Evidence map›Paper›PMID 22898980›Full record

ArticleHepatology (Baltimore, Md.)2013

Ethanol facilitates hepatitis C virus replication via up-regulation of GW182 and heat shock protein 90 in human hepatoma cells.

Terence N Bukong, Wei Hou, Karen Kodys, Gyongyi Szabo

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Alcohol Promotes Exosome Biogenesis and ReleaseFrontiers in cell and developmental biology · 2021
    Article
  7. Article
  8. Cloaked Viruses and Viral Factors in Cutting Edge Exosome-Based Therapies.Frontiers in cell and developmental biology · 2020
    Review
  9. Article
  10. Article
  11. Effect of ethanol on lipid metabolism.Journal of hepatology · 2019
    Review
  12. miRNA Signature in NAFLD: A Turning Point for a Non-Invasive Diagnosis.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Article
  15. Observational
  16. Versican: a novel modulator of hepatic fibrosis.Laboratory investigation; a journal of technical methods and pathology · 2016
    Article
  17. Alcoholic liver disease and hepatitis C virus infection.World journal of gastroenterology · 2016
    Review
  18. Chaperones in hepatitis C virus infection.World journal of hepatology · 2016
    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

4 authors at 1 institution in 1 country.

Terence N BukongDepartment of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Wei Hou
Karen Kodys
Gyongyi Szabo
University of Massachusetts Chan Medical School · US

Funding

HCV, Alcohol and Host DefenseR37AA014372 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SZABO, GYONGYI · 2008 to 2017
$3.7M
NIAAA NIH HHS R37 AA014372NIAAA NIH HHS R37AA014372
6 · The paper itself

Abstract

unlabelledAlcohol use and hepatitis C virus (HCV) infection synergize to cause liver damage, and microRNA-122 (miR-122) appears to play a key role in this process. Argonaute 2 (Ago2), a key component of the RNA-induced silencing complex (RISC), has been shown to be important in modulating miR-122 function during HCV infection. However, GW182, a critical component of processing bodies (GW bodies) that is recruited by Ago2 to target messenger RNA (mRNA), has not been assessed in HCV infection. To characterize the role of GW182 in the pathogenesis of HCV infection, we determined its transcription and protein expression in an HCV J6/JFH1 culture system. Transcript and protein levels of GW182 as well as HCV RNA and protein expression increased with alcohol exposure. Specific silencing of mRNA expression by small interfering RNA against GW182 significantly decreased HCV RNA and protein expression. Overexpression of GW182 significantly increased HCV RNA and protein expression in HCV J6/JFH1 infected Huh7.5 cells. Furthermore, GW182 colocalized and coimmunoprecipitated with heat shock protein 90 (HSP90), which increased upon alcohol exposure with and without HCV infection and enhanced HCV gene expression. The use of an HSP90 inhibitor or knockdown of HSP90 decreased GW182 and miR-122 expression and significantly reduced HCV replication.

conclusionOverall, our results suggest that GW182 protein that is linked to miR-122 biogenesis and HSP90, which has been shown to stabilize the RISC, are novel host proteins that regulate HCV infection during alcohol abuse.

Indexed as

Anti-Infective Agents, LocalAutoantigensCell Line, TumorEthanolHepacivirusHSP90 Heat-Shock ProteinsHumansMicroRNAsRNA-Binding ProteinsUp-RegulationViral ProteinsVirus ReplicationAnti-Infective Agents, LocalAutoantigensEthanolHSP90 Heat-Shock ProteinsMicroRNAsMIRN122 microRNA, humanRNA-Binding ProteinsTNRC6A protein, humanViral Proteins

Identifiers

PMID22898980
PMCPMC3540130
OpenAlexW2148296809

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.