Evidence map›Paper›PMID 27503576›Full record

ArticleAntiviral chemistry & chemotherapy2015

Isolation and characterization of hepatitis C virus resistant to a novel phenanthridinone derivative.

Wataru Ito, Masaaki Toyama, Mika Okamoto, Masanori Ikeda, Koichi Watashi, Takaji Wakita, Yuichi Hashimoto, Masanori Baba

Open access · bronzeAbstract read
In one paragraph

Article in Antiviral chemistry & chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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 3 institutions in 1 country.

Wataru Ito1 Division of Antiviral Chemotherapy, Center for Chronic Viral Diseases, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Masaaki Toyama1 Division of Antiviral Chemotherapy, Center for Chronic Viral Diseases, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Mika Okamoto1 Division of Antiviral Chemotherapy, Center for Chronic Viral Diseases, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Masanori Ikeda2 Division of Persistent and Oncogenic Viruses, Center for Chronic Viral Diseases, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Koichi Watashi3 Department of Virology II, National Institute of Infectious Diseases, Tokyo, Japan.
Takaji Wakita3 Department of Virology II, National Institute of Infectious Diseases, Tokyo, Japan.
Yuichi Hashimoto4 Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Masanori Baba1 Division of Antiviral Chemotherapy, Center for Chronic Viral Diseases, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Kagoshima University · JPNational Institute of Infectious Diseases · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe novel phenanthridinone derivative HA-719 has recently been identified as a highly potent and selective inhibitor of hepatitis C virus replication. To elucidate its mechanism of inhibition, we have isolated and analyzed a clone of hepatitis C virus replicon cells resistant to HA-719.

methodsTo isolate HA-719-resistant replicon cells, Huh-7 cells containing subgenomic hepatitis C virus replicons (genotype 1b) with a luciferase reporter (LucNeo#2) were cultured in the presence of G418 and escalating concentrations of HA-719. After several passages, total RNA was extracted from the growing cells, and Huh-7 cells were transfected with the extracted RNA. Limiting dilution of the transfected cells was performed to obtain an HA-719-resistant clone.

resultsThe 50% effective concentration (EC

conclusionNone of the amino acid mutations in the resistant clone corresponds to those reported to confer drug-resistance to current anti-hepatitis C virus agents, suggesting that the target of HA-719 for hepatitis C virus inhibition differs from those of the existing agents.

Indexed as

Antiviral AgentsCell Line, TumorDose-Response Relationship, DrugDrug Resistance, ViralHepacivirusHumansMicrobial Sensitivity TestsMolecular StructurePhenanthrenesStructure-Activity RelationshipVirus ReplicationAntiviral AgentsPhenanthrenesphenanthridoneDrug resistancehepatitis C virusinhibitors

Identifiers

PMID27503576
PMCPMC5890506
OpenAlexW2521817174

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.