Evidence map›Paper›PMID 20573816›Full record

ArticleJournal of virology2010

Activation of the interferon response by human cytomegalovirus occurs via cytoplasmic double-stranded DNA but not glycoprotein B.

Victor R DeFilippis, Tina Sali, David Alvarado, Laura White, Wade Bresnahan, Klaus J Früh

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. ZBP1 and heatstroke.Frontiers in immunology · 2023
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Cytomegalovirus immune evasion of myeloid lineage cells.Medical microbiology and immunology · 2015
    Review
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Victor R DeFilippisOregon Health and Science University, Vaccine and Gene Therapy Institute, Portland, Oregon 97006, USA. defilipp@ohsu.edu
Tina Sali
David Alvarado
Laura White
Wade Bresnahan
Klaus J Früh
Oregon Health & Science University · USUniversity of Minnesota · US

Funding

Modulation of Innate Immune Responses by CytomegalovirusR01AI070890 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI FRUH, KLAUS J · 2008 to 2012
$2.4M
Functional Analysis of Cytomegalovirus Tegument ProteinsR01AI059340 · NIAID · UNIVERSITY OF MINNESOTA · PI BRESNAHAN, WADE A · 2006 to 2010
$1.4M
NIAID NIH HHS R01 AI059340NIAID NIH HHS R01 AI070890NIAID NIH HHS R01AI070890
6 · The paper itself

Abstract

In vitro infection of cells with the betaherpesvirus human cytomegalovirus (HCMV) stimulates an innate immune response characterized by phosphorylation of the transcription factor interferon regulatory factor 3 (IRF3) and subsequent expression of IRF3-dependent genes. While previous work suggests that HCMV envelope glycoprotein B is responsible for initiating this reaction, the signaling pathways stimulated by virus infection that lead to IRF3 phosphorylation have largely been uncharacterized. Recently, we identified Z DNA binding protein 1 (ZBP1), a sensor of cytoplasmic DNA, as an essential protein for this response. We now describe a human fibroblast cell line exhibiting a recessive defect that results in the absence of activation of IRF3 following treatment with HCMV but not Sendai virus or double-stranded RNA. In addition, we show that while exposure of these cells to soluble HCMV glycoprotein B is capable of triggering IRF3-dependent gene transcription, transfection of the cells with double-stranded DNA is not. Furthermore, we show that overexpression of ZBP1 in these cells reestablishes their ability to secrete interferon in response to HCMV and that multiple ZBP1 transcriptional variants exist in both wild-type and mutant cells. These results have two major implications for the understanding of innate immune stimulation by HCMV. First, they demonstrate that HCMV glycoprotein B is not the essential molecular pattern that induces an IRF3-dependent innate immune response. Second, IRF3-terminal signaling triggered by HCMV particles closely resembles that which is activated by cytoplasmic double-stranded DNA.

Indexed as

Cell LineCytomegalovirusCytomegalovirus InfectionsCytoplasmDNAHumansInterferon-betaInterferon Regulatory Factor-3PhosphorylationProtein TransportViral Envelope ProteinsDNAInterferon-betaInterferon Regulatory Factor-3Viral Envelope Proteins

Identifiers

PMID20573816
PMCPMC2919031
OpenAlexW2102875889

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.