Evidence map›Paper›PMID 14671101›Full record

ArticleJournal of virology2004

Evasion of cellular antiviral responses by human cytomegalovirus TRS1 and IRS1.

Stephanie J Child, Morgan Hakki, Katherine L De Niro, Adam P Geballe

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

94 citing papers in PubMed, 139 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Antagonism of Protein Kinase R by Large DNA Viruses.Pathogens (Basel, Switzerland) · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. The integrated stress response in pulmonary disease.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  14. Article
  15. 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
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

34 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

4 authors at 2 institutions in 1 country.

Stephanie J ChildDivisions of Human Biology and Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA.
Morgan Hakki
Katherine L De Niro
Adam P Geballe
University of Washington · USFred Hutch Cancer Center · US

Funding

TRANSLATIONAL CONTROL OF CYTOMEGALOVIRUS GENE EXPRESSIONR01AI026672 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GEBALLE, ADAM P. · 1994 to 2017
$6.9M
Translational Control of Cytomegalovirus Gene ExpressionR56AI026672 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GEBALLE, ADAM P. · 2018 to 2018
$440k
TRANSLATIONAL CONTROL OF CYTOMEGALOVIRUS GENE EXPRESSIONR29AI026672 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GEBALLE, ADAM P. · 1988 to 1992
–
NIAID NIH HHS AI26672NIAID NIH HHS R01 AI026672NIAID NIH HHS R56 AI026672
6 · The paper itself

Abstract

During infection with human cytomegalovirus (HCMV), cellular protein synthesis continues even as viral proteins are being synthesized in abundance. Thus, HCMV may have a mechanism for counteracting host cell antiviral pathways that act by shutting off translation. Consistent with this view, HCMV infection of human fibroblasts rescues the replication of a vaccinia virus mutant lacking the double-stranded RNA-binding protein gene E3L (VVdeltaE3L). HCMV also prevents the phosphorylation of the eukaryotic translation initiation factor eIF-2alpha, the activation of RNase L, and the shutoff of viral and cellular protein synthesis that otherwise result from VVdeltaE3L infection. To identify the HCMV gene(s) responsible for these effects, we prepared a library of VVdeltaE3L recombinants containing HCMV genomic fragments. By infecting nonpermissive cells with this library and screening for VV gene expression and replication, we isolated a virus containing a 2.8-kb HCMV fragment that rescues replication of VVdeltaE3L. The fragment comprises the 3' end of the J1S open reading frame through the entire TRS1 gene. Analyses of additional VVdeltaE3L recombinants revealed that the protein encoded by TRS1, pTRS1, as well as the closely related IRS1 gene, rescues VVdeltaE3L replication and prevent the shutoff of protein synthesis, the phosphorylation of eIF-2alpha, and activation of RNase L. These results demonstrate that TRS1 and IRS1 are able to counteract critical host cell antiviral response pathways.

Indexed as

AnimalsCell LineCricetinaeCytomegalovirusEndoribonucleasesEnzyme ActivationEukaryotic Initiation Factor-2HumansNucleotidyltransferasesProteinsRecombination, GeneticRNA-Binding ProteinsVaccinia virusViral ProteinsVirus Replication2-5A-dependent ribonucleaseE3L protein, Vaccinia virusEndoribonucleasesEukaryotic Initiation Factor-2NucleotidyltransferasesProteinsRNA-Binding ProteinsTRS1 protein, Human herpesvirus 5Viral Proteins

Identifiers

PMID14671101
PMCPMC303427
OpenAlexW2102032614

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.