Evidence map›Paper›PMID 15699349›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Hepatitis C virus RNA replication is regulated by host geranylgeranylation and fatty acids.

Sharookh B Kapadia, Francis V Chisari

2 registry-linked trialsOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 245 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
245citing papers in PubMed, 1 pooled it
14.3field-weighted citation impact, top 1% 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.

NCT00371579 nawithdrawnnot on this mapstarted 2006, after this paper: background citation

Treatment With Rosuvastatin in Patients With Hepatitis C

TypeinterventionalSponsorUMC UtrechtRan2006 to 2007Enrolled0ConditionsHepatitis CArmsrosuvastatin
NCT00403533 phase2completednot on this mapstarted 2006, after this paper: background citation

Assessment of the Antiviral Effect of Atorvastatin on Hepatitis C Virus

TypeinterventionalSponsorMassachusetts General HospitalRan2006 to 2006Enrolled10ConditionsHepatitis CArms20 mg of atorvastatin daily
3 · Its place in the literature

Who cites it

245 citing papers in PubMed, 1 synthesis or guideline pooled it, 499 citations in OpenAlex.

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185 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Sharookh B KapadiaDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
Francis V Chisari
Scripps Research Institute · US

Funding

HEPATITIS C VIRUS IMMUNOBIOLOGY AND PATHOGENESISR01CA076403 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI CHISARI, FRANCIS VINCENT · 1998 to 2007
$4.0M
NCI NIH HHS CA76403NCI NIH HHS CA A1053988NCI NIH HHS R01 CA076403
6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Our laboratory has previously demonstrated that high-level HCV replication during acute infection of chimpanzees is associated with the modulation of multiple genes involved in lipid metabolism, and that drugs that regulate cholesterol and fatty acid biosynthesis regulate the replication of the subgenomic HCV replicon in Huh-7 cells. In this article, we demonstrate that Huh-7 cells harboring replicating, full-length HCV RNAs express elevated levels of ATP citrate lyase and acetyl-CoA synthetase genes, both of which are involved in cholesterol and fatty acid biosynthesis. Further, we confirm that the cholesterol-biosynthetic pathway controls HCV RNA replication by regulating the cellular levels of geranylgeranyl pyrophosphate, we demonstrate that the impact of geranylgeranylation depends on the fatty acid content of the cell, and we show that fatty acids can either stimulate or inhibit HCV replication, depending on their degree of saturation. These results illustrate a complex cellular-regulatory network that controls HCV RNA replication, presumably by modulating the trafficking and association of cellular and/or viral proteins with cellular membranes, suggesting that pharmacologic manipulation of these pathways may have a therapeutic effect in chronic HCV infection.

Indexed as

Acetate-CoA LigaseATP Citrate (pro-S)-LyaseBase SequenceCCAAT-Enhancer-Binding ProteinsCell LineDNA-Binding ProteinsDNA ProbesFatty AcidsFatty Acids, UnsaturatedGene ExpressionHepacivirusHumansLiver X ReceptorsOrphan Nuclear ReceptorsProtein PrenylationReceptors, Cytoplasmic and NuclearAcetate-CoA LigaseATP Citrate (pro-S)-LyaseCCAAT-Enhancer-Binding ProteinsDNA-Binding ProteinsDNA ProbesFatty AcidsFatty Acids, UnsaturatedLiver X ReceptorsOrphan Nuclear ReceptorsReceptors, Cytoplasmic and NuclearRNA, ViralSREBF1 protein, humanSterol Regulatory Element Binding Protein 1Transcription FactorsViral Proteins

Identifiers

PMID15699349
PMCPMC549027
OpenAlexW2101177020

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.