Evidence map›Paper›PMID 32611756›Full record

ArticleJournal of virology2020

Interferon-Induced Protein 44 and Interferon-Induced Protein 44-Like Restrict Replication of Respiratory Syncytial Virus.

D C Busse, D Habgood-Coote, S Clare, C Brandt, I Bassano, M Kaforou, J Herberg, M Levin, J-F Eléouët, P Kellam and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing 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

72 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Gingipain proteases from the bacteriumProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Article
  19. Seasonal PMParticle and fibre toxicology · 2025
    Article
  20. Article

12 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

11 authors at 4 institutions in 2 countries.

D C BusseDepartment of Infectious Disease, Imperial College London, St. Mary's Campus, London, United Kingdom.ORCID 0000-0003-3872-3557
D Habgood-CooteDepartment of Infectious Disease, Imperial College London, St. Mary's Campus, London, United Kingdom.
S ClareWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, United Kingdom.
C BrandtWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, United Kingdom.
I BassanoDepartment of Infectious Disease, Imperial College London, St. Mary's Campus, London, United Kingdom.ORCID 0000-0002-6948-2568
M KaforouDepartment of Infectious Disease, Imperial College London, St. Mary's Campus, London, United Kingdom.ORCID 0000-0001-9878-4007
J HerbergDepartment of Infectious Disease, Imperial College London, St. Mary's Campus, London, United Kingdom.ORCID 0000-0001-6941-6491
M LevinDepartment of Infectious Disease, Imperial College London, St. Mary's Campus, London, United Kingdom.ORCID 0000-0003-2767-6919
J-F EléouëtUnité De Virologie et Immunologie Moléculaires (UR892), INRA, Université Paris-Saclay, Jouy-en-Josas, France.ORCID 0000-0002-7361-4885
P KellamDepartment of Infectious Disease, Imperial College London, St. Mary's Campus, London, United Kingdom.ORCID 0000-0003-3166-4734
J S TregoningDepartment of Infectious Disease, Imperial College London, St. Mary's Campus, London, United Kingdom john.tregoning@imperial.ac.uk.ORCID 0000-0001-8093-8741
Imperial College London · GBWellcome Sanger Institute · GBKymab (United Kingdom) · GBUniversité Paris-Saclay · FR

Funding

Wellcome Trust 109056/Z/15/AWellcome Trust 206508/Z/17/Z
6 · The paper itself

Abstract

Cellular intrinsic immunity, mediated by the expression of an array of interferon-stimulated antiviral genes, is a vital part of host defense. We have previously used a bioinformatic screen to identify two interferon-stimulated genes (ISG) with poorly characterized function, interferon-induced protein 44 (IFI44) and interferon-induced protein 44-like (IFI44L), as potentially being important in respiratory syncytial virus (RSV) infection. Using overexpression systems, CRISPR-Cas9-mediated knockout, and a knockout mouse model, we investigated the antiviral capability of these genes in the control of RSV replication. Overexpression of IFI44 or IFI44L was sufficient to restrict RSV infection at an early time postinfection. Knocking out these genes in mammalian airway epithelial cells increased levels of infection. Both genes express antiproliferative factors that have no effect on RSV attachment but reduce RSV replication in a minigenome assay. The loss of

Indexed as

A549 CellsAnimalsAntigensBiological AssayCell Line, TumorCRISPR-Cas SystemsCytoskeletal ProteinsDisease Models, AnimalEpithelial CellsGene EditingGene Expression RegulationHEK293 CellsHost-Pathogen InteractionsHumansImmunity, InnateInfantAntigensCytoskeletal ProteinsIFI44L protein, humanIFI44 protein, humanTumor Suppressor ProteinsIFI44innate immunityintrinsic immunityrestriction factorRSV

Identifiers

PMID32611756
PMCPMC7459546
OpenAlexW3039872072

What Socratic 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 Socratic graph.