Evidence map›Paper›PMID 20949077›Full record

ArticlePLoS pathogens2010

Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.

Richard O Adeyemi, Sebastien Landry, Meredith E Davis, Matthew D Weitzman, David J Pintel

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

75 citing papers in PubMed, 121 citations in OpenAlex.

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15 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Richard O AdeyemiUniversity of Missouri-Columbia, School of Medicine, Columbia, Missouri, United States of America.
Sebastien Landry
Meredith E Davis
Matthew D Weitzman
David J Pintel
University of Missouri · USSalk Institute for Biological Studies · US

Funding

Viral Modulation of Genetic StabilityR01CA097093 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI WEITZMAN, MATTHEW D. · 2003 to 2019
$5.2M
Parvovirus RNA Processing and Gene Expression StrategiesR01AI046458 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI PINTEL, DAVID J. · 2000 to 2018
$4.6M
MOLECULAR &GENETIC ANALYSIS OF MVM GENE EXPRESSIONR01AI021302 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI PINTEL, DAVID J. · 1985 to 2008
$2.4M
INITIAL STEPS IN RAAV TRANSDUCTIONR01AI043341 · NIAID · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI WEITZMAN, MATTHEW D. · 2000 to 2003
$1.2M
Parvovirus RNA Processing and Gene Expression StrategiesR56AI046458 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI PINTEL, DAVID J. · 2013 to 2013
$374k
NCI NIH HHS CA97093NCI NIH HHS R01 CA097093NIAID NIH HHS AI21302NIAID NIH HHS AI43341NIAID NIH HHS AI46458NIAID NIH HHS R01 AI021302NIAID NIH HHS R01 AI046458NIAID NIH HHS R56 AI046458
6 · The paper itself

Abstract

Infection by DNA viruses can elicit DNA damage responses (DDRs) in host cells. In some cases the DDR presents a block to viral replication that must be overcome, and in other cases the infecting agent exploits the DDR to facilitate replication. We find that low multiplicity infection with the autonomous parvovirus minute virus of mice (MVM) results in the activation of a DDR, characterized by the phosphorylation of H2AX, Nbs1, RPA32, Chk2 and p53. These proteins are recruited to MVM replication centers, where they co-localize with the main viral replication protein, NS1. The response is seen in both human and murine cell lines following infection with either the MVMp or MVMi strains. Replication of the virus is required for DNA damage signaling. Damage response proteins, including the ATM kinase, accumulate in viral-induced replication centers. Using mutant cell lines and specific kinase inhibitors, we show that ATM is the main transducer of the signaling events in the normal murine host. ATM inhibitors restrict MVM replication and ameliorate virus-induced cell cycle arrest, suggesting that DNA damage signaling facilitates virus replication, perhaps in part by promoting cell cycle arrest. Thus it appears that MVM exploits the cellular DNA damage response machinery early in infection to enhance its replication in host cells.

Indexed as

DNA DamageAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCells, CulturedCHO CellsCricetinaeCricetulusDNA-Binding ProteinsDNA Repair EnzymesHumansMiceMinute Virus of MiceMRE11 Homologue ProteinParvoviridae InfectionsParvovirusAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsDNA Repair EnzymesMre11a protein, mouseMRE11 Homologue ProteinPhosphotransferasesProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID20949077
PMCPMC2951379
OpenAlexW2066647642

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.