Evidence map›Paper›PMID 25577150›Full record

Trial reportVirology2015

Interferon-λ4 is a cell-autonomous type III interferon associated with pre-treatment hepatitis C virus burden.

Yi-Fan Lu, David B Goldstein, Thomas J Urban, Shelton S Bradrick

Abstract readClinical Trial
In one paragraph

Trial report in Virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Interferon lambda 4 is a gut antimicrobial protein.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. IFN-λ3 is induced byInfection and immunity · 2024
    Article
  4. Article
  5. Article
  6. Innate Immunity in Hepatitis C Virus Infection.Cold Spring Harbor perspectives in medicine · 2021
    Review
  7. The Role of Ku70 as a Cytosolic DNA Sensor in Innate Immunity and Beyond.Frontiers in cellular and infection microbiology · 2021
    Review
  8. Review
  9. Genetics of the Human Interferon Lambda Region.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2019
    Review
  10. The IFN-λ4 Conundrum: When a Good Interferon Goes Bad.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

Yi-Fan LuDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, NC 27710, USA; Center for Human Genome Variation, Duke University Medical Center, NC 27710, USA.
David B GoldsteinDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, NC 27710, USA; Center for Human Genome Variation, Duke University Medical Center, NC 27710, USA.
Thomas J UrbanCenter for Human Genome Variation, Duke University Medical Center, NC 27710, USA.
Shelton S BradrickDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, NC 27710, USA; Center for Human Genome Variation, Duke University Medical Center, NC 27710, USA; Center for RNA Biology, Duke University Medical Center, NC 27710, USA.
Center for Human Genetics · US

Funding

Host-pathogen interactions in hepatitis C virus replicationK01DK082613 · NIDDK · DUKE UNIVERSITY · PI BRADRICK, SHELTON STEWART · 2009 to 2013
$546k
NIDDK NIH HHS DK082613NIDDK NIH HHS K01 DK082613
6 · The paper itself

Abstract

Genetic variants surrounding the interferon-λ3 (IFNL3) gene are strongly associated with clearance of hepatitis C virus (HCV). A variant (rs368234815 TT/ΔG) upstream of IFNL3 was recently implicated to control expression of a novel gene termed IFNL4. We conducted genetic analysis of rs368234815 in a chronic HCV patient cohort and molecular studies of IFNL4 in primary human hepatocytes (PHHs). Analysis of PHHs that are heterozygous at rs368234815 revealed that the IFNL4 transcript isoform is rare, accounting for 2% of transcripts arising from the IFNL4 locus. Nevertheless, IFNL4 over-expression inhibited replication of multiple Flaviviridae and IFNL4 anti-viral potency required the IFNL receptor. In contrast to IFNL3, IFNL4 was inefficiently secreted and appeared to act in a cell-autonomous manner. Genetic analysis revealed associations of rs368234815 with sustained virological response and pre-treatment viral load. The findings suggest that IFNL4 is an atypical IFNL whose activity may be maladaptive to clearance of HCV infection.

Indexed as

Antiviral AgentsCohort StudiesGenotypeHepacivirusHepatitis C, ChronicHepatocytesHumansInterferon LambdaInterleukinsMalePolymorphism, Single NucleotideRibavirinTreatment OutcomeViral LoadAntiviral AgentsIFNL4 protein, humanInterferon LambdaInterleukinsRibavirinFlaviviridaeGenome-wide association studyHepatitis C virusIL28BSustained virological response

Identifiers

PMID25577150
PMCPMC4494652
OpenAlexW1994914448

What OpenQuestion holds

Textmetadata
LicenceTDM
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.