Evidence map›Paper›PMID 12805464›Full record

ArticleJournal of virology2003

Classical swine fever virus interferes with cellular antiviral defense: evidence for a novel function of N(pro).

Nicolas Ruggli, Jon-Duri Tratschin, Matthias Schweizer, Kenneth C McCullough, Martin A Hofmann, Artur Summerfield

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
17.0field-weighted citation impact, top 1% 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

58 citing papers in PubMed, 136 citations in OpenAlex.

  1. Review
  2. Article
  3. Strategies of Classical Swine Fever Immune Evasion.International journal of molecular sciences · 2025
    Review
  4. Article
  5. New Generation Self-Replicating RNA Vaccines Derived from Pestivirus Genome.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Classical swine fever virus NJournal of virology · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

6 authors at 2 institutions in 2 countries.

Nicolas RuggliInstitute of Virology and Immunoprophylaxis, Mittelhäusern, Switzerland. nicolas.ruggli@ivi.admin.ch
Jon-Duri Tratschin
Matthias Schweizer
Kenneth C McCullough
Martin A Hofmann
Artur Summerfield
Institute of Virology of the Slovak Academy of Sciences · SKUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Classical swine fever virus (CSFV) replicates efficiently in cell lines and monocytic cells, including macrophages (MPhi), without causing a cytopathic effect or inducing interferon (IFN) secretion. In the present study, the capacity of CSFV to interfere with cellular antiviral activity was investigated. When the porcine kidney cell line SK-6 was infected with CSFV, there was a 100-fold increased capacity to resist to apoptosis induced by polyinosinic-polycytidylic acid [poly(IC)], a synthetic double-stranded RNA. In MPhi, the virus infection inhibited poly(IC)-induced alpha/beta IFN (type I IFN) synthesis. This interference with cellular antiviral defense correlated with the presence of the viral N(pro) gene. Mutants lacking the N(pro) gene (DeltaN(pro) CSFV) did not protect SK-6 cells from poly(IC)-induced apoptosis, despite growth properties and protein expression levels similar to those of the wild-type virus. Furthermore, DeltaN(pro) CSFV did not prevent poly(IC)-induced type I IFN production in MPhi but rather induced type I IFN in the absence of poly(IC) in both MPhi and the porcine kidney cell line PK-15, but not in SK-6 cells. With MPhi and PK-15, an impaired replication of the DeltaN(pro) CSFV compared with wild-type virus was noted. In addition, DeltaN(pro) CSFV, but not wild-type CSFV, could interfere with vesicular stomatitis virus replication in PK-15 cells. Taken together, these results provide evidence for a novel function associated with CSFV N(pro) with respect to the inhibition of the cellular innate immune system.

Indexed as

AnimalsAntiviral AgentsApoptosisCell LineClassical Swine Fever VirusImmunohistochemistrySwineVirus ReplicationAntiviral Agents

Identifiers

PMID12805464
PMCPMC164809
OpenAlexW2122615118

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.