Evidence map›Paper›PMID 27094861›Full record

ArticleInfection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases2016

Human norovirus hyper-mutation revealed by ultra-deep sequencing.

José M Cuevas, Marine Combe, Manoli Torres-Puente, Raquel Garijo, Susana Guix, Javier Buesa, Jesús Rodríguez-Díaz, Rafael Sanjuán

Open access · greenAbstract read
In one paragraph

Article in Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Novel and emerging mutations of SARS-CoV-2: Biomedical implications.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Transmission routes of rare seasonal diseases: the case of norovirus infections.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Mechanisms of viral mutation.Cellular and molecular life sciences : CMLS · 2016
    Review
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.

José M CuevasInstituto Cavanilles de Biodiversidad y Biología Evolutiva, Universitat de València, Valencia, Spain.
Marine CombeInstituto Cavanilles de Biodiversidad y Biología Evolutiva, Universitat de València, Valencia, Spain.
Manoli Torres-PuenteFundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana, Valencia, Spain.
Raquel GarijoInstituto Cavanilles de Biodiversidad y Biología Evolutiva, Universitat de València, Valencia, Spain.
Susana GuixDepartament de Microbiologia, Universitat de Barcelona, Barcelona, Spain.
Javier BuesaDepartament de Microbiologia, Universitat de València, Valencia, Spain.
Jesús Rodríguez-DíazDepartament de Microbiologia, Universitat de València, Valencia, Spain.
Rafael SanjuánInstituto Cavanilles de Biodiversidad y Biología Evolutiva, Universitat de València, Valencia, Spain; Departament de Genètica, Universitat de València, Valencia, Spain. Electronic address: rafael.sanjuan@uv.e.
Universitat de València · ESFundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana · ESUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human noroviruses (NoVs) are a major cause of gastroenteritis worldwide. It is thought that, similar to other RNA viruses, high mutation rates allow NoVs to evolve fast and to undergo rapid immune escape at the population level. However, the rate and spectrum of spontaneous mutations of human NoVs have not been quantified previously. Here, we analyzed the intra-patient diversity of the NoV capsid by carrying out RT-PCR and ultra-deep sequencing with 100,000-fold coverage of 16 stool samples from symptomatic patients. This revealed the presence of low-frequency sequences carrying large numbers of U-to-C or A-to-G base transitions, suggesting a role for hyper-mutation in NoV diversity. To more directly test for hyper-mutation, we performed transfection assays in which the production of mutations was restricted to a single cell infection cycle. This confirmed the presence of sequences with multiple U-to-C/A-to-G transitions, and suggested that hyper-mutation contributed a large fraction of the total NoV spontaneous mutation rate. The type of changes produced and their sequence context are compatible with ADAR-mediated editing of the viral RNA.

Indexed as

Mutation RateVirus ReplicationBase SequenceCaliciviridae InfectionsCloning, MolecularFecesGastroenteritisGene ExpressionHEK293 CellsHigh-Throughput Nucleotide SequencingHumansNorovirusRNA, ViralTransfectionViral ProteinsRNA, ViralViral ProteinsHyper-mutationNext-generation sequencingNorovirusRNA virus

Identifiers

PMID27094861
PMCPMC7172324
OpenAlexW2336161158

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.