Evidence map›Paper›PMID 15596827›Full record

ArticleJournal of virology2005

Role for tumor necrosis factor alpha in murine cytomegalovirus transcriptional reactivation in latently infected lungs.

Christian O Simon, Christof K Seckert, Doris Dreis, Matthias J Reddehase, Natascha K A Grzimek

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

63 citing papers in PubMed, 110 citations in OpenAlex.

  1. Mechanisms and Determinants of CMV Reactivation in Kidney Transplantation.International journal of molecular sciences · 2026
    Review
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  14. A clinically relevant murine model unmasks a "two-hit" mechanism for reactivation and dissemination of cytomegalovirus after kidney transplant.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019
    Article
  15. Impact of cytomegalovirus load on host response to sepsis.Medical microbiology and immunology · 2019
    Review
  16. Impact of CMV upon immune aging: facts and fiction.Medical microbiology and immunology · 2019
    Review
  17. Cytomegalovirus memory inflation and immune protection.Medical microbiology and immunology · 2019
    Review
  18. Article
  19. Cytomegalovirus reactivation in inflammatory bowel disease: an uncommon occurrence related to corticosteroid dependence.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019
    Article
  20. Article

3 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

5 authors at 1 institution in 1 country.

Christian O SimonInstitute for Virology, Johannes Gutenberg University, Mainz, Germany.
Christof K Seckert
Doris Dreis
Matthias J Reddehase
Natascha K A Grzimek
Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interstitial pneumonia is a major clinical manifestation of primary or recurrent cytomegalovirus (CMV) infection in immunocompromised recipients of a bone marrow transplant. In a murine model, lungs were identified as a prominent site of CMV latency and recurrence. Pulmonary latency of murine CMV is characterized by high viral genome burden and a low incidence of variegated immediate-early (IE) gene expression, reflecting a sporadic activity of the major IE promoters (MIEPs) and enhancer. The enhancer-flanking promoters MIEP1/3 and MIEP2 are switched on and off during latency in a ratio of approximately 2:1. MIEP1/3 latency-associated activity generates the IE1 transcript of the ie1/3 transcription unit but not the alternative splicing product IE3 that encodes the essential transactivator of early gene expression. Splicing thus appeared to be an important checkpoint for maintenance of latency. In accordance with previous work of others, we show here that signaling by the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) activates IE1/3 transcription in vivo. As an addition to current knowledge, Poisson distribution analysis revealed an increased incidence of IE1/3 transcriptional events as well as a higher amount of transcripts per event. Notably, TNF-alpha promoted the splicing to IE3 transcripts, but transcription did not proceed to the M55/gB early gene. Moreover, the activated transcriptional state induced by TNF-alpha did not predispose latently infected mice to a higher incidence of virus recurrence after hematoablative treatment. In conclusion, TNF-alpha is an important inductor of IE gene transcriptional reactivation, whereas early genes downstream in the viral replicative cycle appear to be the rate-limiting checkpoint(s) for virus recurrence.

Indexed as

Gene Expression Regulation, ViralTranscription, GeneticVirus ActivationVirus LatencyAnimalsBone Marrow TransplantationDisease Models, AnimalFemaleHerpesviridae InfectionsHumansImmediate-Early ProteinsLungMiceMice, Inbred BALB CMuromegalovirusTransplantation, IsogeneicIE1 protein, cytomegalovirusIE3 protein, cytomegalovirusImmediate-Early ProteinsTumor Necrosis Factor-alphaViral Proteins

Identifiers

PMID15596827
PMCPMC538715
OpenAlexW2149269468

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.