Evidence map›Paper›PMID 26122475›Full record

ReviewNature reviews. Gastroenterology & hepatology2015

Modelling hepatitis C therapy--predicting effects of treatment.

Alan S Perelson, Jeremie Guedj

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 78 citations in OpenAlex.

  1. Trial
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  7. Moderate Sustained Virologic Response Rates With 6-Week Combination Directly Acting Anti-Hepatitis C Virus Therapy in Patients With Advanced Liver Disease.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2016
    Trial
  8. Article
  9. Bemnifosbuvir: An HCV NS5B Inhibitor With Multiple Modes of Action.Clinical pharmacology and therapeutics · 2026
    Article
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  11. Review
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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 2 institutions in 2 countries.

Alan S PerelsonTheoretical Biology and Biophysics, MS-K710, Los Alamos National Laboratory, Los Alamos, NM 87545, USA.
Jeremie GuedjINSERM, IAME, UMR 1137, 16 Rue Henri Huchard, F-75018 Paris, France.
Inserm · FRLos Alamos National Laboratory · US

Funding

Collaborative Integration of HCV Molecular Virology and Mathematical ModelingR01AI078881 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PERELSON, ALAN S, UPRICHARD, SUSAN L. · 2011 to 2025
$7.5M
Modeling Viral and T Lymphocyte DynamicsR01OD011095 · OD · TRIAD NATIONAL SECURITY, LLC · PI PERELSON, ALAN S · 2012 to 2024
$5.0M
Immune System Modeling/HIVR01AI028433 · NIAID · UNIVERSITY OF CALIF-LOS ALAMOS NAT LAB · PI PERELSON, ALAN S · 1990 to 2021
$3.7M
Viral kinetic models of HCV clearance in hemophiliacs treated with telaprevirR34HL109334 · NHLBI · UNIVERSITY OF CINCINNATI · PI SHERMAN, KENNETH E · 2012 to 2013
$713k
NHLBI NIH HHS R01-HL109334NHLBI NIH HHS R34 HL109334NIAID NIH HHS R01 AI028433NIAID NIH HHS R01-AI028433NIAID NIH HHS R01 AI078881NIAID NIH HHS R01-AI078881NIH HHS R01 OD011095NIH HHS R01-OD011095
6 · The paper itself

Abstract

Mathematically modelling changes in HCV RNA levels measured in patients who receive antiviral therapy has yielded many insights into the pathogenesis and effects of treatment on the virus. By determining how rapidly HCV is cleared when viral replication is interrupted by a therapy, one can deduce how rapidly the virus is produced in patients before treatment. This knowledge, coupled with estimates of the HCV mutation rate, enables one to estimate the frequency with which drug resistant variants arise. Modelling HCV also permits the deduction of the effectiveness of an antiviral agent at blocking HCV replication from the magnitude of the initial viral decline. One can also estimate the lifespan of an HCV-infected cell from the slope of the subsequent viral decline and determine the duration of therapy needed to cure infection. The original understanding of HCV RNA decline under interferon-based therapies obtained by modelling needed to be revised in order to interpret the HCV RNA decline kinetics seen when using direct-acting antiviral agents (DAAs). There also exist unresolved issues involving understanding therapies with combinations of DAAs, such as the presence of detectable HCV RNA at the end of therapy in patients who nonetheless have a sustained virologic response.

Indexed as

Antiviral AgentsBiomarkersDrug Resistance, ViralDrug Therapy, CombinationHepatitis C, ChronicHumansInterferon-alphaLiver RegenerationModels, BiologicalRNA, ViralTime FactorsTreatment OutcomeViral LoadVirionAntiviral AgentsBiomarkersInterferon-alphaRNA, Viral

Identifiers

PMID26122475
PMCPMC4692721
OpenAlexW1505788137

What OpenQuestion holds

Textmetadata
LicenceTDM
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.