Evidence map›Paper›PMID 17108037›Full record

ArticleJournal of virology2007

Variable deficiencies in the interferon response enhance susceptibility to vesicular stomatitis virus oncolytic actions in glioblastoma cells but not in normal human glial cells.

Guido Wollmann, Michael D Robek, Anthony N van den Pol

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

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  8. The brain parenchyma has a type I interferon response that can limit virus spread.Proceedings of the National Academy of Sciences of the United States of America · 2017
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  17. Interferon-β sensitivity of tumor cells correlates with poor response to VA7 virotherapy in mouse glioma models.Molecular therapy : the journal of the American Society of Gene Therapy · 2012
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  18. Inhibition of type I interferon-mediated antiviral action in human glioma cells by the IKK inhibitors BMS-345541 and TPCA-1.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2012
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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

3 authors at 1 institution in 1 country.

Guido WollmannDepartment of Neurosurgery, Yale University School of Medicine, 333 Cedar St., New Haven, CT 06520, USA.
Michael D Robek
Anthony N van den Pol
Yale University · US

Funding

Cytomegalovirus in the BrainR01AI048854 · NIAID · YALE UNIVERSITY · PI VAN DEN POL, ANTHONY N · 2001 to 2010
$3.8M
Modulation of HBV Replication by the ImmunoproteasomeK22AI064757 · NIAID · YALE UNIVERSITY · PI ROBEK, MICHAEL D · 2005 to 2006
$268k
NIAID NIH HHS AI48854NIAID NIH HHS K22 AI064757NIAID NIH HHS R01 AI048854
6 · The paper itself

Abstract

With little improvement in the poor prognosis for humans with high-grade glioma brain tumors, alternative therapeutic strategies are needed. As such, selective replication-competent oncolytic viruses may be useful as a potential treatment modality. Here we test the hypothesis that defects in the interferon (IFN) pathway could be exploited to enhance the selective oncolytic profile of vesicular stomatitis virus (VSV) in glioblastoma cells. Two green fluorescent protein-expressing VSV strains, recombinant VSV and the glioma-adapted recombinant VSV-rp30a, were used to study infection of a variety of human glioblastoma cell lines compared to a panel of control cells, including normal human astrocytes, oligodendrocyte precursor cells, and primary explant cultures from human brain tissue. Infection rate, cell viability, viral replication, and IFN-alpha/beta-related gene expression were compared in the absence and presence of IFN-alpha or polyriboinosinic polyribocytidylic acid [poly(I:C)], a synthetic inducer of the IFN-alpha/beta pathway. Both VSV strains caused rapid and total infection and death of all tumor cell lines tested. To a lesser degree, normal cells were also subject to VSV infection. In contrast, IFN-alpha or poly(I:C) completely attenuated the infection of all primary control brain cells, whereas most glioblastoma cell lines treated with IFN-alpha or poly(I:C) showed little or no sign of protection and were killed by VSV. Together, our results demonstrate that activation of the interferon pathway protects normal human brain cells from VSV infection while maintaining the vulnerability of human glioblastoma cells to viral destruction.

Indexed as

Cell LineGlioblastomaHumansInterferonsNeurogliaOncolytic VirusesVesicular stomatitis Indiana virusVirus ReplicationInterferons

Identifiers

PMID17108037
PMCPMC1797501
OpenAlexW2144015889

What OpenQuestion holds

Textmetadata
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.