Evidence map›Paper›PMID 26297201›Full record

ArticleThe Journal of general virology2015

CX3CR1 is an important surface molecule for respiratory syncytial virus infection in human airway epithelial cells.

Tatiana Chirkova, Songbai Lin, Antonius G P Oomens, Kelsey A Gaston, Seyhan Boyoglu-Barnum, Jia Meng, Christopher C Stobart, Calvin U Cotton, Tina V Hartert, Martin L Moore and 2 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of general virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
7.9field-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

115 citing papers in PubMed, 158 citations in OpenAlex.

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  15. Exploring Therapeutic Targets From Spreading Patterns Against Respiratory Syncytial Virus.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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55 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

12 authors at 5 institutions in 1 country.

Tatiana ChirkovaDepartment of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA.
Songbai LinDepartment of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA.
Antonius G P OomensCenter for Veterinary Health Sciences, Oklahoma State University, Stillwater, Oklahoma, USA.
Kelsey A GastonDepartment of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA.
Seyhan Boyoglu-BarnumDepartment of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA.
Jia MengDepartment of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA.
Christopher C StobartDepartment of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA.
Calvin U CottonDivision of Pediatric Pulmonology, Case Western University, Cleveland, Ohio, USA.
Tina V HartertDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine and Vanderbilt Center for Asthma and Environmental Health Sciences Research, Vanderbilt University, Nashville, Tennessee, USA.
Martin L MooreDepartment of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA.
Assem G ZiadyDepartment of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA.
Larry J AndersonDepartment of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA.
Children's Healthcare of Atlanta · USEmory University · USCase Western Reserve University · USOklahoma State University · USVanderbilt 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
Role of the Respiratory Syncytial Virus Fusion Protein in Airway Mucus InductionR01AI087798 · NIAID · EMORY UNIVERSITY · PI MOORE, MARTIN LAWRENCE · 2010 to 2014
$1.9M
Midcareer Investigator Patient-oriented Research Award in Bronchiolitis & AsthmaK24AI077930 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARTERT, TINA V · 2008 to 2017
$1.6M
Dysregulation of Nrf2 in CF epitheliaR01HL109362 · NHLBI · EMORY UNIVERSITY · PI ZIADY, ASSEM G · 2011 to 2014
$1.5M
NHLBI NIH HHS 5R01HL109362NHLBI NIH HHS R01 HL109362NIAID NIH HHS 1R01AI087798NIAID NIH HHS 1U19AI095227NIAID NIH HHS 5T32AI074492-03NIAID NIH HHS K24 AI077930NIAID NIH HHS R01 AI087798NIAID NIH HHS T32 AI074492NIAID NIH HHS U19 AI095227
6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is a major cause of severe pneumonia and bronchiolitis in infants and young children, and causes disease throughout life. Understanding the biology of infection, including virus binding to the cell surface, should help develop antiviral drugs or vaccines. The RSV F and G glycoproteins bind cell surface heparin sulfate proteoglycans (HSPGs) through heparin-binding domains. The G protein also has a CX3C chemokine motif which binds to the fractalkine receptor CX3CR1. G protein binding to CX3CR1 is not important for infection of immortalized cell lines, but reportedly is so for primary human airway epithelial cells (HAECs), the primary site for human infection. We studied the role of CX3CR1 in RSV infection with CX3CR1-transfected cell lines and HAECs with variable percentages of CX3CR1-expressing cells, and the effect of anti-CX3CR1 antibodies or a mutation in the RSV CX3C motif. Immortalized cells lacking HSPGs had low RSV binding and infection, which was increased markedly by CX3CR1 transfection. CX3CR1 was expressed primarily on ciliated cells, and ∼50 % of RSV-infected cells in HAECs were CX3CR1+. HAECs with more CX3CR1-expressing cells had a proportional increase in RSV infection. Blocking G binding to CX3CR1 with anti-CX3CR1 antibody or a mutation in the CX3C motif significantly decreased RSV infection in HAECs. The kinetics of cytokine production suggested that the RSV/CX3CR1 interaction induced RANTES (regulated on activation normal T-cell expressed and secreted protein), IL-8 and fractalkine production, whilst it downregulated IL-15, IL1-RA and monocyte chemotactic protein-1. Thus, the RSV G protein/CX3CR1 interaction is likely important in infection and infection-induced responses of the airway epithelium, the primary site of human infection.

Indexed as

Amino Acid MotifsCell LineCX3C Chemokine Receptor 1Epithelial CellsHumansProtein BindingReceptors, ChemokineRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsRespiratory SystemViral Envelope ProteinsCX3C Chemokine Receptor 1CX3CR1 protein, humanReceptors, ChemokineViral Envelope Proteins

Identifiers

PMID26297201
PMCPMC4635495
OpenAlexW2114446982

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.