Evidence map›Paper›PMID 28275194›Full record

ArticleJournal of virology2017

Internal Disequilibria and Phenotypic Diversification during Replication of Hepatitis C Virus in a Noncoevolving Cellular Environment.

Elena Moreno, Isabel Gallego, Josep Gregori, Adriana Lucía-Sanz, María Eugenia Soria, Victoria Castro, Nathan M Beach, Susanna Manrubia, Josep Quer, Juan Ignacio Esteban and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  5. Review
  6. Quasispecies productivity.Die Naturwissenschaften · 2024
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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

15 authors at 10 institutions in 2 countries.

Elena MorenoCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.
Isabel GallegoCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.
Josep GregoriLiver Unit, Internal Medicine Hospital Universitari Vall d'Hebron, Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain.
Adriana Lucía-SanzCentro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.
María Eugenia SoriaLiver Unit, Internal Medicine Hospital Universitari Vall d'Hebron, Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain.
Victoria CastroCentro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.
Nathan M BeachCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.
Susanna ManrubiaCentro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.
Josep QuerCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd) del Instituto de Salud Carlos III, Madrid, Spain.
Juan Ignacio EstebanCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd) del Instituto de Salud Carlos III, Madrid, Spain.
Charles M RiceCenter for the Study of Hepatitis C, Laboratory of Virology and Infectious Disease, Rockefeller University, New York, New York, USA.
Jordi GómezCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd) del Instituto de Salud Carlos III, Madrid, Spain.
Pablo GastaminzaCentro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain.
Esteban DomingoCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain edomingo@cbm.csic.es cperales@cbm.csic.es.
Celia PeralesCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), Consejo Superior de Investigaciones Científicas (CSIC), Campus de Cantoblanco, Madrid, Spain edomingo@cbm.csic.es cperales@cbm.csic.es.
Centro Nacional de Biotecnología · ESUniversidad Autónoma de Madrid · ESConsejo Superior de Investigaciones Científicas · ESCentro de Biología Molecular Severo Ochoa · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESInstituto de Parasitología y Biomedicina "López - Neyra" · ESInstituto de Salud Carlos III · ESRoche (Spain) · ESRockefeller University · USVall d'Hebron Institut de Recerca · ES

Funding

Structure and function of the HCV RNA replicaseR01CA057973 · NCI · WASHINGTON UNIVERSITY · PI RICE, CHARLES M · 1992 to 2013
$4.7M
Hepatitis C antivirals: Mechanism of action, combination efficacy and resistanceR01AI099284 · NIAID · ROCKEFELLER UNIVERSITY · PI RICE, CHARLES M · 2012 to 2016
$3.6M
NCI NIH HHS R01 CA057973NIAID NIH HHS R01 AI099284
6 · The paper itself

Abstract

Viral quasispecies evolution upon long-term virus replication in a noncoevolving cellular environment raises relevant general issues, such as the attainment of population equilibrium, compliance with the molecular-clock hypothesis, or stability of the phenotypic profile. Here, we evaluate the adaptation, mutant spectrum dynamics, and phenotypic diversification of hepatitis C virus (HCV) in the course of 200 passages in human hepatoma cells in an experimental design that precluded coevolution of the cells with the virus. Adaptation to the cells was evidenced by increase in progeny production. The rate of accumulation of mutations in the genomic consensus sequence deviated slightly from linearity, and mutant spectrum analyses revealed a complex dynamic of mutational waves, which was sustained beyond passage 100. The virus underwent several phenotypic changes, some of which impacted the virus-host relationship, such as enhanced cell killing, a shift toward higher virion density, and increased shutoff of host cell protein synthesis. Fluctuations in progeny production and failure to reach population equilibrium at the genomic level suggest internal instabilities that anticipate an unpredictable HCV evolution in the complex liver environment.

Indexed as

Evolution, MolecularVirus ReplicationAdaptation, BiologicalCarcinoma, HepatocellularDNA ReplicationGenome, ViralHepacivirusHost-Pathogen InteractionsHumansLiverMutationPhenotypeRNA, ViralRNA, Viralmutant spectrumpopulation instabilityquasispeciesRNA virus

Identifiers

PMID28275194
PMCPMC5411618
OpenAlexW2594425558

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.