Evidence map›Paper›PMID 21318239›Full record

ArticleVirus genes2011

Classical swine fever virus NS2 protein promotes interleukin-8 expression and inhibits MG132-induced apoptosis.

Qinghai Tang, Kangkang Guo, Kai Kang, Yanming Zhang, Lei He, Jing Wang

Abstract read
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Article in Virus genes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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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.

Qinghai TangCollege of Veterinary Medicine, Northwest A & F University, Yangling, Shaanxi, 712100, People's Republic of China.
Kangkang Guo
Kai Kang
Yanming Zhang
Lei He
Jing Wang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Classical swine fever (CSF) caused by virulent strains of classical swine fever virus (CSFV) is a hemorrhagic disease of pigs and is characterized by disseminated intravascular coagulation, thrombocytopenia, and immunosuppression. Until now, the role of the NS2 protein produced by CSFV in the pathogenesis of CSF is not well understood. In this report, we investigated the function of CSFV NS2 by examining its effects on the pro-inflammatory CXC chemokine, interleukin-8 (IL-8) expression, and cell survival. Stable swine umbilical vein endothelial cell line (SUVEC) expressing CSFV NS2 were established and showed that CSFV NS2 expressing SUVEC cells express approximately 16-fold higher levels of IL-8 as compared to control vector GFP-expressing cells, GFP-E2 expressing cells, and untransfected cells. Further studies showed that CSFV NS2 induced endoplasmic reticulum stress and activated the nuclear transcription factor kappa B (NF-κB), which is responsible for the up-regulation of IL-8 and the anti-apoptotic protein, Bcl-2, expression. In addition, the GFPNS2-expressing SUVEC cells were resistant to MG132-induced apoptosis. This study suggested that CSFV NS2 plays an important role in the inflammatory response and in persistent CSFV infection. These findings provide novel information on the function of the poorly characterized CSFV NS2.

Indexed as

AnimalsApoptosisCell LineClassical Swine FeverClassical Swine Fever VirusDown-RegulationInterleukin-8LeupeptinsSwineUp-RegulationViral Nonstructural Proteinsbenzyloxycarbonylleucyl-leucyl-leucine aldehydeInterleukin-8LeupeptinsViral Nonstructural Proteins

Identifiers

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Registered trials

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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.