Evidence map›Paper›PMID 26579391›Full record

ReviewActa pharmaceutica Sinica. B2014

Recent advances in the anti-HCV mechanisms of interferon.

Menghao Huang, Jian-Dong Jiang, Zonggen Peng

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Acta pharmaceutica Sinica. B, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Type I Interferon Production of Plasmacytoid Dendritic Cells under Control.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Review
  12. Review
  13. Reinforced reasoning in medicine.Journal of evaluation in clinical practice · 2020
    Article
  14. Review
  15. Virusdisease · 2019
    Article
  16. Article
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

Menghao HuangInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
Jian-Dong JiangInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China ; Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
Zonggen PengInstitute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon (IFN) in combination with ribavirin has been the standard of care (SOC) for chronic hepatitis C for the past few decades. Although the current SOC lacks the desired efficacy, and 4 new direct-acting antiviral agents have been recently approved, interferons are still likely to remain the cornerstone of therapy for some time. Moreover, as an important cytokine system of innate immunity, host interferon signaling provides a powerful antiviral response. Nevertheless, the mechanisms by which HCV infection controls interferon production, and how interferons, in turn, trigger anti-HCV activities as well as control the outcome of HCV infection remain to be clarified. In this report, we review current progress in understanding the mechanisms of IFN against HCV, and also summarize the knowledge of induction of interferon signaling by HCV infection.

Indexed as

Antiviral agentCHC, chronic hepatitis CDCs, dendritic cellsDNAM1, DNAX accessory molecule-1dsRNA, double-stranded RNAE2, envelop 2GAS, IFN-γ-activated siteGWAS, genome-wide association studiesHepatitis C virusIFNAR1, interferon-alpha receptor 1IFNAR2, interferon-alpha receptor 2IFNGR1, interferon gamma receptor 1IFNGR2, interferon gamma receptor 2IFN, interferonIFNL4, IFN-lambda 4IFN-α, interferon-αIL-10R2, interleukin-10 receptor 2IL-29, interleukin-29InterferonIRF-3, interferon regulatory factor 3IRGs, IFN regulatory genesISG15, interferon-stimulated gene 15ISGF3, IFN-stimulated gene factor 3ISGs, IFN-stimulated genesISREs, IFN-stimulated response elementsJAKs, Janus activated kinasesMAVS, mitochondrial antiviral signaling proteinMDA-5, melanoma differentiation-associated gene-5MHC, major histocompatibility complexMolecular mechanismNKCs, natural killer cellsNKTCs, natural killer T cellsOAS, 2′-5′-oligoadenylate synthetasePAMPs, pathogen-associated molecular patternsPBMCs, peripheral blood mononuclear cellspDC, plasmacytoid dendritic cellPKR, protein kinase RPRRs, pattern recognition receptorsRdRp, RNA dependent RNA polymeraseRIG-I, retinoic acid-inducible gene-IRLRs, RIG-I-like receptorsSNPs, single-nucleotide polymorphismsSOC, standard of careSTAT1, signal transducer and activator of transcription 1STAT2, signal transducer and activator of transcription 2SVR, sustained virological responseTH1, T-helper-1TH2, T-helper-2TLRs, Toll-like receptorsTYK2, tyrosine kinase 2USP18, ubiquitin specific peptidase 18

Identifiers

PMID26579391
PMCPMC4629091
OpenAlexW2043161692

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.