erik Dietzel, Larissa Kolesnikova, Bevan Sawatsky, Anja Heiner, Michael Weis, Gary P Kobinger, Stephan Becker, Veronika von Messling, Andrea Maisner

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

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  19. Twenty Years of Nipah Virus Research: Where Do We Go From Here?The Journal of infectious diseases · 2020
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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

9 authors at 5 institutions in 2 countries.

Erik DietzelInstitute of Virology, Philipps University Marburg, Marburg, Germany.
Larissa KolesnikovaInstitute of Virology, Philipps University Marburg, Marburg, Germany.
Bevan SawatskyINRS-Institut Armand-Frappier, University of Quebec, Laval, Quebec, Canada Veterinary Medicine Division, Paul-Ehrlich-Institut, Langen, Germany.
Anja HeinerInstitute of Virology, Philipps University Marburg, Marburg, Germany.
Michael WeisInstitute of Virology, Philipps University Marburg, Marburg, Germany.
Gary P KobingerNational Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada.
Stephan BeckerInstitute of Virology, Philipps University Marburg, Marburg, Germany German Center for Infection Research, Partner Site Giessen-Marburg-Langen, Germany.
Veronika von MesslingINRS-Institut Armand-Frappier, University of Quebec, Laval, Quebec, Canada Veterinary Medicine Division, Paul-Ehrlich-Institut, Langen, Germany German Center for Infection Research, Partner Site Giessen-Marburg-Langen, Germany.
Andrea MaisnerInstitute of Virology, Philipps University Marburg, Marburg, Germany maisner@staff.uni-marburg.de.
Philipps University of Marburg · DEGerman Center for Infection Research · DEInstitut National de la Recherche Scientifique · CAPaul Ehrlich Institut · DEPublic Health Agency of Canada · CA

Funding

Canadian Institutes of Health Research MOP66989
6 · The paper itself

Abstract

unlabelledNipah virus (NiV) causes fatal encephalitic infections in humans. To characterize the role of the matrix (M) protein in the viral life cycle, we generated a reverse genetics system based on NiV strain Malaysia. Using an enhanced green fluorescent protein (eGFP)-expressing M protein-deleted NiV, we observed a slightly increased cell-cell fusion, slow replication kinetics, and significantly reduced peak titers compared to the parental virus. While increased amounts of viral proteins were found in the supernatant of cells infected with M-deleted NiV, the infectivity-to-particle ratio was more than 100-fold reduced, and the particles were less thermostable and of more irregular morphology. Taken together, our data demonstrate that the M protein is not absolutely required for the production of cell-free NiV but is necessary for proper assembly and release of stable infectious NiV particles. IMPORTANCE: Henipaviruses cause a severe disease with high mortality in human patients. Therefore, these viruses can be studied only in biosafety level 4 (BSL-4) laboratories, making it more challenging to characterize their life cycle. Here we investigated the role of the Nipah virus matrix protein in virus-mediated cell-cell fusion and in the formation and release of newly produced particles. We found that even though low levels of infectious viruses are produced in the absence of the matrix protein, it is required for the release of highly infectious and stable particles. Fusogenicity of matrixless viruses was slightly enhanced, further demonstrating the critical role of this protein in different steps of Nipah virus spread.

Indexed as

Virus AssemblyVirus ReleaseAnimalsCell LineGene DeletionHumansMicrobial ViabilityMicroscopy, Electron, TransmissionMicroscopy, FluorescenceMicroscopy, ImmunoelectronNipah VirusReverse GeneticsTemperatureViral LoadViral Matrix ProteinsVirionViral Matrix Proteins

Identifiers

PMID26676785
PMCPMC4810686
OpenAlexW2257747806

What OpenQuestion holds

Textmetadata
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.