Evidence map›Paper›PMID 26447351›Full record

ArticleScientific reports2015

The antiviral drug ganciclovir does not inhibit microglial proliferation and activation.

Thomas Skripuletz, Laura Salinas Tejedor, Chittappen K Prajeeth, Florian Hansmann, Chintan Chhatbar, Valeria Kucman, Ning Zhang, Barbara B Raddatz, Claudia N Detje, Kurt-Wolfram Sühs and 5 more

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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

15 authors.

Thomas SkripuletzDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Laura Salinas TejedorDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Chittappen K PrajeethDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Florian HansmannCenter for Systems Neuroscience, Hannover, Germany.
Chintan ChhatbarInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research; a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.
Valeria KucmanDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Ning ZhangCenter for Systems Neuroscience, Hannover, Germany.
Barbara B RaddatzCenter for Systems Neuroscience, Hannover, Germany.
Claudia N DetjeInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research; a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.
Kurt-Wolfram SühsDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Refik PulDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Viktoria GudiDepartment of Neurology, Hannover Medical School, Hannover, Germany.
Ulrich KalinkeInstitute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research; a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.
Wolfgang BaumgärtnerCenter for Systems Neuroscience, Hannover, Germany.
Martin StangelDepartment of Neurology, Hannover Medical School, Hannover, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ganciclovir is effective in the treatment of human infections with viruses of the Herpesviridae family. Beside antiviral properties, recently ganciclovir was described to inhibit microglial proliferation and disease severity of experimental autoimmune encephalomyelitis, an inflammatory model of multiple sclerosis. Microglial activation and proliferation are main characteristics of neuroinflammatory CNS diseases and inhibition of microglial functions might be beneficial in autoimmune diseases, or detrimental in infectious diseases. The objective of this study was to determine potential inhibitory effects of ganciclovir in three different murine animal models of CNS neuroinflammation in which microglia play an important role: Theiler´s murine encephalomyelitis, the cuprizone model of de- and remyelination, and the vesicular stomatitis virus encephalitis model. In addition, in vitro experiments with microglial cultures were performed to test the hypothesis that ganciclovir inhibits microglial proliferation. In all three animal models, neither microglial proliferation or recruitment nor disease activity was changed by ganciclovir. In vitro experiments confirmed that microglial proliferation was not affected by ganciclovir. In conclusion, our results show that the antiviral drug ganciclovir does not inhibit microglial activation and proliferation in the murine CNS.

Indexed as

AnimalsAnimals, NewbornAntiviral AgentsBrainCell ProliferationCells, CulturedCuprizoneDemyelinating DiseasesDisease Models, AnimalEncephalomyelitisGanciclovirHost-Pathogen InteractionsHumansImmunohistochemistryMacrophage ActivationMice, Inbred C57BLAntiviral AgentsCuprizoneGanciclovir

Identifiers

PMID26447351
PMCPMC4597339

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.