Evidence map›Paper›PMID 28750037›Full record

ArticlePloS one2017

Generation and characterization of interferon-lambda 1-resistant H1N1 influenza A viruses.

Natalia A Ilyushina, Vladimir Y Lugovtsev, Anastasia P Samsonova, Faruk G Sheikh, Nicolai V Bovin, Raymond P Donnelly

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 22 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

6 authors at 3 institutions in 2 countries.

Natalia A IlyushinaDivision of Biotechnology Research and Review II, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, Maryland, United States of America.ORCID http://orcid.org/0000-0001-8178-0472
Vladimir Y LugovtsevDivision of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, Maryland, United States of America.
Anastasia P SamsonovaDivision of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, Maryland, United States of America.
Faruk G SheikhDivision of Biotechnology Research and Review II, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, Maryland, United States of America.
Nicolai V BovinCarbohydrate Chemistry Laboratory, Shemyakin Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, Russia.
Raymond P DonnellyDivision of Biotechnology Research and Review II, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, Maryland, United States of America.
United States Food and Drug Administration · USCenter for Biologics Evaluation and Research · USInstitute of Bioorganic Chemistry · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Influenza A viruses pose a constant potential threat to human health. In view of the innate antiviral activity of interferons (IFNs) and their potential use as anti-influenza agents, it is important to know whether viral resistance to these antiviral proteins can arise. To examine the likelihood of emergence of IFN-λ1-resistant H1N1 variants, we serially passaged the A/California/04/09 (H1N1) strain in a human lung epithelial cell line (Calu-3) in the presence of increasing concentrations of recombinant IFN-λ1 protein. To monitor changes associated with adaptation of this virus to growth in Calu-3 cells, we also passaged the wild-type virus in the absence of IFN-λ1. Under IFN-λ1 selective pressure, the parental virus developed two neuraminidase (NA) mutations, S79L and K331N, which significantly reduced NA enzyme activity (↓1.4-fold) and sensitivity to IFN-λ1 (↓˃20-fold), respectively. These changes were not associated with a reduction in viral replication levels. Mutants carrying either K331N alone or S79L and K331N together induced weaker phosphorylation of IFN regulatory factor 3 (IRF3), and, as a consequence, much lower expression of the IFN genes (IFNB1, IFNL1 and IFNL2/3) and proteins (IFN-λ1 and IFN-λ2/3). The lower levels of IFN expression correlated with weaker induction of tyrosine-phosphorylated STAT1 and reduced RIG-I protein levels. Our findings demonstrate that influenza viruses can develop increased resistance to the antiviral activity of type III interferons.

Indexed as

Amino Acid SubstitutionAnimalsAntiviral AgentsCell LineDEAD Box Protein 58DNA-Directed RNA PolymerasesDogsDrug Resistance, ViralEnzyme-Linked Immunosorbent AssayGene Expression RegulationHumansImmunity, InnateInfluenza A Virus, H1N1 SubtypeInterferon LambdaInterferon Regulatory Factor-3InterferonsAntiviral AgentsDEAD Box Protein 58DNA-Directed RNA PolymerasesInterferon Lambdainterferon-lambda, humanInterferon Regulatory Factor-3InterferonsInterleukinsIRF3 protein, humanNeuraminidaseReceptors, ImmunologicReceptors, VirusRIGI protein, humanSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID28750037
PMCPMC5531537
OpenAlexW2742052119

What OpenQuestion holds

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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.