Evidence map›Paper›PMID 12610112›Full record

ArticleJournal of virology2003

Induction of apoptosis by paramyxovirus simian virus 5 lacking a small hydrophobic gene.

Yuan Lin, Angela C Bright, Terri A Rothermel, Biao He

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 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.4field-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

49 citing papers in PubMed, 78 citations in OpenAlex.

  1. Frontiers in immunology · 2026
    Article
  2. Article
  3. Small hydrophobic (SH) proteins ofJournal of virology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. NovelViruses · 2019
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Targeting the Channel Activity of Viroporins.Advances in protein chemistry and structural biology · 2016
    Review
  17. Article
  18. Article
  19. Review
  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

4 authors at 1 institution in 1 country.

Yuan LinDepartment of Veterinary Science, Pennsylvania State University, University Park, Pennsylvania 16802, USA.
Angela C Bright
Terri A Rothermel
Biao He
Pennsylvania State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Simian virus 5 (SV5) is a member of the paramyxovirus family, which includes emerging viruses such as Hendra virus and Nipah virus as well as many important human and animal pathogens that have been known for years. SV5 encodes eight known viral proteins, including a small hydrophobic integral membrane protein (SH) of 44 amino acids. SV5 without the SH gene (rSV5deltaSH) is viable, and growth of rSV5deltaSH in tissue culture cells and viral protein and mRNA production in rSV5deltaSH-infected cells are indistinguishable from those of the wild-type SV5 virus. However, rSV5deltaSH causes increased cytopathic effect (CPE) and apoptosis in MDBK cells and is attenuated in vivo, suggesting the SH protein plays an important role in SV5 pathogenesis. How rSV5deltaSH induces apoptosis in infected cells has been examined in this report. Tumor necrosis factor alpha (TNF-alpha), a proinflammatory cytokine, was detected in culture media of rSV5deltaSH-infected cells. Apoptosis induced by rSV5deltaSH was inhibited by neutralizing antibodies against TNF-alpha and TNF-alpha receptor 1 (TNF-R1), suggesting that TNF-alpha played an essential role in rSV5deltaSH-induced apoptosis in a TNF-R1-dependent manner. Examination of important proteins in the TNF-alpha signaling pathway showed that p65, a major NF-kappaB subunit whose activation can lead to transcription of TNF-alpha, was first translocated to the nucleus and was capable of binding to DNA and then was targeted for degradation in rSV5deltaSH-infected cells while expression levels of TNF-R1 remained relatively constant. Thus, rSV5deltaSH induced cell death by activating TNF-alpha expression, possibly through activation of the NF-kappaB subunit p65 and then targeting p65 for degradation, leading to apoptosis.

Indexed as

ApoptosisAnimalsCattleCell LineCell NucleusCulture Media, ConditionedCytopathogenic Effect, ViralDNA-Binding ProteinsMiceNF-kappa BRetroviridae Proteins, OncogenicRubulavirusTranscription Factor RelATumor Necrosis Factor-alphaCulture Media, ConditionedDNA-Binding ProteinsNF-kappa BRetroviridae Proteins, Oncogenicsmall hydrophobic protein, virusTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID12610112
PMCPMC149502
OpenAlexW2038272126

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.