Evidence map›Paper›PMID 30918505›Full record

ArticleFrontiers in immunology2019

Senecavirus A 3C Protease Mediates Host Cell Apoptosis Late in Infection.

Maureen H V Fernandes, Mayara F Maggioli, Jaelin Otta, Lok R Joshi, Steve Lawson, Diego G Diel

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.2field-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

33 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Porcine Teschovirus 2 3CMicroorganisms · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Seneca Valley virus 3CFrontiers in microbiology · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Seneca Valley Virus 3CMicrobiology spectrum · 2022
    Article
  19. Article
  20. Seneca Valley Virus 3CFrontiers in microbiology · 2022
    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

6 authors at 1 institution in 1 country.

Maureen H V FernandesAnimal Disease Research And Diagnostic Laboratory, Department of Veterinary and Biomedical Sciences, South Dakota State University, Brookings, SD, United States.
Mayara F MaggioliAnimal Disease Research And Diagnostic Laboratory, Department of Veterinary and Biomedical Sciences, South Dakota State University, Brookings, SD, United States.
Jaelin OttaAnimal Disease Research And Diagnostic Laboratory, Department of Veterinary and Biomedical Sciences, South Dakota State University, Brookings, SD, United States.
Lok R JoshiAnimal Disease Research And Diagnostic Laboratory, Department of Veterinary and Biomedical Sciences, South Dakota State University, Brookings, SD, United States.
Steve LawsonAnimal Disease Research And Diagnostic Laboratory, Department of Veterinary and Biomedical Sciences, South Dakota State University, Brookings, SD, United States.
Diego G DielAnimal Disease Research And Diagnostic Laboratory, Department of Veterinary and Biomedical Sciences, South Dakota State University, Brookings, SD, United States.
South Dakota State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senecavirus A (SVA), an oncolytic picornavirus used for cancer treatment in humans, has recently emerged as a vesicular disease (VD)-causing agent in swine worldwide. Notably, SVA-induced VD is indistinguishable from foot-and-mouth disease (FMD) and other high-consequence VDs of pigs. Here we investigated the role of apoptosis on infection and replication of SVA. Given the critical role of the nuclear factor-kappa B (NF-κB) signaling pathway on modulation of cell death, we first assessed activation of NF-κB during SVA infection. Results here show that while early during infection SVA induces activation of NF-κB, as evidenced by nuclear translocation of NF-κB-p65 and NF-κB-mediated transcription, late in infection a cleaved product corresponding to the C-terminus of NF-κB-p65 is detected in infected cells, resulting in lower NF-κB transcriptional activity. Additionally, we assessed the potential role of SVA 3C protease (3C

Indexed as

ApoptosisHost-Pathogen Interactions3C Viral ProteasesAnimalsCell LineCysteine EndopeptidasesFlow CytometryGenes, ReporterHumansInflammation MediatorsModels, MolecularNF-kappa BPicornaviridaePicornaviridae InfectionsProtein ConformationProteolysis3C Viral ProteasesCysteine EndopeptidasesInflammation MediatorsNF-kappa BViral Proteins3C proteaseapoptosisSeneca Valley virusSenecavirus Avirus egress

Identifiers

PMID30918505
PMCPMC6424860
OpenAlexW2916537610

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.