Evidence map›Paper›PMID 27713835›Full record

ArticleVirus evolution2016

Sequence amplification via cell passaging creates spurious signals of positive adaptation in influenza virus H3N2 hemagglutinin.

Claire D McWhite, Austin G Meyer, Claus O Wilke

Abstract read
In one paragraph

Article in Virus evolution, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Article
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  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Allele-specific nonstationarity in evolution of influenza A virus surface proteins.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Deep mutational scanning of hemagglutinin helps predict evolutionary fates of human H3N2 influenza variants.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  16. Article
  17. Article
  18. Review
  19. The evolution of seasonal influenza viruses.Nature reviews. Microbiology · 2018
    Review
  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.

Claire D McWhiteCenter for Systems and Synthetic Biology and Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 78712; Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712.
Austin G MeyerCenter for Systems and Synthetic Biology and Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 78712; Center for Computational Biology and Bioinformatics, The University of Texas at Austin, Austin, TX 78712; Department of Integrative Biology, The University of Texas at Austin, Austin, TX 78712.
Claus O WilkeCenter for Systems and Synthetic Biology and Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX 78712; Center for Computational Biology and Bioinformatics, The University of Texas at Austin, Austin, TX 78712; Department of Integrative Biology, The University of Texas at Austin, Austin, TX 78712.

Funding

The biophysical basis of translational selectionR01GM088344 · NIGMS · UNIVERSITY OF TEXAS AT AUSTIN · PI BARRICK, JEFFREY EVAN, WILKE, CLAUS O · 2009 to 2023
$3.5M
NIEHS NIH HHS 27398C0007NIGMS NIH HHS R01 GM088344United States NIGMS
6 · The paper itself

Abstract

Clinical influenza A virus isolates are frequently not sequenced directly. Instead, a majority of these isolates (~70% in 2015) are first subjected to passaging for amplification, most commonly in non-human cell culture. Here, we find that this passaging leaves distinct signals of adaptation, which can confound evolutionary analyses of the viral sequences. We find distinct patterns of adaptation to Madin-Darby (MDCK) and monkey cell culture absent from unpassaged hemagglutinin sequences. These patterns also dominate pooled datasets not separated by passaging type, and they increase in proportion to the number of passages performed. By contrast, MDCK-SIAT1 passaged sequences seem mostly (but not entirely) free of passaging adaptations. Contrary to previous studies, we find that using only internal branches of influenza virus phylogenetic trees is insufficient to correct for passaging artifacts. These artifacts can only be safely avoided by excluding passaged sequences entirely from subsequent analysis. We conclude that future influenza virus evolutionary analyses should appropriately control for potentially confounding effects of passaging adaptations.

Identifiers

PMID27713835
PMCPMC5049878

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Registered trials

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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.