Evidence map›Paper›PMID 20485673›Full record

Trial reportPloS one2010

Rhinovirus genome evolution during experimental human infection.

Samuel Cordey, Thomas Junier, Daniel Gerlach, Francesca Gobbini, Laurent Farinelli, Evgeny M Zdobnov, Birgit Winther, Caroline Tapparel, Laurent Kaiser

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The usual suspects: Respiratory syncytial virus and rhinovirus drive asthma development and exacerbation.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2025
    Review
  6. Article
  7. Article
  8. Observational
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Malaria medicines: a glass half full?Nature reviews. Drug discovery · 2015
    Review
  15. Article
  16. Article
  17. Article
  18. Effects of rhinovirus species on viral replication and cytokine production.The Journal of allergy and clinical immunology · 2014
    Article
  19. Emerging and resistant infections.Annals of the American Thoracic Society · 2014
    Review
  20. Co-circulation of multiple genotypes of human rhinovirus during a large outbreak of respiratory illness in a veterans' long-term care home.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2013
    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

9 authors at 3 institutions in 2 countries.

Samuel CordeyLaboratory of Virology, Division of Infectious Diseases and Division of Laboratory Medicine, University of Geneva Hospitals, Geneva, Switzerland. samuel.cordey@hcuge.ch
Thomas Junier
Daniel Gerlach
Francesca Gobbini
Laurent Farinelli
Evgeny M Zdobnov
Birgit Winther
Caroline Tapparel
Laurent Kaiser
University of Geneva · CHUniversity Hospital of Geneva · CHUniversity of Virginia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human rhinoviruses (HRVs) evolve rapidly due in part to their error-prone RNA polymerase. Knowledge of the diversity of HRV populations emerging during the course of a natural infection is essential and represents a basis for the design of future potential vaccines and antiviral drugs. To evaluate HRV evolution in humans, nasal wash samples were collected daily for five days from 15 immunocompetent volunteers experimentally infected with a reference stock of HRV-39. In parallel, HeLa-OH cells were inoculated to compare HRV evolution in vitro. Nasal wash in vivo assessed by real-time PCR showed a viral load that peaked at 48-72 h. Ultra-deep sequencing was used to compare the low-frequency mutation populations present in the HRV-39 inoculum in two human subjects and one HeLa-OH supernatant collected 5 days post-infection. The analysis revealed hypervariable mutation locations in VP2, VP3, VP1, 2C and 3C genes and conserved regions in VP4, 2A, 2B, 3A, 3B and 3D genes. These results were confirmed by classical sequencing of additional samples, both from inoculated volunteers and independent cell infections, and suggest that HRV inter-host transmission is not associated with a strong bottleneck effect. A specific analysis of the VP1 capsid gene of 15 human cases confirmed the high mutation incidence in this capsid region, but not in the antiviral drug-binding pocket. We could also estimate a mutation frequency in vivo of 3.4x10(-4) mutations/nucleotides and 3.1x10(-4) over the entire ORF and VP1 gene, respectively. In vivo, HRV generate new variants rapidly during the course of an acute infection due to mutations that accumulate in hot spot regions located at the capsid level, as well as in 2C and 3C genes.

Indexed as

Evolution, MolecularAdolescentAdultAgedAmino Acid SequenceConsensus SequenceDNA Mutational AnalysisGenetic LociGenome, ViralHeLa CellsHumansKineticsMiddle AgedMolecular Sequence DataMutationOpen Reading Framesviral protein 1, rhinovirusViral Proteins

Identifiers

PMID20485673
PMCPMC2868056
OpenAlexW1963520707

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.