Evidence map›Paper›PMID 22761372›Full record

ArticleJournal of virology2012

A myeloid progenitor cell line capable of supporting human cytomegalovirus latency and reactivation, resulting in infectious progeny.

Christine M O'Connor, Eain A Murphy

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
4.3field-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

103 citing papers in PubMed, 133 citations in OpenAlex.

  1. Review
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  5. N6-methyladenosine modification of HCMV IE1 transcript promotes the repressive state of viral genome to achieve latent infection.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  11. The Pentamer glycoprotein complex inhibits viral Immediate Early transcription during Human Cytomegalovirus infections.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  15. Murine cytomegalovirus promotes renal allograft inflammation via Th1/17 cells and IL-17A.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
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  19. Review
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43 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

2 authors at 1 institution in 1 country.

Christine M O'ConnorDepartment of Molecular Genetics, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Eain A Murphy
Cleveland Clinic Lerner College of Medicine · US

Funding

Clinical and Translational Science Collaborative of ClevelandUL1TR000439 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI KONSTAN, MICHAEL W. · 2012 to 2016
$50.0M
Mechanisms of Human Cytomegalovirus LatencyR01AI101080 · NIAID · EVRYS BIO, LLC · PI MURPHY, EAIN A · 2013 to 2016
$1.6M
NCATS NIH HHS UL1 TR000439NIAID NIH HHS R01 AI101080
6 · The paper itself

Abstract

Human cytomegalovirus (HCMV) is a herpesvirus that establishes a lifelong, latent infection within a host. At times when the immune system is compromised, the virus undergoes a lytic reactivation producing infectious progeny. The identification and understanding of the biological mechanisms underlying HCMV latency and reactivation are not completely defined. To this end, we have developed a tractable in vitro model system to investigate these phases of viral infection using a clonal population of myeloid progenitor cells (Kasumi-3 cells). Infection of these cells results in maintenance of the viral genome with restricted viral RNA expression that is reversed with the addition of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA, also known as PMA). Additionally, a latent viral transcript (LUNA) is expressed at times where viral lytic transcription is suppressed. Infected Kasumi-3 cells initiate production of infectious virus following TPA treatment, which requires cell-to-cell contact for efficient transfer of virus to other cell types. Importantly, lytically infected fibroblast, endothelial, or epithelial cells can transfer virus to Kasumi-3 cells, which fail to initiate lytic replication until stimulated with TPA. Finally, inflammatory cytokines, in addition to the pharmacological agent TPA, are sufficient for transcription of immediate-early (IE) genes following latent infection. Taken together, our findings argue that the Kasumi-3 cell line is a tractable in vitro model system with which to study HCMV latency and reactivation.

Indexed as

Base SequenceCell LineCytokinesCytomegalovirusCytomegalovirus InfectionsDNA, ViralGene ExpressionGenes, Immediate-EarlyGenome, ViralHumansInflammation MediatorsModels, BiologicalMyeloid Progenitor CellsTetradecanoylphorbol AcetateVirus ActivationVirus LatencyCytokinesDNA, ViralInflammation MediatorsTetradecanoylphorbol Acetate

Identifiers

PMID22761372
PMCPMC3446554
OpenAlexW2153723315

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.