Evidence map›Paper›PMID 21680513›Full record

ArticleJournal of virology2011

Hepatitis C virus infection causes cell cycle arrest at the level of initiation of mitosis.

Rathi P Kannan, Lucinda L Hensley, Lauren E Evers, Stanley M Lemon, David R McGivern

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 91 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

5 authors at 2 institutions in 1 country.

Rathi P KannanDivision of Infectious Diseases, Department of Medicine, Center for Translational Research, Inflammatory Diseases Institute, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7295, USA. mcgivern@med.unc.edu
Lucinda L Hensley
Lauren E Evers
Stanley M Lemon
David R McGivern
The University of Texas Medical Branch at Galveston · USUniversity of North Carolina at Chapel Hill · US

Funding

Synthetic Organic Chemistry CoreP30ES006676 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ELFERINK, CORNELIS JOHAN · 1995 to 2017
$21.7M
Virus-Host Interactions in Hepatitis C Virus (HCV) InfectionsU19AI040035 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI LEMON, STANLEY M. · 1996 to 2009
$12.0M
NCI NIH HHS P50-CA127004NIAID NIH HHS U19 AI040035NIAID NIH HHS U19-AI40035NIEHS NIH HHS P30 ES006676NIEHS NIH HHS P30-ES006676
6 · The paper itself

Abstract

Chronic infection with the hepatitis C virus (HCV) is associated with increased risk for hepatocellular carcinoma (HCC). Chronic immune-mediated inflammation is likely to be an important factor in the development of HCV-associated HCC, but direct effects of HCV infection on the host cell cycle may also play a role. Although overexpression studies have revealed multiple interactions between HCV-encoded proteins and host cell cycle regulators and tumor suppressor proteins, the relevance of these observations to HCV-associated liver disease is not clear. We determined the net effect of these interactions on regulation of the cell cycle in the context of virus infection. Flow cytometry of HCV-infected carboxyfluorescein succinimidyl ester-labeled hepatoma cells indicated a slowdown in proliferation that correlated with abundance of viral antigen. A decrease in the proportions of infected cells in G(1) and S phases with an accumulation of cells in G(2)/M phase was observed, compared to mock-infected controls. Dramatic decreases in markers of mitosis, such as phospho-histone H3, in infected cells suggested a block to mitotic entry. In common with findings described in the published literature, we observed caspase 3 activation, suggesting that cell cycle arrest is associated with apoptosis. Differences were observed in patterns of cell cycle disturbance and levels of apoptosis with different strains of HCV. However, the data suggest that cell cycle arrest at the interface of G(2) and mitosis is a common feature of HCV infection.

Indexed as

ApoptosisCell CycleMitosisCaspase 3Cell Line, TumorCell ProliferationFlow CytometryFluoresceinsFluorescent Antibody TechniqueHepacivirusHepatocytesHistonesHumansSuccinimides5-(6)-carboxyfluorescein diacetate succinimidyl esterCaspase 3FluoresceinsHistonesSuccinimides

Identifiers

PMID21680513
PMCPMC3147967
OpenAlexW2000050023

What OpenQuestion holds

Textmetadata
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.