Evidence map›Paper›PMID 25411182›Full record

ArticleJournal of clinical microbiology2015

Ultradeep pyrosequencing of NS3 to predict response to triple therapy with protease inhibitors in previously treated chronic hepatitis C patients.

Sylvie Larrat, Om Kulkarni, Jean-Baptiste Claude, Réjane Beugnot, Michaël G B Blum, Katia Fusillier, Julien Lupo, Pauline Tremeaux, Agnès Plages, Alice Marlu and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of clinical microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Trial
  2. 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

16 authors at 6 institutions in 1 country.

Sylvie LarratLaboratoire de Virologie, Département des Agents Infectieux, Pôle Biologie, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France Unit of Virus Host Cell Interactions UMI 3265 UJF-EMBL-CNRS, BP 181, Grenoble, France slarrat@chu-grenoble.fr.
Om KulkarniLaboratoire TIMC-IMAG/University of Grenoble Alpes/CNRS/UMR 5525, Grenoble, France.
Jean-Baptiste ClaudeGenostar-Bioinformatics Solutions, Montbonnot Saint Martin, France.
Réjane BeugnotLaboratoire de Virologie, Département des Agents Infectieux, Pôle Biologie, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France.
Michaël G B BlumLaboratoire TIMC-IMAG/University of Grenoble Alpes/CNRS/UMR 5525, Grenoble, France.
Katia FusillierLaboratoire de Virologie, Département des Agents Infectieux, Pôle Biologie, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France.
Julien LupoLaboratoire de Virologie, Département des Agents Infectieux, Pôle Biologie, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France Unit of Virus Host Cell Interactions UMI 3265 UJF-EMBL-CNRS, BP 181, Grenoble, France.
Pauline TremeauxLaboratoire de Virologie, Département des Agents Infectieux, Pôle Biologie, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France Unit of Virus Host Cell Interactions UMI 3265 UJF-EMBL-CNRS, BP 181, Grenoble, France.
Agnès PlagesClinique Universitaire d'Hépato-gastroentérologie, Pôle Digidune, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France.
Alice MarluClinique Universitaire d'Hépato-gastroentérologie, Pôle Digidune, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France.
Hervé DuborjalFloralis, Gieres, France.
Anne Signori-SchmuckLaboratoire de Virologie, Département des Agents Infectieux, Pôle Biologie, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France.
Olivier FrancoisLaboratoire TIMC-IMAG/University of Grenoble Alpes/CNRS/UMR 5525, Grenoble, France.
Jean-Pierre ZarskiClinique Universitaire d'Hépato-gastroentérologie, Pôle Digidune, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France Unité INSERM/University Grenoble Alpes U823, IAPC Institut Albert Bonniot, Grenoble, France.
Patrice MorandLaboratoire de Virologie, Département des Agents Infectieux, Pôle Biologie, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France Unit of Virus Host Cell Interactions UMI 3265 UJF-EMBL-CNRS, BP 181, Grenoble, France.
Vincent LeroyClinique Universitaire d'Hépato-gastroentérologie, Pôle Digidune, Centre Hospitalier Universitaire Grenoble, CS10217, Grenoble, France Unité INSERM/University Grenoble Alpes U823, IAPC Institut Albert Bonniot, Grenoble, France.
Centre Hospitalier Universitaire de Grenoble · FRTranslational Innovation in Medicine and Complexity · FRCentre National de la Recherche Scientifique · FRFloralis (France) · FRUnit of Virus Host Cell Interactions · FRUniversité Grenoble Alpes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the gain in sustained virological responses (SVR) provided by protease inhibitors (PIs), failures still occur. The aim of this study was to determine if a baseline analysis of the NS3 region using ultradeep pyrosequencing (UDPS) can help to predict an SVR. Serum samples from 40 patients with previously nonresponding genotype 1 chronic hepatitis C who were retreated with triple therapy, including a PI, were analyzed. Baseline UDPS of the NS3 gene was performed on plasma and peripheral blood mononuclear cells (PBMC). Mutations conferring resistance to PIs were sought. The overall diversity of the quasispecies was evaluated by calculating the Shannon entropy (SE). Resistance mutations were found in plasma and PBMC but were not discriminating enough to predict an SVR. NS3 quasispecies heterogeneity was significantly lower at baseline in patients achieving an SVR than in those not achieving an SVR (SE of 26.98 ± 16.64 × 10(-3) versus 44.93 ± 19.58 × 10(-3), P = 0.0047). With multivariate analysis, the independent predictors of an SVR were fibrosis of stage F ≤2 (odds ratio [OR], 13.3; 95% confidence interval [CI], 1.25 to 141.096; P < 0.03) and SE below the median (OR, 5.4; 95% CI, 1.22 to 23.87; P < 0.03). More than the presence of minor mutations at the baseline in plasma or in PBMC, the NS3 viral heterogeneity determined by UDPS is an independent factor for an SVR in previously treated patients receiving triple therapy that includes a PI.

Indexed as

Drug Resistance, ViralHigh-Throughput Nucleotide SequencingAdultAgedAged, 80 and overAntiviral AgentsDEAD-box RNA HelicasesDrug Therapy, CombinationFemaleGenetic VariationHepatitis C, ChronicHumansMaleMiddle AgedMutation, MissenseNucleoside-TriphosphataseAntiviral AgentsDEAD-box RNA HelicasesNS3 protein, hepatitis C virusNucleoside-TriphosphataseProtease InhibitorsSerine EndopeptidasesViral Nonstructural ProteinsViral Proteases

Identifiers

PMID25411182
PMCPMC4298514
OpenAlexW2149404629

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.