Evidence map›Paper›PMID 30698808›Full record

ArticleNucleic acids research2019

Dysregulation of the cohesin subunit RAD21 by Hepatitis C virus mediates host-virus interactions.

Shira Perez, Michael Gevor, Ateret Davidovich, Antony Kaspi, Katreena Yamin, Tom Domovich, Tomer Meirson, Avi Matityahu, Yehuda Brody, Salomon M Stemmer and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

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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

14 authors at 5 institutions in 4 countries.

Shira PerezMolecular Virology Lab, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Michael GevorMolecular Virology Lab, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Ateret DavidovichMolecular Virology Lab, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Antony KaspiEpigenetics in Human Health and Disease Laboratory, Department of Diabetes, Central Clinical School, Monash University, Melbourne, Australia.
Katreena YaminChromosome Instability and Dynamics Lab, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Tom DomovichMolecular Virology Lab, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Tomer MeirsonCell Migration and Invasion Laboratory, Azrieli Faculty of Medicine in the Galilee, Bar-Ilan University, Safed, Israel.
Avi MatityahuChromosome Instability and Dynamics Lab, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Yehuda BrodyThe Broad institute of Harvard and MIT, Cambridge, MA, USA.
Salomon M StemmerDavidoff Center, Rabin Medical Center, Beilinson Campus, Petach Tikva, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Assam El-OstaEpigenetics in Human Health and Disease Laboratory, Department of Diabetes, Central Clinical School, Monash University, Melbourne, Australia.
Izhak HavivCancer Personalized Medicine and Diagnostic Genomics Lab, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Itay OnnChromosome Instability and Dynamics Lab, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Meital Gal-TanamyMolecular Virology Lab, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Bar-Ilan University · ILBroad Institute · USChinese University of Hong Kong · CNMonash University · AUTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection is the leading cause of chronic hepatitis, which often results in liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC). HCV possesses an RNA genome and its replication is confined to the cytoplasm. Yet, infection with HCV leads to global changes in gene expression, and chromosomal instability (CIN) in the host cell. The mechanisms by which the cytoplasmic virus affects these nuclear processes are elusive. Here, we show that HCV modulates the function of the Structural Maintenance of Chromosome (SMC) protein complex, cohesin, which tethers remote regions of chromatin. We demonstrate that infection of hepatoma cells with HCV leads to up regulation of the expression of the RAD21 cohesin subunit and changes cohesin residency on the chromatin. These changes regulate the expression of genes associated with virus-induced pathways. Furthermore, siRNA downregulation of viral-induced RAD21 reduces HCV infection. During mitosis, HCV infection induces hypercondensation of chromosomes and the appearance of multi-centrosomes. We provide evidence that the underlying mechanism involves the viral NS3/4 protease and the cohesin regulator, WAPL. Altogether, our results provide the first evidence that HCV induces changes in gene expression and chromosome structure of infected cells by modulating cohesin.

Indexed as

Carrier ProteinsCell Cycle ProteinsCell Line, TumorCell NucleusChromatinChromosomal InstabilityChromosomal Proteins, Non-HistoneCohesinsCytoplasmDNA-Binding ProteinsHepacivirusHepatitis CHepatocytesHost-Pathogen InteractionsHumansMitosisCarrier ProteinsCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinsNS3-4A serine protease, Hepatitis C virusNuclear ProteinsPhosphoproteinsProto-Oncogene ProteinsRAD21 protein, humanSerine ProteasesViral Nonstructural ProteinsWAPL protein, human

Identifiers

PMID30698808
PMCPMC6412124
OpenAlexW2913507422

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.