Evidence map›Paper›PMID 23637397›Full record

ArticleJournal of virology2013

Response of hepatitis C virus to long-term passage in the presence of alpha interferon: multiple mutations and a common phenotype.

Celia Perales, Nathan M Beach, Isabel Gallego, Maria Eugenia Soria, Josep Quer, Juan Ignacio Esteban, Charles Rice, Esteban Domingo, Julie Sheldon

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
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  7. Article
  8. Immunomodulatory Role of Interferons in Viral and Bacterial Infections.International journal of molecular sciences · 2023
    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

9 authors at 6 institutions in 2 countries.

Celia PeralesCentro de Biología Molecular Severo Ochoa (CSIC-UAM), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.
Nathan M Beach
Isabel Gallego
Maria Eugenia Soria
Josep Quer
Juan Ignacio Esteban
Charles Rice
Esteban Domingo
Julie Sheldon
Consejo Superior de Investigaciones Científicas · ESUniversidad Autónoma de Madrid · ESUniversitat Autònoma de Barcelona · ESCentro de Biología Molecular Severo Ochoa · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESRockefeller University · US

Funding

Identification and characterization of cellular factors involved in HCV entryR01AI072613 · NIAID · ROCKEFELLER UNIVERSITY · PI RICE, CHARLES M · 2007 to 2016
$4.7M
NIAID NIH HHS AI072613NIAID NIH HHS R01 AI072613
6 · The paper itself

Abstract

Cell culture-produced hepatitis C virus (HCV) has been subjected to up to 100 serial passages in human hepatoma cells in the absence or presence of different doses of alpha interferon (IFN-α). Virus survival, genetic changes, fitness levels, and phenotypic traits have been examined. While high initial IFN-α doses (increasing from 1 to 4 IU/ml) did not allow HCV survival beyond passage 40, a gradual exposure (from 0.25 to 10 IU/ml) allowed the virus to survive for at least 100 passages. The virus passaged in the presence of IFN-α acquired IFN-α resistance as evidenced by enhanced progeny production and viral protein expression in an IFN-α environment. A partial IFN-α resistance was also noted in populations passaged in the absence of IFN-α. All lineages acquired adaptative mutations, and multiple, nonsynonymous mutations scattered throughout the genome were present in IFN-α-selected populations. Comparison of consensus sequences indicates a dominance of synonymous versus nonsynonymous substitutions. IFN-α-resistant populations displayed decreased sensitivity to a combination of IFN-α and ribavirin. A phenotypic trait common to all assayed viral populations is the ability to increase shutoff host cell protein synthesis, accentuated in infections with IFN-α-selected populations carried out in the presence of IFN-α. The trait was associated with enhanced phosphorylation of protein kinase R (PKR) and eIF2α, although other contributing factors are likely. The results suggest that multiple, independent mutational pathways can confer IFN-α resistance to HCV and might explain why no unified picture has been obtained regarding IFN-α resistance in vivo.

Indexed as

PhenotypeAdaptation, BiologicalBase SequenceBlotting, WesternCell Line, TumorDNA PrimersDose-Response Relationship, DrugDrug ResistanceHepacivirusHumansInterferon-alphaMolecular Sequence DataMutationReal-Time Polymerase Chain ReactionSequence Analysis, DNASerial PassageDNA PrimersInterferon-alpha

Identifiers

PMID23637397
PMCPMC3700284
OpenAlexW2035914469

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.