Evidence map›Paper›PMID 24786669›Full record

ReviewJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2014

IFN-λ4: the paradoxical new member of the interferon lambda family.

Thomas R O'Brien, Ludmila Prokunina-Olsson, Raymond P Donnelly

Abstract readReview
In one paragraph

Review in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
–field-weighted citation impact
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

88 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Variants ofGenes · 2023
    Article
  13. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023
    Article
  14. The Interferon-Lambda Family Celebrates 20 Years of Scientific Discovery.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023
    Article
  15. Unlocking STING as a Therapeutic Antiviral Strategy.International journal of molecular sciences · 2023
    Review
  16. Article
  17. No Association of IFNL4 Genotype With Opportunistic Infections and Cancers Among Men With Human Immunodeficiency Virus 1 Infection.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023
    Article
  18. Article
  19. Article
  20. Distribution ofMicroorganisms · 2022
    Article

28 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

3 authors.

Thomas R O'Brien1 Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute , National Institutes of Health, Bethesda, Maryland.
Ludmila Prokunina-Olsson
Raymond P Donnelly

Funding

Epidemiology of Oncogenic VirusesZIACP005782 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI O'BRIEN, THOMAS R · 2009 to 2025
$6.7M
CLINICAL/IMMUNOLOGIC/GENETIC ANALYSES OF AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROMEZ01AI000732 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI RAO, VEMULKONDA · 1995 to 2008
$1.1M
Intramural NIH HHS
6 · The paper itself

Abstract

Interferons (IFNs) are generally considered antiviral cytokines, yet the newly discovered IFN-λ4 is linked with the failure to clear hepatitis C virus (HCV) infection either spontaneously or in response to treatment. IFN-λ4 can be generated only by individuals who carry the IFNL4-ΔG allele (rs368234815), which is the strongest known host factor for predicting clearance of HCV. The ancestral IFNL4-ΔG allele is the major variant in Africans while the minor variant in Asians, suggesting very strong negative genetic selection for this allele-most likely driven by an infectious agent other than HCV. IFN-λ4 most closely resembles IFN-λ3, but these proteins share only 29% amino-acid identity, and, in contrast to IFN-λ3, IFN-λ4 is only weakly secreted. Nevertheless, IFN-λ4 signals through the IFN-λ receptor complex and induces expression of IFN-stimulated genes via the Janus kinase-signal transducer and activator of transcription signaling pathway. Although the IFNL4-ΔG variant is strongly associated with the failure to clear HCV infection, HCV-infected patients who carry this allele have lower baseline HCV RNA levels in the absence of treatment. Resolving the paradoxical functions of IFN-λ4, which appears to induce antiviral activity yet impair effective clearance of HCV, may yield critical new insights into the immunologic response to HCV infection and IFN biology.

Indexed as

AllelesAnimalsBlack PeopleGenetic Predisposition to DiseaseHepacivirusHepatitis CHumansInterferon LambdaInterleukinsPolymorphism, Single NucleotideRNA, ViralSignal TransductionViral LoadIFNL4 protein, humanInterferon LambdaInterleukinsRNA, Viral

Identifiers

PMID24786669
PMCPMC4217005

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.