Evidence map›Paper›PMID 16699040›Full record

ArticleJournal of virology2006

Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation.

Michael A Jarvis, Jamie A Borton, Amy M Keech, John Wong, William J Britt, Bruce E Magun, Jay A Nelson

Abstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
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

47 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Deletion of the non-adjacent genesFrontiers in immunology · 2023
    Article
  5. Article
  6. Article
  7. TheCells · 2021
    Article
  8. Article
  9. Review
  10. MicroRNA Involvement in Signaling Pathways During Viral Infection.Frontiers in cell and developmental biology · 2020
    Review
  11. UJournal of virology · 2019
    Article
  12. Article
  13. 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
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

7 authors.

Michael A JarvisVaccine and Gene Therapy Institute, Oregon Health Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA. jarvismi@ohsu.edu
Jamie A Borton
Amy M Keech
John Wong
William J Britt
Bruce E Magun
Jay A Nelson

Funding

MOLECULAR ASPECTS OF CYTOMEGALOVIRUS LATENCYR01AI021640 · NIAID · UNIVERSITY OF GUELPH · PI Meaghan H Hancock · 1985 to 2026
$8.1M
ENVELOPE ASSEMBLY OF HUMAN CYTOMEGALOVIRUSR01AI035602 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRITT, WILLIAM JARVIS · 1995 to 2018
$4.5M
Molecular Aspects of Cytomegalovirus LatencyR37AI021640 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI HANCOCK, MEAGHAN H · 2018 to 2024
$4.0M
INFLAMMATORY RESPONSES IN THE TOXICITY OF RICINR01AI059335 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI MAGUN, BRUCE E. · 2004 to 2009
$1.9M
Inflammatory mechanisms in the toxicity of ricinR56AI059335 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI MAGUN, BRUCE E. · 2010 to 2010
$385k
NIAID NIH HHS AI 059335NIAID NIH HHS AI 21640NIAID NIH HHS AI 35602NIAID NIH HHS R01 AI021640NIAID NIH HHS R01 AI035602NIAID NIH HHS R37 AI021640
6 · The paper itself

Abstract

Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. The effect on these pathways was limited to cells infected with the virus, occurred at late times of infection, and was independent of cell type or virus strain. IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. We believe that the ability of HCMV to inhibit these two major proinflammatory pathways reveals a critical aspect of HCMV biology, with possible importance for immune evasion, as well as establishment of infection in cell types persistently infected by this virus.

Indexed as

CytomegalovirusHumansInterleukin-1betaNF-kappa BSignal TransductionTumor Cells, CulturedTumor Necrosis Factor-alphaInterleukin-1betaNF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID16699040
PMCPMC1472148

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.