Evidence map›Paper›PMID 17455911›Full record

ArticleBiochemistry2007

Biochemical mechanism of hepatitis C virus inhibition by the broad-spectrum antiviral arbidol.

Eve-Isabelle Pécheur, Dimitri Lavillette, Fanny Alcaras, Jennifer Molle, Yury S Boriskin, Michael Roberts, François-Loïc Cosset, Stephen J Polyak

Open access · greenAbstract read
In one paragraph

Article in Biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.6field-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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Umifenovir Epigenetically Targets theMicrobiology spectrum · 2023
    Article
  7. Article
  8. Disease-drug and drug-drug interaction in COVID-19: Risk and assessment.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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

8 authors at 1 institution in 1 country.

Eve-Isabelle PécheurIFR128 Biosciences Lyon Gerland, Institut de Biologie et Chimie des Protéines, UMR 5086 CNRS-Université Claude Bernard Lyon I, 7 passage du Vercors, 69367 Lyon Cedex 07, France. e.pecheur@ ibcp.fr
Dimitri Lavillette
Fanny Alcaras
Jennifer Molle
Yury S Boriskin
Michael Roberts
François-Loïc Cosset
Stephen J Polyak
Université Claude Bernard Lyon 1 · FR

Funding

Suppression of HCV-specific CD4+ T Cells by Core ProteinU19AI066328 · NIAID · UNIVERSITY OF COLORADO DENVER · PI ROSEN, HUGO RAMON · 2005 to 2014
$6.8M
Hepatitis C Virus Induced IL-8 &Inhibition of InterferonR01DK062187 · NIDDK · UNIVERSITY OF WASHINGTON · PI POLYAK, STEPHEN J. · 2003 to 2007
$1.4M
NIAID NIH HHS U19 AI066328NIDDK NIH HHS R01 DK062187NIDDK NIH HHS R01 DK62187PHS HHS U19 A1066328
6 · The paper itself

Abstract

Hepatitis C affects approximately 3% of the world population, yet its current treatment options are limited to interferon-ribavirin drug regimens which achieve a 50-70% cure rate depending on the hepatitis C virus (HCV) genotype. Besides extensive screening for HCV-specific compounds, some well-established medicinal drugs have recently demonstrated an anti-HCV effect in HCV replicon cells. One of these drugs is arbidol (ARB), a Russian-made broad-spectrum antiviral agent, which we have previously shown to inhibit acute and chronic HCV infection. Here we show that ARB inhibits the cell entry of HCV pseudoparticles of genotypes 1a, 1b, and 2a in a dose-dependent fashion. ARB also displayed a dose-dependent inhibition of HCV membrane fusion, as assayed by using HCV pseudoparticles (HCVpp) and fluorescent liposomes. ARB inhibition of HCVpp fusion was found to be more effective on genotype 1a than on genotypes 1b and 2a. In vitro biochemical studies revealed association of ARB with membranelike environments such as detergents and with lipid membranes. This association was particularly prominent at acidic pH which is optimal for HCV-mediated fusion. Our results suggest that the affinity of ARB for lipid membranes could account for its anti-HCV actions, together with a differential level of interaction with key motifs in HCV glycoproteins of different genotypes.

Indexed as

Antiviral AgentsCell Line, TumorDetergentsHepacivirusHumansIndolesLiposomesMembrane FusionMembrane LipidsMicellesSulfidesVirionAntiviral AgentsDetergentsIndolesLiposomesMembrane LipidsMicellesSulfidesumifenovir

Identifiers

PMID17455911
PMCPMC2532706
OpenAlexW2067214744

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.