Evidence map›Paper›PMID 29970470›Full record

ArticlemBio2018

Avian Influenza Virus PB1 Gene in H3N2 Viruses Evolved in Humans To Reduce Interferon Inhibition by Skewing Codon Usage toward Interferon-Altered tRNA Pools.

Bartram L Smith, Guifang Chen, Claus O Wilke, Robert M Krug

Open access · goldAbstract read
In one paragraph

Article in mBio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 37 citations in OpenAlex.

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  8. Emerging translation strategies during virus-host interaction.Wiley interdisciplinary reviews. RNA · 2021
    Review
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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.

Bartram L SmithDepartment of Molecular Biosciences, John Ring LaMontagne Center for Infectious Disease, Institute for Cellular and Molecular Biology, the University of Texas at Austin, Austin, Texas, USA.
Guifang ChenDepartment of Molecular Biosciences, John Ring LaMontagne Center for Infectious Disease, Institute for Cellular and Molecular Biology, the University of Texas at Austin, Austin, Texas, USA.
Claus O WilkeDepartment of Integrative Biology, Center for Computational Biology and Bioinformatics, Institute for Cellular and Molecular Biology, the University of Texas at Austin, Austin, Texas, USA.ORCID 0000-0002-7470-9261
Robert M KrugDepartment of Molecular Biosciences, John Ring LaMontagne Center for Infectious Disease, Institute for Cellular and Molecular Biology, the University of Texas at Austin, Austin, Texas, USA rkrug@austin.utexas.edu.
The University of Texas at Austin · US

Funding

REPLICATION OF INFLUENZA VIRUSR01AI011772 · NIAID · UNIVERSITY OF TEXAS AUSTIN · PI KRUG, ROBERT M · 1985 to 2017
$10.7M
The biophysical basis of translational selectionR01GM088344 · NIGMS · UNIVERSITY OF TEXAS AT AUSTIN · PI BARRICK, JEFFREY EVAN, WILKE, CLAUS O · 2009 to 2023
$3.5M
Identifying Mutations that Promote Microbial EvolvabilityK99GM087550 · NIGMS · MICHIGAN STATE UNIVERSITY · PI BARRICK, JEFFREY EVAN · 2009 to 2010
$180k
NIAID NIH HHS R01 AI011772NIGMS NIH HHS K99 GM087550NIGMS NIH HHS R01 GM088344
6 · The paper itself

Abstract

Influenza A viruses cause an annual contagious respiratory disease in humans and are responsible for periodic high-mortality human pandemics. Pandemic influenza A viruses usually result from the reassortment of gene segments between human and avian influenza viruses. These avian influenza virus gene segments need to adapt to humans. Here we focus on the human adaptation of the synonymous codons of the avian influenza virus PB1 gene of the 1968 H3N2 pandemic virus. We generated recombinant H3N2 viruses differing only in codon usage of PB1 mRNA and demonstrated that codon usage of the PB1 mRNA of recent H3N2 virus isolates enhances replication in interferon (IFN)-treated human cells without affecting replication in untreated cells, thereby partially alleviating the interferon-induced antiviral state. High-throughput sequencing of tRNA pools explains the reduced inhibition of replication by interferon: the levels of some tRNAs differ between interferon-treated and untreated human cells, and evolution of the codon usage of H3N2 PB1 mRNA is skewed toward interferon-altered human tRNA pools. Consequently, the avian influenza virus-derived PB1 mRNAs of modern H3N2 viruses have acquired codon usages that better reflect tRNA availabilities in IFN-treated cells. Our results indicate that the change in tRNA availabilities resulting from interferon treatment is a previously unknown aspect of the antiviral action of interferon, which has been partially overcome by human-adapted H3N2 viruses.

Indexed as

Adaptation, BiologicalCodonVirus ReplicationAnimalsCell LineHumansInfluenza A Virus, H3N2 SubtypeInterferonsReassortant VirusesRNA, TransferViral ProteinsCodoninfluenza virus polymerase basic protein 1InterferonsRNA, TransferViral Proteinscodon usageevolutioninfluenza A virusinfluenza PB1 proteininterferon

Identifiers

PMID29970470
PMCPMC6030557
OpenAlexW2811511509

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.