Evidence map›Paper›PMID 36718430›Full record

ArticleJHEP reports : innovation in hepatology2023

Hepatitis C virus replication requires integrity of mitochondria-associated ER membranes.

Sarah Duponchel, Lea Monnier, Jennifer Molle, Nadia Bendridi, Muhammad Rizwan Alam, Ahmed Gaballah, Boyan Grigorov, Alexander Ivanov, Marcel Schmiel, Margarete Odenthal and 4 more

Open access · goldAbstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  5. Article
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  8. Article
  9. Article
  10. Article
  11. Review
  12. HCV-induced autophagy and innate immunity.Frontiers in immunology · 2024
    Review
  13. Endoplasmic reticulum stress and mitochondrial dysfunction during aging: Role of sphingolipids.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023
    Article
  14. Host mitochondria: more than an organelle in SARS-CoV-2 infection.Frontiers in cellular and infection microbiology · 2023
    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

14 authors at 3 institutions in 4 countries.

Sarah DuponchelUniv Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Centre de Recherche en Cancérologie de Lyon, Lyon, 69434, France.
Lea MonnierUniv Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Centre de Recherche en Cancérologie de Lyon, Lyon, 69434, France.
Jennifer MolleUniv Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Centre de Recherche en Cancérologie de Lyon, Lyon, 69434, France.
Nadia BendridiLaboratoire CarMeN, INSERM U-1060, INRA U-1397, Université Lyon, Université Claude Bernard Lyon 1, Pierre Bénite, 69495, France.
Muhammad Rizwan AlamCarMeN Laboratory, Hôpital Louis Pradel, Hospices Civils de Lyon, Université de Lyon and Explorations Fonctionnelles Cardiovasculaires, INSERM U1060, Lyon, France.
Ahmed GaballahUniv Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Centre de Recherche en Cancérologie de Lyon, Lyon, 69434, France.
Boyan GrigorovUniv Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Centre de Recherche en Cancérologie de Lyon, Lyon, 69434, France.
Alexander IvanovEngelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.
Marcel SchmielInstitute of Pathology, University Hospital of Cologne and Center for Molecular Medicine (CMMC), University of Cologne, Germany.
Margarete OdenthalInstitute of Pathology, University Hospital of Cologne and Center for Molecular Medicine (CMMC), University of Cologne, Germany.
Michel OvizeCarMeN Laboratory, Hôpital Louis Pradel, Hospices Civils de Lyon, Université de Lyon and Explorations Fonctionnelles Cardiovasculaires, INSERM U1060, Lyon, France.
Jennifer RieussetLaboratoire CarMeN, INSERM U-1060, INRA U-1397, Université Lyon, Université Claude Bernard Lyon 1, Pierre Bénite, 69495, France.
Fabien ZoulimUniv Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Centre de Recherche en Cancérologie de Lyon, Lyon, 69434, France.
Birke BartoschUniv Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Centre de Recherche en Cancérologie de Lyon, Lyon, 69434, France.
Université Claude Bernard Lyon 1 · FRUniversity of Cologne · DEEngelhardt Institute of Molecular Biology · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: Chronic HCV infection causes cellular stress, fibrosis and predisposes to hepatocarcinogenesis. Mitochondria play key roles in orchestrating stress responses by regulating bioenergetics, inflammation and apoptosis. To better understand the role of mitochondria in the viral life cycle and disease progression of chronic hepatitis C, we studied morphological and functional mitochondrial alterations induced by HCV using productively infected hepatoma cells and patient livers. Methods: Biochemical and imaging assays were used to assess localization of cellular and viral proteins and mitochondrial functions in cell cultures and liver biopsies. Cyclophilin D (CypD) knockout was performed using CRISPR/Cas9 technology. Viral replication was quantified by quantitative reverse-transcription PCR and western blotting. Results: Several HCV proteins were found to associate with mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs), the points of contact between the ER and mitochondria. Downregulation of CypD, which is known to disrupt MAM integrity, reduced viral replication, suggesting that MAMs play an important role in the viral life cycle. This process was rescued by ectopic CypD expression. Furthermore, HCV proteins were found to associate with voltage dependent anion channel 1 (VDAC1) at MAMs and to reduce VDAC1 protein levels at MAMs Conclusions: HCV proteins associate specifically with MAMs and MAMs play an important role in viral replication. The association between viral proteins and MAMs did not impact Ca Impact and implications: Hepatitis C virus infects the liver, where it causes inflammation, cell damage and increases the long-term risk of liver cancer. We show that several HCV proteins interact with mitochondria in liver cells and alter the composition of mitochondrial subdomains. Importantly, HCV requires the architecture of these mitochondrial subdomains to remain intact for efficient viral replication.

Indexed as

CypD, cyclophilin DDMVs, double membrane vesiclesdpi, days post infectionEM, electron microscopyER, endoplasmic reticulumfibrosisGrp75, glucose-regulated protein 75HCC, hepatocellular carcinomaHCVcc, cell culture-derived HCVhepatitis C virusIP3R1, inositol trisphosphate receptor 1IP, immunoprecipitationKO, knockoutMAMs, mitochondria-associated ER membranesmitochondria-associated ER membranesMOI, multiplicity of infectionOMM, outer mitochondrial membranePLA, proximity ligation assayS1R, sigma 1 receptorVDAC, voltage-dependent anion channelvoltage-dependent anion channel 1

Identifiers

PMID36718430
PMCPMC9883273
OpenAlexW4311145936

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.