Evidence map›Paper›PMID 19793818›Full record

ArticleJournal of virology2009

Apolipoprotein E but not B is required for the formation of infectious hepatitis C virus particles.

Jieyun Jiang, Guangxiang Luo

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 131 papers.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed
11.0field-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

131 citing papers in PubMed, 240 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Apolipoprotein E and viral infection: Risks and Mechanisms.Molecular therapy. Nucleic acids · 2023
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. HCV Assembly and Egress via Modifications in Host Lipid Metabolic Systems.Cold Spring Harbor perspectives in medicine · 2021
    Review
  15. Hepatitis C virus infection and tight junction proteins: The ties that bind.Biochimica et biophysica acta. Biomembranes · 2020
    Review
  16. Review
  17. Article
  18. The Role of ApoE in HCV Infection and Comorbidity.International journal of molecular sciences · 2019
    Review
  19. Review
  20. Article

71 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jieyun JiangDepartment of Microbiology, Immunology and Molecular Genetics, University of Kentucky College of Medicine, 800 Rose Street, Lexington, KY 40536, USA.
Guangxiang Luo
University of Kentucky · US

Funding

Transgenic mouse models of HCV infection and replicationR21AI092074 · NIAID · UNIVERSITY OF KENTUCKY · PI JIANG, JIEYUN · 2011 to 2012
$408k
Transgenic mouse models of hepatitis C virus replicationR21DK079293 · NIDDK · UNIVERSITY OF KENTUCKY · PI LUO, GUANGXIANG GEORGE · 2007 to 2008
$399k
Hepatitis C virus infection and lipoproteinsR21AI070769 · NIAID · UNIVERSITY OF KENTUCKY · PI LUO, GUANGXIANG GEORGE · 2007 to 2008
$399k
NIAID NIH HHS AI070769NIAID NIH HHS R21 AI070769NIAID NIH HHS R21 AI092074NIDDK NIH HHS DK079293NIDDK NIH HHS R21 DK079293
6 · The paper itself

Abstract

Our previous studies have found that hepatitis C virus (HCV) particles are enriched in apolipoprotein E (apoE) and that apoE is required for HCV infectivity and production. Studies by others, however, suggested that both microsomal transfer protein (MTP) and apoB are important for HCV production. To define the roles of apoB and apoE in the HCV life cycle, we developed a single-cycle HCV growth assay to determine the correlation of HCV assembly with apoB and apoE expression, as well as the influence of MTP inhibitors on the formation of HCV particles. The small interfering RNA (siRNA)-mediated knockdown of apoE expression remarkably suppressed the formation of HCV particles. However, apoE expressed ectopically could restore the defect of HCV production posed by the siRNA-mediated knockdown of endogenous apoE expression. In contrast, apoB-specific antibodies and siRNAs had no significant effect on HCV infectivity and production, respectively, suggesting that apoB does not play a significant role in the HCV life cycle. Additionally, two MTP inhibitors, CP-346086 and BMS-2101038, efficiently blocked secretion of apoB-containing lipoproteins but did not affect HCV production unless apoE expression and secretion were inhibited. At higher concentrations, however, MTP inhibitors blocked apoE expression and secretion and consequently suppressed the formation of HCV particles. Furthermore, apoE was found to be sensitive to trypsin digestion and to interact with NS5A in purified HCV particles and HCV-infected cells, as demonstrated by coimmunoprecipitation. Collectively, these findings demonstrate that apoE but not apoB is required for HCV assembly, probably via a specific interaction with NS5A.

Indexed as

Apolipoproteins BApolipoproteins ECell Line, TumorHepacivirusHumansIsoquinolinesRNA-Dependent RNA PolymeraseRNA, Small InterferingRNA, ViralTriazolesTrypsinViral Nonstructural ProteinsVirionVirus AssemblyApolipoproteins BApolipoproteins ECP-346086IsoquinolinesNS-5 protein, hepatitis C virusRNA-Dependent RNA PolymeraseRNA, Small InterferingRNA, ViralTriazolesTrypsinViral Nonstructural Proteins

Identifiers

PMID19793818
PMCPMC2786834
OpenAlexW2084858225

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.