Evidence map›Paper›PMID 20855726›Full record

ArticleAntimicrobial agents and chemotherapy2010

Susceptibility of treatment-naive hepatitis C virus (HCV) clinical isolates to HCV protease inhibitors.

Andrew Bae, Siu-Chi Sun, Xiaoping Qi, Xiaowu Chen, Karin Ku, Angela Worth, Kelly A Wong, Jeanette Harris, Michael D Miller, Hongmei Mo

Abstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Guideline
  2. Infrequent development of resistance in genotype 1-6 hepatitis C virus-infected subjects treated with sofosbuvir in phase 2 and 3 clinical trials.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2014
    Trial
  3. Trial
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  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
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  15. Article
  16. Review
  17. Hepatitis C (chronic).BMJ clinical evidence · 2015
    Review
  18. Article
  19. Prevalence of HCV NS3 pre-treatment resistance associated amino acid variants within a Scottish cohort.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2015
    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

10 authors at 1 institution in 1 country.

Andrew BaeDepartment of Clinical Virology, Gilead Sciences, 333 Lakeside Dr., Foster City, CA 94404, USA.
Siu-Chi Sun
Xiaoping Qi
Xiaowu Chen
Karin Ku
Angela Worth
Kelly A Wong
Jeanette Harris
Michael D Miller
Hongmei Mo
Gilead Sciences (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In order to assess the natural variation in susceptibility to hepatitis C virus (HCV) NS3 protease inhibitors (PIs) among untreated HCV patient samples, the susceptibilities of 39 baseline clinical isolates were determined using a transient-replication assay on a panel of HCV PIs, including two α-ketoamides (VX-950 and SCH-503034) and three macrocyclic inhibitors (MK-7009, ITMN-191, and TMC-435350). Some natural variation in susceptibility to all HCV PIs tested was observed among the baseline clinical isolates. The susceptibility to VX-950 correlated strongly with the susceptibility to SCH-503034. A moderate correlation was observed between the susceptibilities to ITMN-191 and MK-7009. In contrast, the phenotypic correlations between the α-ketoamides and macrocyclic inhibitors were significantly lower. This difference is partly attributable to reduced susceptibility of the HCV variants containing the NS3 polymorphism Q80K (existing in 47% of genotype 1a isolates) to the macrocyclic compounds but no change in the sensitivity of the same variants to the α-ketoamides tested. Our results suggest that the natural variation in baseline susceptibility may contribute to different degrees of antiviral response among patients in vivo, particularly at lower doses.

Indexed as

Antiviral AgentsCell Line, TumorCyclopropanesHepacivirusHeterocyclic Compounds, 3-RingHumansIndolesIsoindolesLactamsLactams, MacrocyclicLeucineMolecular StructureOligopeptidesProlineProtease InhibitorsSimeprevirAntiviral AgentsCyclopropanesdanoprevirHeterocyclic Compounds, 3-RingIndolesIsoindolesLactamsLactams, MacrocyclicLeucineN-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamideOligopeptidesProlineProtease InhibitorsSimeprevirSulfonamidestelaprevirvaniprevir

Identifiers

PMID20855726
PMCPMC2981235
OpenAlexW1983818291

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.