Evidence map›Paper›PMID 31332246›Full record

ArticleScientific reports2019

Virus Genotype-Dependent Transcriptional Alterations in Lipid Metabolism and Inflammation Pathways in the Hepatitis C Virus-infected Liver.

W M H d'Avigdor, M A Budzinska, M Lee, R Lam, J Kench, M Stapelberg, S V McLennan, G Farrell, J George, G W McCaughan and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Observational
  6. Article
  7. Article
  8. Review
  9. Genotype 3-hepatitis C virus' last line of defense.World journal of gastroenterology · 2021
    Review
  10. Impact of virus subtype and hostRNA (New York, N.Y.) · 2020
    Article
  11. Article
  12. 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

12 authors at 4 institutions in 2 countries.

W M H d'AvigdorLiver Injury and Cancer Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, Sydney, NSW, Australia.
M A BudzinskaLiver Injury and Cancer Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0002-3624-431X
M LeeLiver Injury and Cancer Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, Sydney, NSW, Australia.
R LamLiver Injury and Cancer Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, Sydney, NSW, Australia.
J KenchSydney Medical School, University of Sydney, Sydney, NSW, Australia.
M StapelbergLiver Injury and Cancer Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, Sydney, NSW, Australia.
S V McLennanSydney Medical School, University of Sydney, Sydney, NSW, Australia.
G FarrellAustralian National University, Canberra, ACT, Australia.
J GeorgeStorr Liver Centre, Westmead Institute for Medical Research, University of Sydney and Westmead Hospital, Westmead, NSW, 2145, Australia.ORCID http://orcid.org/0000-0002-8421-5476
G W McCaughanLiver Injury and Cancer Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, Sydney, NSW, Australia.
T TuLiver Injury and Cancer Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, Sydney, NSW, Australia. thomas.tu.phd@gmail.com.ORCID http://orcid.org/0000-0002-0482-4387
N A ShackelLiver Injury and Cancer Laboratory, Centenary Institute of Cancer Medicine and Cell Biology, Sydney, NSW, Australia. n.shackel@unsw.edu.au.
The University of Sydney · AUCentenary Institute · AUAustralian National University · AUHeidelberg University · DE

Funding

CHRONIC HEPATITIS C: MOLECULAR &CELLULAR MARKERSR01DK056402 · NIDDK · UNIVERSITY OF SYDNEY · PI FARRELL, GEOFFREY · 1999 to 2003
$528k
NIDDK NIH HHS R01 DK056402
6 · The paper itself

Abstract

Despite advances in antiviral therapy, molecular drivers of Hepatitis C Virus (HCV)-related liver disease remain poorly characterised. Chronic infection with HCV genotypes (1 and 3) differ in presentation of liver steatosis and virological response to therapies, both to interferon and direct acting antivirals. To understand what drives these clinically important differences, liver expression profiles of patients with HCV Genotype 1 or 3 infection (n = 26 and 33), alcoholic liver disease (n = 8), and no liver disease (n = 10) were analysed using transcriptome-wide microarrays. In progressive liver disease, HCV genotype was the major contributor to altered liver gene expression with 2151 genes differentially expressed >1.5-fold between HCV Genotype 1 and 3. In contrast, only 6 genes were altered between the HCV genotypes in advanced liver disease. Induction of lipogenic, lipolytic, and interferon stimulated gene pathways were enriched in Genotype 1 injury whilst a broad range of immune-associated pathways were associated with Genotype 3 injury. The results are consistent with greater lipid turnover in HCV Genotype 1 patients. Moreover, the lower activity in inflammatory pathways associated with HCV genotype 1 is consistent with relative resistance to interferon-based therapy. This data provides a molecular framework to explain the clinical manifestations of HCV-associated liver disease.

Indexed as

Lipid MetabolismAdolescentAdultFemaleGene Expression ProfilingGene Expression Regulation, ViralGenotypeHepacivirusHepatitis CHumansInflammationLiverLiver CirrhosisLiver Diseases, AlcoholicMaleMetabolic Networks and Pathways

Identifiers

PMID31332246
PMCPMC6646375
OpenAlexW2963907475

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.