Evidence map›Paper›PMID 23365443›Full record

ArticleJournal of virology2013

Reassortment complements spontaneous mutation in influenza A virus NP and M1 genes to accelerate adaptation to a new host.

William L Ince, Aissatou Gueye-Mbaye, Jack R Bennink, Jonathan W Yewdell

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 69 citations in OpenAlex.

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  16. H5N8 and H7N9 packaging signals constrain HA reassortment with a seasonal H3N2 influenza A virus.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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.

William L InceLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA.
Aissatou Gueye-Mbaye
Jack R Bennink
Jonathan W Yewdell
National Institute of Allergy and Infectious Diseases · US

Funding

Biology, Evolution and Pathogenesis of Influenza A VirusZIAAI001014 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BENNINK, JACK R · 2009 to 2020
$5.6M
Antigenic Drift in Influenza A VirusZIAAI001055 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI YEWDELL, JONATHAN W · 2009 to 2015
$3.1M
Intramural NIH HHS
6 · The paper itself

Abstract

Influenza A virus (IAV) infects a remarkably wide variety of avian and mammalian hosts. Evolution finely hones IAV genes to optimally infect and be transmitted in a particular host species. Sporadically, IAV manages to jump between species, introducing novel antigenic strains into the new host population that wreak havoc until herd immunity develops. IAV adaptation to new hosts typically involves reassortment of IAV gene segments from coinfecting virus strains adapted to different hosts in conjunction with multiple adaptive mutations in the various IAV genes. To better understand host adaptation between mammalian species in real time, we passaged mouse-adapted A/PR8/34 (PR8) in guinea pigs. Guinea pigs, unlike mice, support spontaneous and robust IAV transmission. For some IAV strains, including PR8, adaptation is required for a virus to attain transmissibility, providing an opportunity to understand the evolution of transmissibility in guinea pigs. Multiple guinea pig-adapted PR8 mutants generated by serial nasal wash passaging in independent lines replicated more efficiently and were transmitted by cocaging. All transmissible variants possessed one of two nonsynonymous mutations in M1, either alone or in combination with mutations in PB2, HA, NP, or NA. Rapid reassortment between independently selected variants combined beneficial mutations in NP and M1 to form the fittest virus capable of being transmitted. These findings provide further insight into genetic determinants in NP and M1 involved in PR8 IAV adaptation to be transmitted in a new host and clearly show the benefit of a segmented genome in rapidly generating optimal combinations of mutations in IAV evolution.

Indexed as

Adaptation, BiologicalMutation, MissenseRecombination, GeneticAnimalsDisease Models, AnimalFemaleGuinea PigsInfluenza A virusMiceNasal CavityNucleocapsid ProteinsOrthomyxoviridae InfectionsRNA-Binding ProteinsSerial PassageViral Core ProteinsViral Matrix ProteinsM1 protein, Influenza A virusNP protein, Influenza A virusNucleocapsid ProteinsRNA-Binding ProteinsViral Core ProteinsViral Matrix Proteins

Identifiers

PMID23365443
PMCPMC3624365
OpenAlexW1999495439

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.