Evidence map›Paper›PMID 26703877›Full record

ArticleJournal of neuroinflammation2015

Interferon-stimulated genes-essential antiviral effectors implicated in resistance to Theiler's virus-induced demyelinating disease.

Lin Li, Reiner Ulrich, Wolfgang Baumgärtner, Ingo Gerhauser

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. 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
0.6field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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  10. Rapid Expansion of Virus-Specific CD4International journal of molecular sciences · 2020
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  15. Animal Models of Zika Virus.Comparative medicine · 2017
    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

4 authors at 1 institution in 1 country.

Lin LiDepartment of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559, Hannover, Germany. Lin.Li@tiho-hannover.de.
Reiner UlrichDepartment of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559, Hannover, Germany. Reiner.Ulrich@fli.bund.de.
Wolfgang BaumgärtnerDepartment of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559, Hannover, Germany. Wolfgang.Baumgaertner@tiho-hannover.de.
Ingo GerhauserDepartment of Pathology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559, Hannover, Germany. Ingo.Gerhauser@tiho-hannover.de.
University of Veterinary Medicine Hannover, Foundation · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExperimental infection of mice with Theiler's murine encephalomyelitis virus (TMEV) is used as an animal model of human multiple sclerosis. TMEV persists in susceptible mouse strains and causes a biphasic disease consisting of acute polioencephalomyelitis and chronic demyelinating leukomyelitis. In contrast, resistant mice eliminate the virus within 2 to 4 weeks, which seems to be based on a strong antiviral innate immune response including the activation of the type I interferon (IFN) pathway. Several interferon-stimulated genes (ISGs) such as IFN-stimulated protein of 15 kDa (ISG15), protein kinase R (PKR), and 2'5'-oligoadenylate synthetase (OAS) function as antiviral effectors and might contribute to virus elimination. Nevertheless, detailed investigations of the type I IFN pathway during TMEV-induced demyelinating disease (TMEV-IDD) are lacking.

methodsThe present study evaluated microarray data of the spinal cord obtained from susceptible SJL/J mice after TMEV infection focusing on IFN-related genes. Moreover, ISG gene and protein expression was determined in mock- and TMEV-infected SJL/J mice and compared to its expression in resistant C57BL/6 mice using real- time PCR, immunohistochemistry, and immunofluorescence.

resultsInterestingly, despite of increased ISG gene expression during TMEV-IDD, ISG protein expression was impaired in SJL/J mice and mainly restricted to demyelinated lesions. In contrast, high ISG protein levels were found in spinal cord gray and white matter of C57BL/6 compared to SJL/J mice in the acute and chronic phase of TMEV-IDD. In both mouse strains, ISG15 was mainly found in astrocytes and endothelial cells, whereas PKR was predominantly expressed by microglia/macrophages, oligodendrocytes, and neurons. Only few cells were immunopositive for OAS proteins.

conclusionsHigh levels of antiviral ISG15 and PKR proteins in the spinal cord of C57BL/6 mice might block virus replication and play an important role in the resistance to TMEV-IDD.

Indexed as

AnimalsCardiovirus InfectionsCytokinesDisease Models, AnimalDisease ResistanceeIF-2 KinaseFemaleFluorescent Antibody TechniqueImmunity, InnateImmunohistochemistryInterferon Type IMiceMice, Inbred C57BLMultiple SclerosisOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionCytokineseIF-2 KinaseG1p2 protein, mouseInterferon Type Iprotein kinase R, mouseUbiquitins

Identifiers

PMID26703877
PMCPMC4690264
OpenAlexW2232435607

What OpenQuestion holds

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LicenceCC BY
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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.