Evidence map›Paper›PMID 24839861›Full record

ReviewAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2014

New cell-signaling pathways for controlling cytomegalovirus replication.

S Roy, R Arav-Boger

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Does human cytomegalovirus provide a novel therapeutic target for patients with glioblastoma?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  5. Review
  6. Article
  7. Anti-CMV therapy, what next? A systematic review.Frontiers in microbiology · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Inflammasome expression and cytomegalovirus viremia in critically ill patients with sepsis.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2017
    Observational
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

S RoyDepartment of Pediatrics, Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD.
R Arav-Boger
Johns Hopkins Medicine · US

Funding

Novel Artemisinin Derivatives for Cytomegalovirus TherapyR01AI093701 · NIAID · JOHNS HOPKINS UNIVERSITY · PI BOGER, RAVIT · 2011 to 2015
$2.0M
NIAID NIH HHS 1R01AI093701NIAID NIH HHS R01 AI093701
6 · The paper itself

Abstract

Cytomegalovirus (CMV) is increasingly recognized as an accomplished modulator of cell-signaling pathways, both directly via interaction between viral and cellular proteins, and indirectly by activating metabolic/energy states of infected cells. Viral genes, as well as captured cellular genes, enable CMV to modify these pathways upon binding to cellular receptors, up until generation of virus progeny. Deregulation of cell-signaling pathways appears to be a well-developed tightly balanced virus strategy to achieve the desired consequences in each infected cell type. Importantly and perhaps surprisingly, identification of new signaling pathways in cancer cells positioned CMV as a sophisticated user and abuser of many such pathways, creating opportunities to develop novel therapeutic strategies for inhibiting CMV replication (in addition to standard of care CMV DNA polymerase inhibitors). Advances in genomics and proteomics allow the identification of CMV products interacting with the cellular machinery. Ultimately, clinical implementation of candidate drugs capable of disrupting the delicate balance between CMV and cell-signaling will depend on the specificity and selectivity index of newly identified targets.

Indexed as

Signal TransductionVirus ReplicationAdenylate KinaseAtaxia Telangiectasia Mutated ProteinsCytomegalovirusDNA DamageHumansProteolysisTOR Serine-Threonine KinasesUbiquitinUnfolded Protein ResponseWnt ProteinsAdenylate KinaseAtaxia Telangiectasia Mutated ProteinsATM protein, humanMTOR protein, humanTOR Serine-Threonine KinasesUbiquitinWnt ProteinsAMPKATMCMVmTORsignal transductionWnt

Identifiers

PMID24839861
PMCPMC4280670
OpenAlexW1561301488

What OpenQuestion holds

Textmetadata
LicenceTDM
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.