Evidence map›Paper›PMID 34663377›Full record

ReviewVirology journal2021

Modulation of host cell signaling during cytomegalovirus latency and reactivation.

Nicholas A Smith, Gary C Chan, Christine M O'Connor

Open access · goldAbstract readReview
In one paragraph

Review in Virology journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Human cytomegalovirus and neonatal infection.Current research in microbial sciences · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Hematopoietic stem cells and betaherpesvirus latency.Frontiers in cellular and infection microbiology · 2023
    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

3 authors at 2 institutions in 1 country.

Nicholas A SmithDepartment of Microbiology & Immunology, SUNY Upstate Medical University, Syracuse, NY, 13210, USA.
Gary C ChanDepartment of Microbiology & Immunology, SUNY Upstate Medical University, Syracuse, NY, 13210, USA. ChanG@upstate.edu.
Christine M O'ConnorDepartment of Genomic Medicine, Infection Biology Program, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA. oconnoc6@ccf.org.ORCID 0000-0003-4943-3774
SUNY Upstate Medical University · USCleveland Clinic Lerner College of Medicine · US

Funding

Novel Anti-HCMV StrategiesR01HL139824 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI CHAN, GARY CHING TAO · 2018 to 2021
$3.0M
Mechanisms of HCMV-induced monocyte-to-macrophage differentiation.R01AI141460 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI CHAN, GARY CHING TAO · 2019 to 2023
$2.7M
Manipulation of host factors that promote HCMV latencyR01AI150931 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI O'CONNOR, CHRISTINE M · 2021 to 2025
$2.4M
HCMV GPCR functions during latency and reactivationR01AI153348 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI O'CONNOR, CHRISTINE M · 2021 to 2025
$2.2M
NHLBI NIH HHS R01 HL139824NIAID NIH HHS R01 AI141460NIAID NIH HHS R01 AI150931NIAID NIH HHS R01 AI153348
6 · The paper itself

Abstract

backgroundHuman cytomegalovirus (HCMV) resides latently in cells of the myeloid compartment, including CD34 MAIN BODY: To establish and maintain latency, HCMV has evolved various means by which it usurps host cell factors to alter the cellular environment to its own advantage, including altering host cell signaling cascades. As early as virus entry into myeloid cells, HCMV usurps cellular signaling to change the cellular milieu, and this regulation includes upregulation, as well as downregulation, of different signaling cascades. Indeed, given proper reactivation cues, this signaling is again altered to allow for transactivation of viral lytic genes.

conclusionsHCMV modulation of host cell signaling is not binary, and many of the cellular pathways altered are finely regulated, wherein the slightest modification imparts profound changes to the cellular milieu. It is also evident that viral-mediated cell signaling differs not only between these phases of infection, but also is myeloid cell type specific. Nonetheless, understanding the exact pathways and the means by which HCMV mediates them will undoubtedly provide novel targets for therapeutic intervention.

Indexed as

CytomegalovirusVirus LatencyCells, CulturedHost-Pathogen InteractionsSignal TransductionCD34+ HPCsCell signalingCytomegalovirusHCMVLatencyMonocytesReactivation

Identifiers

PMID34663377
PMCPMC8524946
OpenAlexW3206086754

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.