Evidence map›Paper›PMID 23716573›Full record

ArticlemBio2013

Human embryonic stem cell lines model experimental human cytomegalovirus latency.

Rhiannon R Penkert, Robert F Kalejta

Open access · goldAbstract read
In one paragraph

Article in mBio, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Using 2D and 3D pluripotent stem cell models to study neurotropic viruses.Frontiers in virology (Lausanne, Switzerland) · 2022
    Article
  6. CD34Journal of virology · 2021
    Article
  7. Review
  8. Control of Cytokines in Latent Cytomegalovirus Infection.Pathogens (Basel, Switzerland) · 2020
    Review
  9. Review
  10. Expanding the Known Functional Repertoire of the Human Cytomegalovirus pp71 Protein.Frontiers in cellular and infection microbiology · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Human cytomegalovirus G protein-coupled receptor US28 promotes latency by attenuating c-fos.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Intestinal organoid as anFrontiers in biology · 2017
    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

2 authors at 1 institution in 1 country.

Rhiannon R PenkertInstitute for Molecular Virology and McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Robert F Kalejta
University of Wisconsin–Madison · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
Role of Daxx degradation by pp71 during the Human Cytomegalovirus life cycleR01AI074984 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI KALEJTA, ROBERT F · 2008 to 2018
$3.5M
NCI NIH HHS P30 CA014520NIAID NIH HHS AI074984NIAID NIH HHS R01 AI074984
6 · The paper itself

Abstract

Herpesviruses are highly successful pathogens that persist for the lifetime of their hosts primarily because of their ability to establish and maintain latent infections from which the virus is capable of productively reactivating. Human cytomegalovirus (HCMV), a betaherpesvirus, establishes latency in CD34(+) hematopoietic progenitor cells during natural infections in the body. Experimental infection of CD34(+) cells ex vivo has demonstrated that expression of the viral gene products that drive productive infection is silenced by an intrinsic immune defense mediated by Daxx and histone deacetylases through heterochromatinization of the viral genome during the establishment of latency. Additional mechanistic details about the establishment, let alone maintenance and reactivation, of HCMV latency remain scarce. This is partly due to the technical challenges of CD34(+) cell culture, most notably, the difficulty in preventing spontaneous differentiation that drives reactivation and renders them permissive for productive infection. Here we demonstrate that HCMV can establish, maintain, and reactivate in vitro from experimental latency in cultures of human embryonic stem cells (ESCs), for which spurious differentiation can be prevented or controlled. Furthermore, we show that known molecular aspects of HCMV latency are faithfully recapitulated in these cells. In total, we present ESCs as a novel, tractable model for studies of HCMV latency.

Indexed as

Host-Pathogen InteractionsVirus LatencyAdaptor Proteins, Signal TransducingAntigens, CD34Cell Culture TechniquesChromatinCo-Repressor ProteinsCytomegalovirusEmbryonic Stem CellsGene SilencingHistone DeacetylasesHumansMolecular ChaperonesNuclear ProteinsVirologyAdaptor Proteins, Signal TransducingAntigens, CD34ChromatinCo-Repressor ProteinsDAXX protein, humanHistone DeacetylasesMolecular ChaperonesNuclear Proteins

Identifiers

PMID23716573
PMCPMC3663570
OpenAlexW2157647639

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.