Evidence map›Paper›PMID 27926942›Full record

ArticlePLoS pathogens2016

Actin-Related Protein 2 (ARP2) and Virus-Induced Filopodia Facilitate Human Respiratory Syncytial Virus Spread.

Masfique Mehedi, Thomas McCarty, Scott E Martin, Cyril Le Nouën, Eugen Buehler, Yu-Chi Chen, Margery Smelkinson, Sundar Ganesan, Elizabeth R Fischer, Linda G Brock and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Viruses · 2026
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  7. Exploring Therapeutic Targets From Spreading Patterns Against Respiratory Syncytial Virus.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
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  13. Intercellular Transport of Viral Proteins.Results and problems in cell differentiation · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Potential role of PIM1 inhibition in the treatment of SARS-CoV-2 infection.Journal, genetic engineering & biotechnology · 2023
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Masfique MehediRNA Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.ORCID http://orcid.org/0000-0003-1728-3126
Thomas McCartyRNA Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Scott E MartinDivision of Pre-Clinical Innovation, National Center for Advancing Translational Sciences, Rockville, Maryland, United States of America.
Cyril Le NouënRNA Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Eugen BuehlerDivision of Pre-Clinical Innovation, National Center for Advancing Translational Sciences, Rockville, Maryland, United States of America.
Yu-Chi ChenDivision of Pre-Clinical Innovation, National Center for Advancing Translational Sciences, Rockville, Maryland, United States of America.
Margery SmelkinsonBiological Imaging Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Sundar GanesanBiological Imaging Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Elizabeth R FischerMicroscopy Unit, Rocky Mountain Laboratories, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, United States of America.
Linda G BrockRNA Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Bo LiangRNA Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Shirin MunirRNA Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Peter L CollinsRNA Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Ursula J BuchholzRNA Viruses Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
National Institutes of Health · USNational Center for Advancing Translational Sciences · US

Funding

Infectious Diseases Research Technologies Core - RMLZICAI001052 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2009 to 2025
$133.3M
Laboratory Studies of Human Respiratory Syncytial Virus and Other PneumovirusesZIAAI000372 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BUCHHOLZ, URSULA · 2009 to 2025
$21.8M
6 · The paper itself

Abstract

Human respiratory syncytial virus (RSV) is an enveloped RNA virus that is the most important viral cause of acute pediatric lower respiratory tract illness worldwide, and lacks a vaccine or effective antiviral drug. The involvement of host factors in the RSV replicative cycle remains poorly characterized. A genome-wide siRNA screen in human lung epithelial A549 cells identified actin-related protein 2 (ARP2) as a host factor involved in RSV infection. ARP2 knockdown did not reduce RSV entry, and did not markedly reduce gene expression during the first 24 hr of infection, but decreased viral gene expression thereafter, an effect that appeared to be due to inhibition of viral spread to neighboring cells. Consistent with reduced spread, there was a 10-fold reduction in the release of infectious progeny virions in ARP2-depleted cells at 72 hr post-infection. In addition, we found that RSV infection induced filopodia formation and increased cell motility in A549 cells and that this phenotype was ARP2 dependent. Filopodia appeared to shuttle RSV to nearby uninfected cells, facilitating virus spread. Expression of the RSV F protein alone from a plasmid or heterologous viral vector in A549 cells induced filopodia, indicating a new role for the RSV F protein, driving filopodia induction and virus spread. Thus, this study identified roles for ARP2 and filopodia in RSV-induced cell motility, RSV production, and RSV cell-to-cell spread.

Indexed as

A549 CellsActin-Related Protein 2Blotting, WesternFlow CytometryGene Knockdown TechniquesHumansMicroscopy, ConfocalMicroscopy, Electron, TransmissionPseudopodiaReal-Time Polymerase Chain ReactionRespiratory Syncytial VirusesRespiratory Syncytial Virus InfectionsVirus InternalizationActin-Related Protein 2ACTR2 protein, human

Identifiers

PMID27926942
PMCPMC5142808
OpenAlexW2559878375

What OpenQuestion holds

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LicenceCC0
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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.