Evidence map›Paper›PMID 23055562›Full record

ArticleJournal of virology2012

Infection of vascular endothelial cells with human cytomegalovirus under fluid shear stress reveals preferential entry and spread of virus in flow conditions simulating atheroprone regions of the artery.

Jenny B DuRose, Julie Li, Shu Chien, Deborah H Spector

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  8. RNA-binding protein CPEB1 remodels host and viral RNA landscapes.Nature structural & molecular biology · 2016
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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

4 authors at 2 institutions in 1 country.

Jenny B DuRoseDepartment of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, California, USA.
Julie Li
Shu Chien
Deborah H Spector
University of California, San Diego · USLa Jolla Bioengineering Institute · US

Funding

Shear Regulation of MicroRNA Transportomes and Targetomes in Vascular HomeostasisR01HL106579 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, SHYY, JOHN YJ · 2011 to 2022
$8.3M
Human Cytomegalovirus Gene ExpressionR01CA034729 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SPECTOR, DEBORAH HYE · 1985 to 2011
$4.8M
Atherosclerosis: Cytomegalovirus, Shear Stress, and Endothelial CellsR21AI094180 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SPECTOR, DEBORAH HYE · 2011 to 2012
$408k
Vessel Shear Stress & Cytomegalovirus Disease: Molecular Basis of AtherosclerosisF32HL099072 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DUROSE, JENNY B · 2010 to 2013
$154k
NCI NIH HHS R01 CA034729NCI NIH HHS R01CA034729NCI NIH HHS T32 CA009532NHLBI NIH HHS F32 HL099072NHLBI NIH HHS R01 HL106579NHLBI NIH HHS R01HL106579NIAID NIH HHS R21 AI094180NIAID NIH HHS R21AI094180
6 · The paper itself

Abstract

Atherosclerosis is a major pathogenic factor in cardiovascular diseases, which are the leading cause of mortality in developed countries. While risk factors for atherosclerosis tend to be systemic, the distribution of atherosclerotic plaques within the vasculature is preferentially located at branch points and curves where blood flow is disturbed and shear stress is low. It is now widely accepted that hemodynamic factors can modulate endothelial gene expression and function and influence the pathophysiological changes associated with atherosclerosis. Human cytomegalovirus (HCMV), a ubiquitous pathogen, has long been proposed as a risk factor for atherosclerosis. To date, the role of HCMV in atherogenesis has been explored only in static conditions, and it is not known how HCMV infection is influenced by the physiological context of flow. In this study, we utilized a parallel-plate flow system to simulate the effects of shear stresses in different regions of the vasculature in vitro. We found that endothelial cells cultured under low shear stress, which simulates the flow condition of atheroprone regions in vivo, are more permissive to HCMV infection than cells experiencing high shear stress or static conditions. Cells exposed to low shear stress show increased entry of HCMV compared to cells exposed to high shear stress or static conditions. Viral structural gene expression, viral titers, and viral spread are also enhanced in endothelial cells exposed to low shear stress. These results suggest that hemodynamic factors modulate HCMV infection of endothelial cells, thus providing new insights into the induction/acceleration of atherosclerosis by HCMV.

Indexed as

Membrane FusionArteriesBase SequenceBlotting, WesternCells, CulturedCytomegalovirusDNA PrimersDNA, ViralEndothelium, VascularFluorescent Antibody TechniqueGene Expression Regulation, ViralGenes, ViralHumansMicroscopy, Electron, TransmissionPolymerase Chain ReactionDNA PrimersDNA, Viral

Identifiers

PMID23055562
PMCPMC3503096
OpenAlexW2026239217

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.