Evidence map›Paper›PMID 10207084›Full record

ArticleMolecular and cellular biology1999

Engagement of the cellular receptor for glycoprotein B of human cytomegalovirus activates the interferon-responsive pathway.

K A Boyle, R L Pietropaolo, T Compton

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

101 citing papers in PubMed, 201 citations in OpenAlex.

  1. Trial
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  11. Human cytomegalovirus induces and exploits Roquin to counteract the IRF1-mediated antiviral state.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Article
  13. Single-Cell Transcriptome Analysis of CD34Frontiers in microbiology · 2019
    Article
  14. Article
  15. Article
  16. Article
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  18. Review
  19. Article
  20. Human cytomegalovirus activation of ERK and myeloid cell leukemia-1 protein correlates with survival of latently infected cells.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article

41 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

3 authors at 1 institution in 1 country.

K A BoyleDepartment of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin 53706-1532, USA.
R L Pietropaolo
T Compton
University of Wisconsin–Madison · US

Funding

Role of Glycoprotein B in HCMV infectionR01AI034998 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI KALEJTA, ROBERT F · 1995 to 2010
$2.8M
NIAID NIH HHS R01 AI034998NIAID NIH HHS R01 AI-34998
6 · The paper itself

Abstract

Cells respond to contact with human cytomegalovirus (HCMV) virions by initiating intracellular signaling and gene expression characteristic of the interferon (IFN)-responsive pathway. Herein, we demonstrate that a principal mechanism of HCMV-induced signal transduction is via an interaction of the primary viral ligand, glycoprotein B (gB), with its cellular receptor. Cells incubated with a purified, soluble form of gB resulted in the transcriptional upregulation of IFN-responsive genes OAS and ISG54 (encoding 2'-5' oligoadenylate synthetase and an IFN-stimulated gene product of 54 kDa) to a comparable level as virions or IFN. Gene induction was an immediate and direct response to gB which did not require de novo protein synthesis. Neither the initial virus attachment site, heparan sulfate proteoglycans, nor the IFN-alpha/beta or IFN-gamma receptors are involved in the response. Pleotropic protein phosphorylation was required for cellular gene induction, and the mitogen-activated protein kinases ERK1 and ERK2 were activated in response to the ligand. Together these data indicate that a principal means by which cytomegalovirus induces intracellular signaling and activation of the interferon-responsive pathway is via an interaction of gB with an as yet unidentified, likely novel cellular receptor that interfaces with the IFN signaling pathway.

Indexed as

2',5'-Oligoadenylate SynthetaseCalcium-Calmodulin-Dependent Protein KinasesCell LineGene Expression RegulationHeparan SulfateHumansInterferonsPhosphorylationProtein DenaturationReceptors, Cell SurfaceRNA, MessengerSignal TransductionTranscriptional ActivationUp-RegulationViral Envelope ProteinsViral Proteins2',5'-Oligoadenylate SynthetaseCalcium-Calmodulin-Dependent Protein Kinasesglycoprotein B, SimplexvirusHeparan SulfateInterferonsReceptors, Cell SurfaceRNA, MessengerViral Envelope ProteinsViral Proteins

Identifiers

PMID10207084
PMCPMC84158
OpenAlexW2114739240

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.