Evidence map›Paper›PMID 31825835›Full record

ArticleCell reports2019

Type-I-IFN-Stimulated Gene TRIM5γ Inhibits HBV Replication by Promoting HBx Degradation.

Guangyun Tan, Zhaohong Yi, Hongxiao Song, Fengchao Xu, Feng Li, Roghiyh Aliyari, Hong Zhang, Peishuang Du, Yanhua Ding, Junqi Niu and 4 more

Registry-linked trialAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05965388 (Predictive Value of HBV pgRNA on Long-term Outcomes in Hepatitis B Patients Treated With Antiviral Therapy), which is not on this map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
–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.

NCT05965388 not yet recruitingnot on this mapstarted 2023, after this paper: background citation

Predictive Value of HBV pgRNA on Long-term Outcomes in Hepatitis B Patients Treated With Antiviral Therapy

TypeobservationalSponsorWen-hong ZhangRan2023 to 2029Enrolled5,000ConditionsHBV, HCCArmsnucleoside analogues or interferon
3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. [Advances of TRIM superfamily proteins in chronic liver disease and hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Observational
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Structural basis of the hepatitis B virus X protein in complex with DDB1.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

14 authors.

Guangyun TanDepartment of Immunology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin 130061, China. Electronic address: tgy0425@jlu.edu.cn.
Zhaohong YiCAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Chaoyang District, Beijing, China.
Hongxiao SongDepartment of Immunology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin 130061, China.
Fengchao XuDepartment of Immunology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin 130061, China.
Feng LiLineberger Comprehensive Cancer Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Roghiyh AliyariDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095, USA.
Hong ZhangPhase I Clinical Research Center, The First Hospital of Jilin University, Jilin 130021, China.
Peishuang DuCAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Chaoyang District, Beijing, China.
Yanhua DingPhase I Clinical Research Center, The First Hospital of Jilin University, Jilin 130021, China.
Junqi NiuDepartment of Hepatology, The First Hospital of Jilin University, Changchun, Jilin 130021, China.
Xiaosong WangDepartment of Immunology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin 130061, China.
Lishan SuDepartment of Immunology, Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin 130061, China; CAS Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Chaoyang District, Beijing, China; Lineberger Comprehensive Cancer Center, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
F Xiao-Feng QinCenter of Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100005, China; Suzhou Institute of Systems Medicine, Suzhou, Jiangsu 215123, China. Electronic address: fqin1@foxmail.com.
Genhong ChengDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095, USA. Electronic address: gcheng@mednet.ucla.edu.

Funding

Viral Mediated Type I Interferon InductionR01AI069120 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHENG, GENHONG · 2006 to 2021
$6.0M
NIAID NIH HHS R01 AI069120
6 · The paper itself

Abstract

To understand the molecular mechanisms that mediate the anti-hepatitis B virus (HBV) effect of interferon (IFN) therapy, we conduct high-throughput bimolecular fluorescence complementation screening to identify potential physical interactions between the HBx protein and 145 IFN-stimulated genes (ISGs). Seven HBx-interacting ISGs have consistent and significant inhibitory effects on HBV replication, among which TRIM5γ suppresses HBV replication by promoting K48-linked ubiquitination and degradation of the HBx protein on the K95 ubiquitin site. The B-Box domain of TRIM5γ under overexpression conditions is sufficient to trigger HBx degradation and is responsible both for interacting with HBx and recruiting TRIM31, which is an ubiquitin ligase that triggers HBx ubiquitination. High expression levels of TRIM5γ in IFN-α-treated HBV patients might indicate a better therapeutic effect. Thus, our studies identify a crucial role for TRIM5γ and TRIM31 in promoting HBx degradation, which may facilitate the development of therapeutic agents for the treatment of patients with IFN-resistant HBV infection.

Indexed as

Virus ReplicationAdultAntiviral Restriction FactorsFemaleHEK293 CellsHepatitis BHepatitis B virusHepatocytesHep G2 CellsHumansInterferon-alphaMaleMiddle AgedProteolysisTrans-ActivatorsTripartite Motif ProteinsAntiviral Restriction Factorshepatitis B virus X proteinInterferon-alphaTrans-ActivatorsTRIM31 protein, humanTRIM5 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesViral Regulatory and Accessory ProteinsHBVHBxTRIM31TRIM5γtype I IFN

Identifiers

PMID31825835
PMCPMC6996557

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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.