Evidence map›Paper›PMID 24421397›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014

A genetic model of differential susceptibility to human respiratory syncytial virus (RSV) infection.

Jonathan M Ciencewicki, Xuting Wang, Jacqui Marzec, M Elina Serra, Douglas A Bell, Fernando P Polack, Steven R Kleeberger

Abstract readMulticenter Study
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Inter-individual variation in health and disease associated with pulmonary infectious agents.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Genetic associations with viral respiratory illnesses and asthma control in children.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2016
    Article
  16. Article
  17. Mx1 and Mx2 key antiviral proteins are surprisingly lost in toothed whales.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
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 3 institutions in 2 countries.

Jonathan M Ciencewicki1Laboratory of Respiratory Biology National Institute of Environmental Health Sciences, 111 T. W. Alexander Dr., Bldg. 101, MD D-201, Research Triangle Park, NC 27709, USA. ciencewickij@niehs.nih.gov.
Xuting Wang
Jacqui Marzec
M Elina Serra
Douglas A Bell
Fernando P Polack
Steven R Kleeberger
National Institutes of Health · USInfant Foundation · ARNational Institute of Environmental Health Sciences · US

Funding

Discovery And Functional Genomics Of Environmental Response GenesZIAES100475 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BELL, DOUGLAS · 2009 to 2025
$24.4M
The Role Of Innate Immunity Genes In Viral Infection and Disease ProgressionZIAES100557 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI KLEEBERGER, STEVEN R · 2009 to 2021
$10.9M
Genetic Susceptibility To Carcinogens and ToxicantsZIAES046008 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BELL, DOUGLAS · 2009 to 2021
$7.8M
Intramural NIH HHS
6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is the primary cause of lower respiratory tract infection during childhood and causes severe symptoms in some patients, which may cause hospitalization and death. Mechanisms for differential responses to RSV are unknown. Our objective was to develop an in vitro model of RSV infection to evaluate interindividual variation in response to RSV and identify susceptibility genes. Populations of human-derived HapMap lymphoblastoid cell lines (LCLs) were infected with RSV. Compared with controls, RSV-G mRNA expression varied from ~1- to 400-fold between LCLs. Basal expression of a number of gene transcripts, including myxovirus (influenza virus) resistance 1 (MX1), significantly correlated with RSV-G expression in HapMap LCLs. Individuals in a case-control population of RSV-infected children who were homozygous (n=94) or heterozygous (n=172) for the predicted deleterious A allele in a missense G/A SNP in MX1 had significantly greater risk for developing severe RSV disease relative to those with the major allele (n=108) (χ(2)=5.305, P=0.021; OR: 1.750, 95% CI: 1.110, 2.758, P=0.021). We conclude that genetically diverse human LCLs enable identification of susceptibility genes (e.g., MX1) for RSV disease severity in children, providing insight for disease risk.

Indexed as

Models, GeneticTranscriptomeCase-Control StudiesCell LineFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHost-Pathogen InteractionsHumansInfantLymphocytesMaleMyxovirus Resistance ProteinsPolymorphism, Single NucleotideProspective StudiesMX1 protein, humanMyxovirus Resistance Proteinsbronchiolitisgene expressionHapMapinfant lung diseaselymphoblastoid cell linesMX1

Identifiers

PMID24421397
PMCPMC3963017
OpenAlexW2150533762

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.