Evidence map›Paper›PMID 31664929›Full record

ArticleBMC infectious diseases2019

Inflammatory responses to a pathogenic West Nile virus strain.

Bixing Huang, Nic West, Jelena Vider, Ping Zhang, Rebecca E Griffiths, Ernst Wolvetang, Peter Burtonclay, David Warrilow

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC infectious diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Organoid Models for Infectious Disease.Annual review of medicine · 2022
    Review
  8. Using 2D and 3D pluripotent stem cell models to study neurotropic viruses.Frontiers in virology (Lausanne, Switzerland) · 2022
    Article
  9. Article
  10. 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

8 authors.

Bixing HuangPublic Health Virology Laboratory, Queensland Health Forensic and Scientific Services, PO Box 594, Archerfield, Queensland, Australia.
Nic WestMenzies Health Institute Queensland and School of Medical Science, Griffith University, Southport, Queensland, Australia.
Jelena ViderMenzies Health Institute Queensland and School of Medical Science, Griffith University, Southport, Queensland, Australia.
Ping ZhangMenzies Health Institute Queensland and School of Medical Science, Griffith University, Southport, Queensland, Australia.
Rebecca E GriffithsAustralian Institute for Bioengineering and Nanotechnology, University of Queensland, Brisbane, Queensland, Australia.
Ernst WolvetangAustralian Institute for Bioengineering and Nanotechnology, University of Queensland, Brisbane, Queensland, Australia.
Peter BurtonclayPublic Health Virology Laboratory, Queensland Health Forensic and Scientific Services, PO Box 594, Archerfield, Queensland, Australia.
David WarrilowPublic Health Virology Laboratory, Queensland Health Forensic and Scientific Services, PO Box 594, Archerfield, Queensland, Australia. David.Warrilow@health.qld.gov.au.ORCID http://orcid.org/0000-0002-3221-7605

Funding

Department of Health, Queensland RSS16-003HSRD VA IIR 16-003
6 · The paper itself

Abstract

backgroundWest Nile virus (WNV) circulates across Australia and was referred to historically as Kunjin virus (WNV

methodsTo better understand the emergence of this virulent phenotype and the mechanism by which pathogenicity is manifested in its host, cells were infected with either the virulent strain (NSW2012), or less pathogenic historical isolates, and their innate immune responses compared by digital immune gene expression profiling. Two different cell systems were used: a neuroblastoma cell line (SK-N-SH cells) and neuronal cells derived from induced pluripotent stem cells (iPSCs).

resultsSignificant innate immune gene induction was observed in both systems. The NSW2012 isolate induced higher gene expression of two genes (IL-8 and CCL2) when compared with cells infected with less pathogenic isolates. Pathway analysis of induced inflammation-associated genes also indicated generally higher activation in infected NSW2012 cells. However, this differential response was not paralleled in the neuronal cultures.

conclusionNSW2012 may have unique genetic characteristics which contributed to the outbreak. The data herein is consistent with the possibility that the virulence of NSW2012 is underpinned by increased induction of inflammatory genes.

Indexed as

Disease OutbreaksAustraliaCell Line, TumorChemokine CCL2Gene ExpressionGene Expression ProfilingHumansImmunity, InnateInduced Pluripotent Stem CellsInflammationInterleukin-8NeuronsPhenotypeVirulenceWest Nile FeverWest Nile virusCCL2 protein, humanChemokine CCL2CXCL8 protein, humanInterleukin-8ArbovirusEncephalitisFlavivirusInflammationInnate immunityStem cell

Identifiers

PMID31664929
PMCPMC6819652

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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.