Evidence map›Paper›PMID 28968805›Full record

ArticleThe Journal of infectious diseases2017

A Link Between a Common Mutation in CFTR and Impaired Innate and Adaptive Viral Defense.

Emma Svedin, Renata Utorova, Michael H Hühn, Pär G Larsson, Virginia M Stone, Manasa Garimella, Katharina Lind, Thomas Hägglöf, Terezia Pincikova, Olli H Laitinen and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

15 authors at 3 institutions in 3 countries.

Emma SvedinCenter for Infectious Medicine, Department of Medicine.
Renata UtorovaCenter for Infectious Medicine, Department of Medicine.
Michael H HühnCenter for Infectious Medicine, Department of Medicine.
Pär G LarssonCenter for Infectious Medicine, Department of Medicine.
Virginia M StoneCenter for Infectious Medicine, Department of Medicine.
Manasa GarimellaDepartment of Microbiology, Tumor and Cell Biology.
Katharina LindCenter for Infectious Medicine, Department of Medicine.
Thomas HägglöfDepartment of Microbiology, Tumor and Cell Biology.
Terezia PincikovaCenter for Infectious Medicine, Department of Medicine.
Olli H LaitinenCenter for Infectious Medicine, Department of Medicine.
Gerald M McInerneyDepartment of Microbiology, Tumor and Cell Biology.
Bob ScholteDepartment of Cell Biology and Pediatric Pulmonology, Erasmus Medical Center, Rotterdam, The Netherlands.
Lena HjelteDepartment of Clinical Science, Intervention and Technology, Karolinska Institutet, and Stockholm Cystic Fibrosis Center, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Mikael C I KarlssonDepartment of Microbiology, Tumor and Cell Biology.
Malin Flodström-TullbergCenter for Infectious Medicine, Department of Medicine.
National Center for Infectious Diseases · USErasmus MC · NLKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute respiratory virus infections predispose the cystic fibrosis (CF) lung to chronic bacterial colonization, which contributes to high mortality. For reasons unknown, respiratory virus infections have a prolonged duration in CF. Here, we demonstrate that mice carrying the most frequent cystic fibrosis transmembrane conductance regulator (CFTR) mutation in humans, ΔF508, show increased morbidity and mortality following infection with a common human enterovirus. ΔF508 mice demonstrated impaired viral clearance, a slower type I interferon response and delayed production of virus-neutralizing antibodies. While the ΔF508 mice had a normal immune cell repertoire, unchanged serum immunoglobulin concentrations and an intact immune response to a T-cell-independent antigen, their response to a T-cell-dependent antigen was significantly delayed. Our studies reveal a novel function for CFTR in antiviral immunity and demonstrate that the ΔF508 mutation in cftr is coupled to an impaired adaptive immune response. This important insight could open up new approaches for patient care and treatment.

Indexed as

MutationAdaptive ImmunityAnimalsAntibodies, NeutralizingAntibodies, ViralCodonCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorDisease Models, AnimalDisease ResistanceGene Expression RegulationHost-Pathogen InteractionsHumansImmunity, InnateImmunizationImmunoglobulin GAntibodies, NeutralizingAntibodies, ViralCFTR protein, humanCodonCystic Fibrosis Transmembrane Conductance RegulatorImmunoglobulin GImmunoglobulin MInterferon-alphaPoly I-Cantibody responseantiviral defenseCoxsackieviruscystic fibrosisimmunity

Identifiers

PMID28968805
PMCPMC5853514
OpenAlexW2752732781

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.