Evidence map›Paper›PMID 18688877›Full record

ArticleHepatology (Baltimore, Md.)2008

Induction of incomplete autophagic response by hepatitis C virus via the unfolded protein response.

Donna Sir, Wen-Ling Chen, Jinah Choi, Takaji Wakita, T S Benedict Yen, Jing-Hsiung James Ou

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed, 2 pooled it
14.8field-weighted citation impact, top 1% 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

226 citing papers in PubMed, 2 syntheses or guidelines pooled it, 354 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Review
  4. Article
  5. Article
  6. Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025
    Review
  7. Review
  8. Article
  9. Review
  10. Viruses and autophagy: bend, but don't break.Nature reviews. Microbiology · 2024
    Review
  11. Review
  12. Article
  13. HCV-induced autophagy and innate immunity.Frontiers in immunology · 2024
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. The role of autophagy in viral infections.Journal of biomedical science · 2023
    Review

166 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

6 authors at 3 institutions in 2 countries.

Donna SirDepartment of Molecular Microbiology and Immunology, University of Southern California, Keck School of Medicine, Los Angeles, CA 90033, USA.
Wen-Ling Chen
Jinah Choi
Takaji Wakita
T S Benedict Yen
Jing-Hsiung James Ou
University of Southern California · USNational Institute of Infectious Diseases · JPUniversity of California, San Francisco · US

Funding

UCSF Liver Core CenterP30DK026743 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Holger Willenbring · 1986 to 2026
$30.7M
Molecular analysis of the HCV F geneR01AI060559 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OU, J.-H. JAMES · 2003 to 2007
$1.4M
NIAID NIH HHS AI060559NIAID NIH HHS R01 AI060559NIDDK NIH HHS P30 DK026743NIDDK NIH HHS P30DK26743
6 · The paper itself

Abstract

unlabelledAutophagy is important for cellular homeostasis and can serve as innate immunity to remove intracellular pathogens. Here, we demonstrate by a battery of morphological and biochemical assays that hepatitis C virus (HCV) induces the accumulation of autophagosomes in cells without enhancing autophagic protein degradation. This induction of autophagosomes depended on the unfolded protein response (UPR), as the suppression of UPR signaling pathways suppressed HCV-induced lipidation of the microtubule-associated protein light chain 3 (LC3) protein, a necessary step for the formation of autophagosomes. The suppression of UPR or the suppression of expression of LC3 or Atg7, a protein that mediates LC3 lipidation, suppressed HCV replication, indicating a positive role of UPR and the incomplete autophagic response in HCV replication.

conclusionOur studies delineate the molecular pathway by which HCV induces autophagic vacuoles and also demonstrate the perturbation of the autophagic response by HCV. These unexpected effects of HCV on the host cell likely play an important role in HCV pathogenesis.

Indexed as

Protein FoldingAutophagyAutophagy-Related Protein 7Carcinoma, HepatocellularCell Line, TumorEndoplasmic ReticulumHepacivirusHepatitis CHumansLiver NeoplasmsMicrotubule-Associated ProteinsPlasmidsRNA, Small InterferingRNA, ViralSignal TransductionTransfectionATG7 protein, humanAutophagy-Related Protein 7MAP1LC3A protein, humanMicrotubule-Associated ProteinsRNA, Small InterferingRNA, ViralUbiquitin-Activating Enzymes

Identifiers

PMID18688877
PMCPMC2562598
OpenAlexW2003682019

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.