Evidence map›Paper›PMID 32306957›Full record

ArticleVirology journal2020

Promoter activity of Merkel cell Polyomavirus variants in human dermal fibroblasts and a Merkel cell carcinoma cell line.

Ibrahim Abdulsalam, Kashif Rasheed, Baldur Sveinbjørnsson, Bernhard Ehlers, Ugo Moens

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Virology journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. 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

5 authors at 2 institutions in 2 countries.

Ibrahim AbdulsalamMolecular Inflammation Research Group, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway.
Kashif RasheedMolecular Inflammation Research Group, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway.
Baldur SveinbjørnssonMolecular Inflammation Research Group, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway.
Bernhard EhlersDivision 12 Measles, Mumps, Rubella and Viruses Affecting Immunocompromised Patients, Robert Koch Institute, Berlin, Germany.
Ugo MoensMolecular Inflammation Research Group, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. ugo.moens@uit.no.
UiT The Arctic University of Norway · NORobert Koch Institute · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMerkel cell polyomavirus (MCPyV) is a human polyomavirus that establishes a life-long harmless infection in most individuals, with dermal fibroblasts believed to be the natural host cell. However, this virus is the major cause of Merkel cell carcinoma (MCC), an aggressive skin cancer. Several MCPyV variants with polymorphism in their promoter region have been isolated, but it is not known whether these differences affect the biological properties of the virus.

methodsUsing transient transfection studies in human dermal fibroblasts and the MCC cell line MCC13, we compared the transcription activity of the early and late promoters of the most commonly described non-coding control region MCPyV variant and six other isolates containing specific mutation patterns.

resultsBoth the early and late promoters were significantly stronger in human dermal fibroblasts compared with MCC13 cells, and a different promoter strength between the MCPyV variants was observed. The expression of full-length large T-antigen, a viral protein that regulates early and late promoter activity, inhibited early and late promoter activities in both cell lines. Nonetheless, a truncated large T-antigen, which is expressed in virus-positive MCCs, stimulated the activity of its cognate promoter.

conclusionThe promoter activities of all MCPyV variants tested was stronger in human dermal fibroblasts, a cell line that supports viral replication, than in MCC13 cells, which are not permissive for MCPyV. Truncated large T-antigen, but not full-length large T-antigen stimulated viral promoter activity. Whether, the difference in promoter strength and regulation by large T-antigen may affect the replication and tumorigenic properties of the virus remains to be determined.

Indexed as

Promoter Regions, GeneticAntigens, Viral, TumorCarcinoma, Merkel CellCell Line, TumorFibroblastsGene Expression Regulation, ViralGenetic VariationHumansMerkel cell polyomavirusTranscription, GeneticTransfectionVirus ReplicationAntigens, Viral, TumorLarge T-antigenLuciferase assayMCC13 cellsMCPyVMutationsNon-coding control region

Identifiers

PMID32306957
PMCPMC7168875
OpenAlexW3016318186

What OpenQuestion 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 OpenQuestion graph.