Evidence map›Paper›PMID 29443378›Full record

ArticleHepatology (Baltimore, Md.)2019

Hepatitis C Virus E2 Envelope Glycoprotein Induces an Immunoregulatory Phenotype in Macrophages.

Young-Chan Kwon, Keith Meyer, Guangyong Peng, Soumya Chatterjee, Daniel F Hoft, Ranjit Ray

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Hepatitis C virus modifiedJournal of virology · 2025
    Article
  3. Review
  4. Review
  5. Review
  6. Hepatitis C virus modified sE2Journal of virology · 2024
    Article
  7. Review
  8. M1/M2 macrophages and their overlaps - myth or reality?Clinical science (London, England : 1979) · 2023
    Article
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  10. Article
  11. Article
  12. Review
  13. Article
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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 1 institution in 1 country.

Young-Chan KwonDepartments of Internal Medicine, Saint Louis University, St. Louis, MO.
Keith MeyerDepartments of Internal Medicine, Saint Louis University, St. Louis, MO.
Guangyong PengDepartments of Internal Medicine, Saint Louis University, St. Louis, MO.
Soumya ChatterjeeDepartments of Internal Medicine, Saint Louis University, St. Louis, MO.
Daniel F HoftDepartments of Internal Medicine, Saint Louis University, St. Louis, MO.
Ranjit RayDepartments of Internal Medicine, Saint Louis University, St. Louis, MO.
Saint Louis University · US

Funding

Hepatitis C virus infection and mechanism of liver disease progressionR01DK113645 · NIDDK · SAINT LOUIS UNIVERSITY · PI RAY, RANJIT, RAY, RATNA B. · 2017 to 2021
$1.7M
Mechanisms of Liver Disease Progression by Hepatitis C VirusR01DK080812 · NIDDK · SAINT LOUIS UNIVERSITY · PI RAY, RANJIT · 2009 to 2013
$1.6M
NIDDK NIH HHS R01 DK080812NIDDK NIH HHS R01 DK113645NIH HHS DK080812Presidential and Liver Center Research Funds of Saint Louis University
6 · The paper itself

Abstract

A comprehensive strategy to control hepatitis C virus (HCV) infection needs a vaccine. Our phase I study with recombinant HCV E1/E2 envelope glycoprotein (EnvGPs) as a candidate vaccine did not induce a strong immune response in volunteers. We analyzed the interactions of HCV EnvGPs with human monocyte-derived macrophages as antigen-presenting cells. HCV E2 induced immune regulatory cytokine interleukin (IL)-10 and soluble CD163 (sCD163) protein expression in macrophages from 7 of 9 blood donors tested. Furthermore, HCV E2 enhanced Stat3 and suppressed Stat1 activation, reflecting macrophage polarization toward M2 phenotype. E2-associated macrophage polarization appeared to be dependent of its interaction with CD81 leading endothelial growth factor receptor (EGFR) activation. Additionally, E2 suppressed the expression of C3 complement, similar to HCV-exposed dendritic cells (DCs), implying potential impairment of immune cell priming. Conclusion: Our results suggest that E2 EnvGP may not be an ideal candidate for HCV vaccine development, and discrete domains within E2 may prove to be more capable of elliciting a protective immune response. (Hepatology 2018).

Indexed as

Antigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenComplement C3Dendritic CellsErbB ReceptorsHost-Pathogen InteractionsHumansInterleukin-10MacrophagesPhenotypeProto-Oncogene Proteins c-aktReceptors, Cell SurfaceTetraspanin 28Viral Envelope ProteinsAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCD81 protein, humanComplement C3EGFR protein, humanErbB Receptorsglycoprotein E2, Hepatitis C virusIL10 protein, humanInterleukin-10Proto-Oncogene Proteins c-aktReceptors, Cell SurfaceTetraspanin 28Viral Envelope Proteins

Identifiers

PMID29443378
PMCPMC6092255
OpenAlexW2793438433

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.