Evidence map›Paper›PMID 29695434›Full record

ArticleJournal of virology2018

Regulation of Apolipoprotein E Trafficking by Hepatitis C Virus-Induced Autophagy.

Ja Yeon Kim, Jing-Hsiung James Ou

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025
    Review
  3. Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024
    Review
  4. Review
  5. Article
  6. HCV-induced autophagy and innate immunity.Frontiers in immunology · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Autophagy in liver diseases.World journal of hepatology · 2021
    Review
  12. Autophagy in HCV Replication and Protein Trafficking.International journal of molecular sciences · 2021
    Review
  13. Review
  14. The Role of ApoE in HCV Infection and Comorbidity.International journal of molecular sciences · 2019
    Review
  15. Diverse Functions of Autophagy in Liver Physiology and Liver Diseases.International journal of molecular sciences · 2019
    Review
  16. The Multifaceted Roles of Autophagy in Flavivirus-Host Interactions.International journal of molecular sciences · 2018
    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

2 authors at 1 institution in 1 country.

Ja Yeon KimDepartment of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, USA.
Jing-Hsiung James OuDepartment of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, Los Angeles, California, USA jamesou@hsc.usc.edu.
University of Southern California · US

Funding

Hepatitis C virus and autophagic responseR01DK094652 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OU, J.-H. JAMES · 2011 to 2020
$3.2M
NIDDK NIH HHS R01 DK094652
6 · The paper itself

Abstract

Apolipoprotein E (ApoE) plays an important role in the maturation and infectivity of hepatitis C virus (HCV). By analyzing the subcellular localization of ApoE in Huh7 hepatoma cells that harbored an HCV subgenomic RNA replicon, we found that ApoE colocalized with autophagosomes. This colocalization was marginally detected in HCV-infected cells, apparently due to the depletion of ApoE by HCV, as treatment with bafilomycin A1 (BafA1), a vacuolar ATPase inhibitor that inhibits autophagic protein degradation, partially restored the ApoE level and enhanced its colocalization with autophagosomes in HCV-infected cells. The role of HCV-induced autophagy in the degradation of ApoE was further supported by the observations that nutrient starvation, which induces autophagic protein degradation, led to the loss of ApoE in HCV subgenomic RNA replicon cells and that the knockdown of ATG7, a protein essential for the formation of autophagic vacuoles, increased the ApoE level in cells with productive HCV replication. Interestingly, the inhibition of autophagy by ATG7 knockdown reduced the colocalization of ApoE with the HCV E2 envelope protein and the HCV titers released from cells. In contrast, the treatment of cells with BafA1 enhanced the colocalization of ApoE and HCV E2 and increased both intracellular and extracellular HCV titers. These results indicated that autophagy played an important role in the trafficking of ApoE in HCV-infected cells. While it led to autophagic degradation of ApoE, it also promoted the interaction between ApoE and HCV E2 to enhance the production of infectious progeny viral particles.

Indexed as

Apolipoproteins EAutophagosomesAutophagyAutophagy-Related Protein 7Cell Line, TumorGene Knockdown TechniquesHepacivirusHepatitis CHost-Pathogen InteractionsHumansViral Envelope ProteinsViral LoadVirus ReplicationApoE protein, humanApolipoproteins EATG7 protein, humanAutophagy-Related Protein 7Viral Envelope Proteinsapolipoprotein Eautophagosomesautophagyhepatitis C virus

Identifiers

PMID29695434
PMCPMC6026764
OpenAlexW2802732121

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.