Evidence map›Paper›PMID 18382670›Full record

ArticlePloS one2008

Different effect of proteasome inhibition on vesicular stomatitis virus and poliovirus replication.

Nickolay Neznanov, Eugenia M Dragunsky, Konstantin M Chumakov, Lubov Neznanova, Ronald C Wek, Andrei V Gudkov, Amiya K Banerjee

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

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  14. The eIF2α kinases: their structures and functions.Cellular and molecular life sciences : CMLS · 2013
    Review
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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

7 authors at 5 institutions in 1 country.

Nickolay NeznanovDepartment of Molecular Genetics, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, United States of America. neznann@ccf.org
Eugenia M Dragunsky
Konstantin M Chumakov
Lubov Neznanova
Ronald C Wek
Andrei V Gudkov
Amiya K Banerjee
Center for Biologics Evaluation and Research · USCleveland Clinic · USCleveland BioLabs (United States) · USCleveland Clinic Lerner College of Medicine · USIndiana University – Purdue University Indianapolis · US

Funding

GENE EXPRESSION OF NEGATIVE STRAND RNA VIRUSESR01AI026585 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI BANERJEE, AMIYA K. · 1988 to 2009
$3.6M
GENETIC ELEMENTS TRANSFORMING MOUSE FIBROBLASTSR01CA060730 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GUDKOV, ANDREI V · 1994 to 2009
$2.6M
STRESS INDUCED BYSTANDER EFFECT IN CANCER TREATMENTR01CA088071 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GUDKOV, ANDREI V · 2000 to 2004
$1.4M
NCI NIH HHS CA60730NCI NIH HHS CA88071NCI NIH HHS R01 CA060730NCI NIH HHS R01 CA088071NIAID NIH HHS AI26585NIAID NIH HHS R01 AI026585
6 · The paper itself

Abstract

Proteasome activity is an important part of viral replication. In this study, we examined the effect of proteasome inhibitors on the replication of vesicular stomatitis virus (VSV) and poliovirus. We found that the proteasome inhibitors significantly suppressed VSV protein synthesis, virus accumulation, and protected infected cells from toxic effect of VSV replication. In contrast, poliovirus replication was delayed, but not diminished in the presence of the proteasome inhibitors MG132 and Bortezomib. We also found that inhibition of proteasomes stimulated stress-related processes, such as accumulation of chaperone hsp70, phosphorylation of eIF2alpha, and overall inhibition of translation. VSV replication was sensitive to this stress with significant decline in replication process. Poliovirus growth was less sensitive with only delay in replication. Inhibition of proteasome activity suppressed cellular and VSV protein synthesis, but did not reduce poliovirus protein synthesis. Protein kinase GCN2 supported the ability of proteasome inhibitors to attenuate general translation and to suppress VSV replication. We propose that different mechanisms of translational initiation by VSV and poliovirus determine their sensitivity to stress induced by the inhibition of proteasomes. To our knowledge, this is the first study that connects the effect of stress induced by proteasome inhibition with the efficiency of viral infection.

Indexed as

Proteasome InhibitorsVirus ReplicationBoronic AcidsBortezomibDNADNA ReplicationEukaryotic Initiation Factor-2HeLa CellsHumansLeupeptinsModels, BiologicalPoliovirusProteasome Endopeptidase ComplexPyrazinesTransfectionVesiculovirusbenzyloxycarbonylleucyl-leucyl-leucine aldehydeBoronic AcidsBortezomibDNAEukaryotic Initiation Factor-2LeupeptinsProteasome Endopeptidase ComplexProteasome InhibitorsPyrazinesViral Proteins

Identifiers

PMID18382670
PMCPMC2268745
OpenAlexW2044105820

What OpenQuestion holds

Textmetadata
LicenceCC0
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.