Evidence map›Paper›PMID 29444943›Full record

ArticleJournal of virology2018

Vaccinia Virus C9 Ankyrin Repeat/F-Box Protein Is a Newly Identified Antagonist of the Type I Interferon-Induced Antiviral State.

Ruikang Liu, Bernard Moss

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
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  7. Article
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  9. Review
  10. A comprehensive review of monkeypox virus and mpox characteristics.Frontiers in cellular and infection microbiology · 2024
    Review
  11. Comprehensive literature review of monkeypox.Emerging microbes & infections · 2022
    Review
  12. Review
  13. Article
  14. Poxvirus Interactions with the Host Ubiquitin System.Pathogens (Basel, Switzerland) · 2021
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

Ruikang LiuLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Bernard MossLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA bmoss@nih.gov.ORCID https://orcid.org/0000-0002-2154-8564
National Institutes of Health · US

Funding

Poxvirus pathogenesis and immunityZIAAI000979 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MOSS, BERNARD · 2009 to 2022
$12.7M
Poxvirus pathogenesis and immunityZ01AI000979 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI MOSS, BERNARD · 2006 to 2008
$2.0M
Intramural NIH HHS Z01 AI000979Intramural NIH HHS ZIA AI000979
6 · The paper itself

Abstract

Type I interferons (IFNs) induce expression of more than 300 cellular genes that provide protection against viruses and other pathogens. For survival, viruses evolved defenses to prevent the IFN response or counteract the IFN-induced antiviral state. However, because viruses and cells coevolved, the dynamic relationship between virus and host is difficult to discern. In the present study, we demonstrated that vaccinia virus with a large deletion near the left end of the genome had a diminished ability to replicate in cells that had been pretreated with beta interferon (IFN-β), suggesting that one or more of the missing 17 open reading frames (ORFs) encode an antagonist of the IFN-induced antiviral state. By systematically deleting groups of ORFs and then individual ORFs, the C9L gene was shown to be required for IFN resistance. Replication of the C9L deletion mutant (vΔC9) was impaired in human cells that had been pretreated with IFN-β. Expression of viral early genes occurred, but subsequent events, including genome uncoating, genome replication, and postreplicative gene expression, were inhibited. Expression of the C9 protein occurred prior to genome replication, consistent with an early role in counteracting the IFN-induced antiviral state. C9 contains six ankyrin repeat motifs and a near C-terminal F-box. Mass spectrometry and immunoblotting identified host proteins that copurified with a functional epitope-tagged C9. The most abundant proteins were components of the SCF (CUL1, SKP1, F-box) and signalosome/deneddylation complexes, which interact with each other, suggesting a possible role in proteolysis of one or more interferon-induced proteins.

Indexed as

Ankyrin RepeatA549 CellsCullin ProteinsDNA, ViralF-Box ProteinsGene Knockout TechniquesGenome, ViralHumansInterferon-betaSequence DeletionSKP Cullin F-Box Protein LigasesVaccinia virusViral ProteinsVirus ReplicationCullin 1Cullin ProteinsDNA, ViralF-Box ProteinsInterferon-betaSKP Cullin F-Box Protein LigasesViral Proteinscullin 1deneddylationinterferonorthopoxviruspoxvirusSCF complexsignalosomeSKP1

Identifiers

PMID29444943
PMCPMC5899206
OpenAlexW2793362905

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.