Evidence map›Paper›PMID 24089561›Full record

ArticleJournal of virology2013

Respiratory syncytial virus G protein CX3C motif impairs human airway epithelial and immune cell responses.

Tatiana Chirkova, Seyhan Boyoglu-Barnum, Kelsey A Gaston, Fahad M Malik, Steven P Trau, Antonius G P Oomens, Larry J Anderson

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 98 citations in OpenAlex.

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  12. 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
  13. The MAPK Response to Virus Infection Is Modified by Probenecid.Current issues in molecular biology · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
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15 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

7 authors at 2 institutions in 1 country.

Tatiana ChirkovaEmory University Department of Pediatrics, Atlanta, Georgia, USA.
Seyhan Boyoglu-Barnum
Kelsey A Gaston
Fahad M Malik
Steven P Trau
Antonius G P Oomens
Larry J Anderson
Emory University · USOklahoma State University · US

Funding

Viral and Host Determinants of Infant and Childhood Allergy and AsthmaU19AI095227 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Dawn C Newcomb · 2011 to 2026
$34.9M
Training a New Generation of VaccinologistsT32AI074492 · NIAID · EMORY UNIVERSITY · PI Rama Rao Amara, Benjamin A Lopman · 2009 to 2026
$6.4M
NIAID NIH HHS 1U19AI095227NIAID NIH HHS T32 5T32AI074492-03NIAID NIH HHS T32 AI074492NIAID NIH HHS U19 AI095227
6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is a major cause of severe lower respiratory infection in infants and young children and causes disease in the elderly and persons with compromised cardiac, pulmonary, or immune systems. Despite the high morbidity rates of RSV infection, no highly effective treatment or vaccine is yet available. The RSV G protein is an important contributor to the disease process. A conserved CX3C chemokine-like motif in G likely contributes to the pathogenesis of disease. Through this motif, G protein binds to CX3CR1 present on various immune cells and affects immune responses to RSV, as has been shown in the mouse model of RSV infection. However, very little is known of the role of RSV CX3C-CX3CR1 interactions in human disease. In this study, we use an in vitro model of human RSV infection comprised of human peripheral blood mononuclear cells (PBMCs) separated by a permeable membrane from human airway epithelial cells (A549) infected with RSV with either an intact CX3C motif (CX3C) or a mutated motif (CX4C). We show that the CX4C virus induces higher levels of type I/III interferon (IFN) in A549 cells, increased IFN-α and tumor necrosis factor alpha (TNF-α) production by human plasmacytoid dendritic cells (pDCs) and monocytes, and increased IFN-γ production in effector/memory T cell subpopulations. Treatment of CX3C virus-infected cells with the F(ab')2 form of an anti-G monoclonal antibody (MAb) that blocks binding to CX3CR1 gave results similar to those with the CX4C virus. Our data suggest that the RSV G protein CX3C motif impairs innate and adaptive human immune responses and may be important to vaccine and antiviral drug development.

Indexed as

Adaptive ImmunityAmino Acid MotifsChemokines, CX3CCX3C Chemokine Receptor 1Epithelial CellsHumansImmunity, InnateInterferonsLeukocytes, MononuclearReceptors, ChemokineRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsViral ProteinsChemokines, CX3CCX3C Chemokine Receptor 1CX3CR1 protein, humanInterferonsReceptors, ChemokineViral Proteins

Identifiers

PMID24089561
PMCPMC3838285
OpenAlexW2128972608

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.