Evidence map›Paper›PMID 19793905›Full record

ArticleThe Journal of general virology2010

Requirement of cellular DDX3 for hepatitis C virus replication is unrelated to its interaction with the viral core protein.

Allan G N Angus, David Dalrymple, Steeve Boulant, David R McGivern, Reginald F Clayton, Martin J Scott, Richard Adair, Susan Graham, Ania M Owsianka, Paul Targett-Adams and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of general virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

62 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. The human DEAD-box helicase DDX3X as a regulator of mRNA translation.Frontiers in cell and developmental biology · 2022
    Review
  11. Review
  12. Cytoplasmic DDX3 as prognosticator in male breast cancer.Virchows Archiv : an international journal of pathology · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

2 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

15 authors at 4 institutions in 3 countries.

Allan G N AngusMRC Virology Unit, Institute of Virology, University of Glasgow, Church Street, Glasgow G11 5JR, UK.
David Dalrymple
Steeve Boulant
David R McGivern
Reginald F Clayton
Martin J Scott
Richard Adair
Susan Graham
Ania M Owsianka
Paul Targett-Adams
Kui Li
Takaji Wakita
John McLauchlan
Stanley M Lemon
Arvind H Patel
University of Glasgow · GBThe University of Texas Medical Branch at Galveston · USNational Institute of Infectious Diseases · JPUniversity of Tennessee Health Science Center · US

Funding

Virus-Host Interactions in Hepatitis C Virus (HCV) InfectionsU19AI040035 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI LEMON, STANLEY M. · 1996 to 2009
$12.0M
Role of TLR3 Signaling in Control of HCVR01AI069285 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI LI, KUI · 2007 to 2016
$2.5M
Role of TLR3 Signaling in Control of HCVR56AI069285 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LI, KUI · 2012 to 2012
$300k
Medical Research Council MC_U130184143Medical Research Council MC_U130184144Medical Research Council MC_UU_12014/1NIAID NIH HHS AI069285NIAID NIH HHS R01 AI069285NIAID NIH HHS R56 AI069285NIAID NIH HHS U19 AI040035NIAID NIH HHS U19-AI40035
6 · The paper itself

Abstract

The cellular DEAD-box protein DDX3 was recently shown to be essential for hepatitis C virus (HCV) replication. Prior to that, we had reported that HCV core binds to DDX3 in yeast-two hybrid and transient transfection assays. Here, we confirm by co-immunoprecipitation that this interaction occurs in cells replicating the JFH1 virus. Consistent with this result, immunofluorescence staining of infected cells revealed a dramatic redistribution of cytoplasmic DDX3 by core protein to the virus assembly sites around lipid droplets. Given this close association of DDX3 with core and lipid droplets, and its involvement in virus replication, we investigated the importance of this host factor in the virus life cycle. Mutagenesis studies located a single amino acid in the N-terminal domain of JFH1 core that when changed to alanine significantly abrogated this interaction. Surprisingly, this mutation did not alter infectious virus production and RNA replication, indicating that the core-DDX3 interaction is dispensable in the HCV life cycle. Consistent with previous studies, siRNA-led knockdown of DDX3 lowered virus production and RNA replication levels of both WT JFH1 and the mutant virus unable to bind DDX3. Thus, our study shows for the first time that the requirement of DDX3 for HCV replication is unrelated to its interaction with the viral core protein.

Indexed as

Host-Pathogen InteractionsVirus ReplicationAmino Acid SequenceAmino Acid SubstitutionCell LineDEAD-box RNA HelicasesGene Knockdown TechniquesHepacivirusHumansImmunoprecipitationMolecular Sequence DataMutagenesis, Site-DirectedProtein BindingProtein Interaction MappingRNA, Small InterferingViral Core ProteinsDDX3X protein, humanDEAD-box RNA Helicasesnucleocapsid protein, Hepatitis C virusRNA, Small InterferingViral Core Proteins

Identifiers

PMID19793905
PMCPMC2885062
OpenAlexW2096166831

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.