Evidence map›Paper›PMID 28835506›Full record

ArticleJournal of virology2017

The K186E Amino Acid Substitution in the Canine Influenza Virus H3N8 NS1 Protein Restores Its Ability To Inhibit Host Gene Expression.

Aitor Nogales, Caroline Chauché, Marta L DeDiego, David J Topham, Colin R Parrish, Pablo R Murcia, Luis Martínez-Sobrido

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. 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
2.1field-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

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Observational
  2. Article
  3. Review
  4. Review
  5. Bacterial Artificial Chromosome Reverse Genetics Approaches for SARS-CoV-2.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Immunity to Influenza Infection in Humans.Cold Spring Harbor perspectives in medicine · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  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

7 authors at 3 institutions in 2 countries.

Aitor NogalesDepartment of Microbiology and Immunology, University of Rochester, Rochester, New York, USA.
Caroline ChauchéMRC-University of Glasgow Centre for Virus Research, Glasgow, United Kingdom.
Marta L DeDiegoDepartment of Microbiology and Immunology, University of Rochester, Rochester, New York, USA.
David J TophamDepartment of Microbiology and Immunology, University of Rochester, Rochester, New York, USA.ORCID http://orcid.org/0000-0002-9435-8673
Colin R ParrishBaker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.ORCID http://orcid.org/0000-0002-1836-6655
Pablo R MurciaMRC-University of Glasgow Centre for Virus Research, Glasgow, United Kingdom.ORCID http://orcid.org/0000-0002-4352-394X
Luis Martínez-SobridoDepartment of Microbiology and Immunology, University of Rochester, Rochester, New York, USA luis_martinez@urmc.rochester.edu.
University of Rochester · USMRC University of Glasgow Centre for Virus Research · GBCornell University · US

Funding

Medical Research Council MC_UU_12014/9NIAID NIH HHS HHSN272201400005C
6 · The paper itself

Abstract

Canine influenza viruses (CIVs) are the causative agents of canine influenza, a contagious respiratory disease in dogs, and include the equine-origin H3N8 and the avian-origin H3N2 viruses. Influenza A virus (IAV) nonstructural protein 1 (NS1) is a virulence factor essential for counteracting the innate immune response. Here, we evaluated the ability of H3N8 CIV NS1 to inhibit host innate immune responses. We found that H3N8 CIV NS1 was able to efficiently counteract interferon (IFN) responses but was unable to block general gene expression in human or canine cells. Such ability was restored by a single amino acid substitution in position 186 (K186E) that resulted in NS1 binding to the 30-kDa subunit of the cleavage and polyadenylation specificity factor (CPSF30), a cellular protein involved in pre-mRNA processing. We also examined the frequency distribution of K186 and E186 among H3N8 CIVs and equine influenza viruses (EIVs), the ancestors of H3N8 CIV, and experimentally determined the impact of amino acid 186 in the ability of different CIV and EIV NS1s to inhibit general gene expression. In all cases, the presence of E186 was responsible for the control of host gene expression. In contrast, the NS1 protein of H3N2 CIV harbors E186 and blocks general gene expression in canine cells. Altogether, our results confirm previous studies on the strain-dependent ability of NS1 to block general gene expression. Moreover, the observed polymorphism on amino acid 186 between H3N8 and H3N2 CIVs might be the result of adaptive changes acquired during long-term circulation of avian-origin IAVs in mammals.

Indexed as

Amino Acid SubstitutionMutation, MissenseAnimalsDogsGene Expression RegulationHEK293 CellsHost-Pathogen InteractionsHumansInfluenza A Virus, H3N8 SubtypeMadin Darby Canine Kidney CellsOrthomyxoviridae InfectionsViral Nonstructural ProteinsINS1 protein, influenza virusViral Nonstructural Proteinshost-pathogen interactionshost responseinfluenzainterferons

Identifiers

PMID28835506
PMCPMC5660486
OpenAlexW2750146440

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.