Evidence map›Paper›PMID 27824949›Full record

ArticlePLoS pathogens2016

Genome-Wide Estimation of the Spontaneous Mutation Rate of Human Adenovirus 5 by High-Fidelity Deep Sequencing.

Jennifer Risso-Ballester, José M Cuevas, Rafael Sanjuán

Abstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
  2. Viral gene replication enhances AAV vector quality and reduces manufacturing costs.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Detection of mutations: from Ames test to duplex sequencing.Frontiers in molecular biosciences · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Genetic diversity of adenovirus in neotropical bats from Brazil.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Virus evolution · 2020
    Article
  19. Article
  20. 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

3 authors.

Jennifer Risso-BallesterInstitute for Integrative Systems Biology (I2SysBio), Universitat de València and Consejo Superior de Investigaciones Científicas, València, Spain.
José M CuevasInstitute for Integrative Systems Biology (I2SysBio), Universitat de València and Consejo Superior de Investigaciones Científicas, València, Spain.
Rafael SanjuánInstitute for Integrative Systems Biology (I2SysBio), Universitat de València and Consejo Superior de Investigaciones Científicas, València, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rates of spontaneous mutation determine the ability of viruses to evolve, infect new hosts, evade immunity and undergo drug resistance. Contrarily to RNA viruses, few mutation rate estimates have been obtained for DNA viruses, because their high replication fidelity implies that new mutations typically fall below the detection limits of Sanger and standard next-generation sequencing. Here, we have used a recently developed high-fidelity deep sequencing technique (Duplex Sequencing) to score spontaneous mutations in human adenovirus 5 under conditions of minimal selection. Based on >200 single-base spontaneous mutations detected throughout the entire viral genome, we infer an average mutation rate of 1.3 × 10-7 per base per cell infection cycle. This value is similar to those of other, large double-stranded DNA viruses, but an order of magnitude lower than those of single-stranded DNA viruses, consistent with the possible action of post-replicative repair. Although the mutation rate did not vary strongly along the adenovirus genome, we found several sources of mutation rate heterogeneity. First, two regions mapping to transcription units L3 and E1B-IVa2 were significantly depleted for mutations. Second, several point insertions/deletions located within low-complexity sequence contexts appeared recurrently, suggesting mutational hotspots. Third, mutation probability increased at GpC dinucleotides. Our findings suggest that host factors may influence the distribution of spontaneous mutations in human adenoviruses and potentially other nuclear DNA viruses.

Indexed as

Mutation RateAdenoviruses, HumanGenome, ViralHigh-Throughput Nucleotide SequencingHumansMutationPolymerase Chain Reaction

Identifiers

PMID27824949
PMCPMC5100877

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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.