Evidence map›Paper›PMID 15890962›Full record

ArticleJournal of virology2005

Loss of interferon regulatory factor 3 in cells infected with classical swine fever virus involves the N-terminal protease, Npro.

S Anna La Rocca, Rebecca J Herbert, Helen Crooke, Trevor W Drew, Thomas E Wileman, Penny P Powell

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
20.3field-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

59 citing papers in PubMed, 117 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Strategies of Classical Swine Fever Immune Evasion.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Pestiviruses infection: Interferon-virus mutual regulation.Frontiers in cellular and infection microbiology · 2023
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. The EViruses · 2021
    Article
  16. Classical swine fever virus NJournal of virology · 2020
    Article
  17. Article
  18. Review
  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

6 authors at 2 institutions in 1 country.

S Anna La RoccaDepartment of Immunology, BBSRC Institute for Animal Health, Ash Road, Pirbright, Surrey GU24 0NF, United Kingdom.
Rebecca J Herbert
Helen Crooke
Trevor W Drew
Thomas E Wileman
Penny P Powell
The Pirbright Institute · GBBiotechnology and Biological Sciences Research Council · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We show that cells infected with the pestivirus classical swine fever virus (CSFV) fail to produce alpha/beta interferon not only following treatment with double-stranded RNA but also after superinfection with a heterologous virus, the alphavirus Sindbis virus, a virus shown to normally induce interferon. We investigated whether the inhibition of interferon synthesis by CSFV involved a block in interferon regulatory factor 3 (IRF3) activity. Cells infected with CSFV exhibited a lack of translocation of green fluorescent protein-IRF3 to the nucleus; however, constitutive shuttling of IRF3 was not blocked, since it could still accumulate in the nucleus in the presence of leptomycin B. Interestingly subcellular fractionation analysis showed that IRF3 was lost from the cytoplasm of infected cells from 18 h postinfection onwards. Using IRF3 promoter-luciferase reporter constructs, we demonstrate that loss of IRF3 was due to an inhibition of transcription of the IRF3 gene in CSFV-infected cells. Further, we investigated which viral protein may be responsible for the inhibition of interferon and loss of IRF3. We used cell lines expressing the CSFV N-terminal protease (Npro) to show that this single viral protein, unique to pestiviruses, inhibited interferon production in response to Sindbis virus. In addition to being lost from CSFV-infected cells, IRF3 was lost from Npro-expressing cells. The results demonstrate a novel viral evasion of innate host defenses, where interferon synthesis is prevented by inhibiting transcription of IRF3 in CSFV-infected cells.

Indexed as

Amino Acid SequenceAnimalsBase SequenceCattleCell LineClassical Swine Fever VirusDNA-Binding ProteinsDNA, ViralImmunity, InnateInterferon Regulatory Factor-3InterferonsMolecular Sequence DataPeptide HydrolasesRNA, ViralSindbis VirusSuperinfectionDNA-Binding ProteinsDNA, ViralInterferon Regulatory Factor-3InterferonsPeptide HydrolasesRNA, ViralTranscription Factors

Identifiers

PMID15890962
PMCPMC1112113
OpenAlexW2104118102

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.