Evidence map›Paper›PMID 20158406›Full record

ArticleJournal of neurovirology2010

Gene expression in the brain during reovirus encephalitis.

Kenneth L Tyler, J Smith Leser, Tzu L Phang, Penny Clarke

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurovirology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Kenneth L TylerDepartment of Neurology, University of Colorado-Denver, Anschutz Medical Campus, Aurora, Colorado, USA.
J Smith Leser
Tzu L Phang
Penny Clarke
University of Colorado Anschutz Medical Campus · USUniversity of Colorado Denver · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR025780 · NCRR · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2008 to 2011
$61.3M
Cellular genes and signaling pathways as therapeutic targets for virus-induced CNR01NS076512 · NINDS · UNIVERSITY OF COLORADO DENVER · PI TYLER, KENNETH L. · 2011 to 2014
$1.4M
Mechanisms of Apoptosis in the central nervous systemR01NS050138 · NINDS · UNIVERSITY OF COLORADO DENVER · PI TYLER, KENNETH L. · 2005 to 2009
$1.3M
Mechanisms of virus-induced apoptosis in neurons and CNSR01NS051403 · NINDS · UNIVERSITY OF COLORADO DENVER · PI TYLER, KENNETH L. · 2006 to 2010
$1.2M
NCRR NIH HHS RR025780NCRR NIH HHS UL1 RR025780NINDS NIH HHS 5R01NS050138NINDS NIH HHS 5R01NS051403NINDS NIH HHS R01 NS050138NINDS NIH HHS R01 NS051403NINDS NIH HHS R01 NS076512
6 · The paper itself

Abstract

Viral encephalitis remains a significant cause of morbidity and mortality throughout the world. We performed microarray analysis to identify genes and pathways that are differentially regulated during reovirus encephalitis and that may provide novel therapeutic targets for virus-induced diseases of the central nervous system (CNS). An increase in the expression of 130 cellular genes was found in the brains of reovirus-infected mice at early times post infection, compared to mock-infected controls. The up-regulation of these genes was consistent with activation of innate immune responses, particularly interferon signaling. At later times post infection, when significant CNS injury is present and mice exhibit signs of severe neurologic disease, many more (1374) genes were up-regulated, indicating that increased gene expression correlates with disease pathology. Virus-induced gene expression at late times post infection was again consistent with the activation of innate immune responses. However, additional significant pathways included those associated with cytokine signaling and apoptosis, both of which can contribute to CNS injury. This is the first report comparing virus-induced cellular gene and pathway regulation at early and late times following virus infection of the brain. The shift of virus-induced gene expression from innate immune responses at early times post infection to cytokine signaling and apoptosis at later times suggests a potential therapeutic strategy that preserves early protective responses whilst inhibiting later responses that contribute to pathogenesis.

Indexed as

Gene Expression RegulationReoviridaeAnimalsApoptosisBrainCaspases, EffectorCell LineDisease ProgressionEncephalitis, ViralGene Expression ProfilingHumansImmunity, InnateInterferon Regulatory FactorsInterferonsMiceNF-kappa BCaspases, EffectorInterferon Regulatory FactorsInterferonsNF-kappa BStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID20158406
PMCPMC2891017
OpenAlexW2130807481

What OpenQuestion holds

Textmetadata
LicenceTDM
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.