Evidence map›Paper›PMID 27867263›Full record

ArticleMediators of inflammation2016

Interferon-Stimulated Gene 15 Conjugation Stimulates Hepatitis B Virus Production Independent of Type I Interferon Signaling Pathway

Yujia Li, Shilin Li, Xiaoqiong Duan, Yanzhao Chen, Baihai Jiao, Haiyan Ye, Min Yao, Limin Chen

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The development of COVID-19 treatment.Frontiers in immunology · 2023
    Review
  6. Article
  7. Review
  8. ISG15 in antiviral immunity and beyond.Nature reviews. Microbiology · 2018
    Review
  9. Article
  10. Article
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

8 authors at 2 institutions in 2 countries.

Yujia LiInstitute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory for Transfusion-Transmitted Diseases of Sichuan Province, Chengdu, Sichuan 610052, China.ORCID 0000-0002-2636-5468
Shilin LiInstitute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory for Transfusion-Transmitted Diseases of Sichuan Province, Chengdu, Sichuan 610052, China.ORCID 0000-0001-7065-6150
Xiaoqiong DuanInstitute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory for Transfusion-Transmitted Diseases of Sichuan Province, Chengdu, Sichuan 610052, China.ORCID 0000-0002-3556-6739
Yanzhao ChenInstitute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory for Transfusion-Transmitted Diseases of Sichuan Province, Chengdu, Sichuan 610052, China.
Baihai JiaoInstitute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory for Transfusion-Transmitted Diseases of Sichuan Province, Chengdu, Sichuan 610052, China.
Haiyan YeInstitute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory for Transfusion-Transmitted Diseases of Sichuan Province, Chengdu, Sichuan 610052, China.
Min YaoInstitute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory for Transfusion-Transmitted Diseases of Sichuan Province, Chengdu, Sichuan 610052, China.
Limin ChenInstitute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory for Transfusion-Transmitted Diseases of Sichuan Province, Chengdu, Sichuan 610052, China; Toronto General Research Institute, University of Toronto, Toronto, ON, Canada M5G 1L6.ORCID 0000-0002-7370-6499
Chinese Academy of Medical Sciences & Peking Union Medical College · CNUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) is an important account of infectious hepatitis and interferon (IFN) remains one of the best treatment options. Activation of type I IFN signaling pathway leads to expressions of IFN-stimulated genes (ISGs) which play important roles in antiviral and immunomodulatory responses to HBV or hepatitis C virus (HCV) infection. Our previous studies indicated that ISG15 and its conjugation (ISGylation) were exploited by HCV to benefit its replication and persistent infection. This study was designed to assess the role of ISG15 and ISGylation in HBV infection

Indexed as

CytokinesDNA, ViralHepacivirusHep G2 CellsHumansInterferon-alphaSignal TransductionUbiquitin-Activating EnzymesUbiquitinsCytokinesDNA, ViralInterferon-alphaISG15 protein, humanUBA7 protein, humanUbiquitin-Activating EnzymesUbiquitins

Identifiers

PMID27867263
PMCPMC5102744
OpenAlexW2543969678

What OpenQuestion 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 OpenQuestion graph.