Evidence map›Paper›PMID 36325033›Full record

ArticleVirus evolution2022

Accumulation of copy-back viral genomes during respiratory syncytial virus infection is preceded by diversification of the copy-back viral genome population followed by selection.

Sébastien A Felt, Emna Achouri, Sydney R Faber, Carolina B López

Open access · goldAbstract read
In one paragraph

Article in Virus evolution, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Sébastien A FeltDepartment of Molecular Microbiology and Center for Women Infectious Disease Research, Washington University School of Medicine, St Louis, MO 63108, USA.
Emna AchouriDepartment of Molecular Microbiology and Center for Women Infectious Disease Research, Washington University School of Medicine, St Louis, MO 63108, USA.
Sydney R FaberDepartment of Molecular Microbiology and Center for Women Infectious Disease Research, Washington University School of Medicine, St Louis, MO 63108, USA.
Carolina B LópezDepartment of Molecular Microbiology and Center for Women Infectious Disease Research, Washington University School of Medicine, St Louis, MO 63108, USA.
Washington University in St. Louis · US

Funding

Defective Viral genomes in RSV pathogenesisR01AI137062 · NIAID · WASHINGTON UNIVERSITY · PI Carolina B. Lopez · 2018 to 2026
$4.2M
Mechanisms of DDO AdjuvancyR01AI134862 · NIAID · WASHINGTON UNIVERSITY · PI LOPEZ, CAROLINA B. · 2018 to 2022
$2.4M
NIAID NIH HHS R01 AI134862NIAID NIH HHS R01 AI137062
6 · The paper itself

Abstract

RNA viruses generate nonstandard viral genomes during their replication, including viral genomes of the copy-back (cbVGs) type that cannot replicate in the absence of a standard virus. cbVGs play a crucial role in shaping virus infection outcomes due to their ability to interfere with virus replication and induce strong immune responses. However, despite their critical role during infection, the principles that drive the selection and evolution of cbVGs within a virus population are poorly understood. As cbVGs are dependent on the virus replication machinery to be generated and replicated, we hypothesized that host factors that affect virus replication exert selective pressure on cbVGs and drive their evolution within a virus population. To test this hypothesis, we used respiratory syncytial virus (RSV) as a model and took an experimental evolution approach by serially passaging RSV in immune-competent human lung adenocarcinoma A549 control and immune-deficient A549 Signal transducer and activator of transcription 1 (STAT1) KO cells, which allow higher levels of virus replication. As predicted, we observed that virus populations accumulated higher amounts of cbVGs in the more permissive A549 STAT1 KO cells over time; however, unexpectedly, the predominant cbVG species after passages in the two conditions were different. While A549 STAT1 KO cells accumulated relatively short cbVGs, A549 control cells mainly contained cbVGs of much longer predicted size, which have not been described previously. These long cbVGs were predominant at first in both cell lines

Indexed as

copy-back viral genomesexperimental evolutionrespiratory syncytial virus

Identifiers

PMID36325033
PMCPMC9615430
OpenAlexW4297991243

What OpenQuestion holds

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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.