Evidence map›Paper›PMID 27215196›Full record

ArticleBMC genomics2016

A de novo transcriptome analysis shows that modulation of the JAK-STAT signaling pathway by salmonid alphavirus subtype 3 favors virus replication in macrophage/dendritic-like TO-cells.

Cheng Xu, Øystein Evensen, Hetron Mweemba Munang'andu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Teleosts Genomics: Progress and Prospects in Disease Prevention and Control.International journal of molecular sciences · 2018
    Review
  5. Review
  6. 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

3 authors at 1 institution in 1 country.

Cheng XuDepartment of Basic Sciences and Aquatic Medicine, Section of Aquatic Medicine and Nutrition, Faculty of Veterinary Medicine and Biosciences, Norwegian University of Life Sciences, P.O Box 8146, Oslo, NO-0033 Dep, Norway.
Øystein EvensenDepartment of Basic Sciences and Aquatic Medicine, Section of Aquatic Medicine and Nutrition, Faculty of Veterinary Medicine and Biosciences, Norwegian University of Life Sciences, P.O Box 8146, Oslo, NO-0033 Dep, Norway.
Hetron Mweemba Munang'anduDepartment of Basic Sciences and Aquatic Medicine, Section of Aquatic Medicine and Nutrition, Faculty of Veterinary Medicine and Biosciences, Norwegian University of Life Sciences, P.O Box 8146, Oslo, NO-0033 Dep, Norway. hetroney.mweemba.munangandu@nmbu.no.
Norwegian University of Life Sciences · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Janus kinase (Jak) and signaling transducer activator of transcription (Stat) pathway mediates the signaling of genes required for cellular development and homeostasis. To elucidate the effect of type I IFN on the Jak/stat pathway in salmonid alphavirus subtype 3 (SAV3) infected macrophage/dendritic like TO-cells derived from Atlantic salmon (Salmo salar L) headkidney leukocytes, we used a differential transcriptome analysis by RNA-seq and the Kyoto encyclopedia of genes and genomes (KEGGs) pathway analysis to generate a repertoire of de novo assembled genes from type I IFN treated and non-treated TO-cells infected with SAV3.

resultsConcurrent SAV3 infection with type I IFN treatment of TO-cells suppressed SAV3 structural protein (SP) expression by 2log10 at 2 days post infection compared to SAV3 infection without IFN treatment which paved way to evaluating the impact of type I IFN on expression of Jak/stat pathway genes in SAV3 infected TO-cells. In the absence of type I IFN treatment, SAV3 downregulated several Jak/stat pathway genes that included type I and II receptor genes, Jak2, tyrosine kinase 2 (Tyk2), Stat3 and Stat5 pointing to possible failure to activate the Jak/stat signaling pathway and inhibition of signal transducers caused by SAV3 infection. Although the suppressor of cytokine signaling (SOCS) genes 1 and 3 were upregulated in the IFN treated cells, only SOCS3 was downregulated in the SAV3 infected cells which points to inhibition of SOCS3 by SAV3 infection in TO-cells.

conclusionData presented in this study shows that SAV3 infection downregulates several genes of the Jak/stat pathway, which could be an immune evasion strategy, used to block the transcription of antiviral genes that would interfere with SAV3 replication in TO-cells. Overall, we have shown that combining de novo assembly with pathway based transcriptome analyses provides a contextual approach to understanding the molecular networks of genes that form the Jak/stat pathway in TO-cells infected by SAV3.

Indexed as

Gene Regulatory NetworksAlphavirusAnimalsCell LineFish ProteinsGene Expression ProfilingGene Expression RegulationGene Expression Regulation, ViralInterferon Type IJanus KinasesMacrophagesMAP Kinase Signaling SystemSalmonidaeSTAT Transcription FactorsViral Structural ProteinsVirus ReplicationFish ProteinsInterferon Type IJanus KinasesSTAT Transcription FactorsViral Structural Proteins

Identifiers

PMID27215196
PMCPMC4878077
OpenAlexW2396592849

What OpenQuestion holds

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LicenceCC BY
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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.