Evidence map›Paper›PMID 26658574›Full record

ArticlePLoS pathogens2015

Respiratory Syncytial Virus Uses CX3CR1 as a Receptor on Primary Human Airway Epithelial Cultures.

Sara M Johnson, Beth A McNally, Ioannis Ioannidis, Emilio Flano, Michael N Teng, Antonius G Oomens, Edward E Walsh, Mark E Peeples

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed, 1 pooled it
12.4field-weighted citation impact, top 1% 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

187 citing papers in PubMed, 1 synthesis or guideline pooled it, 278 citations in OpenAlex.

  1. Frontiers in immunology · 2021
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127 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

8 authors at 5 institutions in 1 country.

Sara M JohnsonCenter for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, United States of America.
Beth A McNallyCenter for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, United States of America.
Ioannis IoannidisCenter for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, United States of America.
Emilio FlanoCenter for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, United States of America.
Michael N TengDivision of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, Florida, United States of America.
Antonius G OomensDepartment of Veterinary Pathobiology, Oklahoma State University, Stillwater, Oklahoma, United States of America.
Edward E WalshSchool of Medicine and Dentistry, University of Rochester Medical Center, Rochester, New York, United States of America.
Mark E PeeplesCenter for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, United States of America.
Nationwide Children's Hospital · USThe Ohio State University · USOklahoma State University · USUniversity of Rochester Medical Center · USUniversity of South Florida · US

Funding

Project 3: Dr. LiP01AI112524 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI LI, JIANRONG · 2015 to 2019
$6.8M
Respiratory Syncytial Virus Targeting of the Human Airway EpitheliumR01AI093848 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI PEEPLES, MARK E. · 2012 to 2023
$3.8M
NIAID NIH HHS P01 AI112524NIAID NIH HHS R01 AI093848
6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is the most frequent cause of lower respiratory disease in infants, but no vaccine or effective therapy is available. The initiation of RSV infection of immortalized cells is largely dependent on cell surface heparan sulfate (HS), a receptor for the RSV attachment (G) glycoprotein in immortalized cells. However, RSV infects the ciliated cells in primary well differentiated human airway epithelial (HAE) cultures via the apical surface, but HS is not detectable on this surface. Here we show that soluble HS inhibits infection of immortalized cells, but not HAE cultures, confirming that HS is not the receptor on HAE cultures. Conversely, a "non-neutralizing" monoclonal antibody against the G protein that does not block RSV infection of immortalized cells, does inhibit infection of HAE cultures. This antibody was previously shown to block the interaction between the G protein and the chemokine receptor CX3CR1 and we have mapped the binding site for this antibody to the CX3C motif and its surrounding region in the G protein. We show that CX3CR1 is present on the apical surface of ciliated cells in HAE cultures and especially on the cilia. RSV infection of HAE cultures is reduced by an antibody against CX3CR1 and by mutations in the G protein CX3C motif. Additionally, mice lacking CX3CR1 are less susceptible to RSV infection. These findings demonstrate that RSV uses CX3CR1 as a cellular receptor on HAE cultures and highlight the importance of using a physiologically relevant model to study virus entry and antibody neutralization.

Indexed as

AnimalsCell LineCells, CulturedCX3C Chemokine Receptor 1GTP-Binding ProteinsHost-Parasite InteractionsHumansImmunohistochemistryMiceMice, Inbred C57BLReceptors, ChemokineRespiratory MucosaRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsTransfectionViral ProteinsCX3C Chemokine Receptor 1CX3CR1 protein, humanGTP-Binding ProteinsReceptors, ChemokineViral Proteins

Identifiers

PMID26658574
PMCPMC4676609
OpenAlexW2198743132

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.