Evidence map›Paper›PMID 39459904›Full record

ArticleViruses2024

Enhanced Transcription of Human Endogenous Retroviruses and TRIM28 Downregulation in Patients with Inflammatory Bowel Disease.

Pier-Angelo Tovo, Davide Giuseppe Ribaldone, Ilaria Galliano, Gian Paolo Caviglia, Maddalena Dini, Valentina Veglio, Cristina Calvi, Paola Montanari, Demis Pitoni, Simone Frara and 3 more

Abstract read
In one paragraph

Article in Viruses, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

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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

13 authors.

Pier-Angelo TovoDepartment of Public Health and Pediatric Sciences, University of Turin, Piazza Polonia 94, 10126 Turin, Italy.
Davide Giuseppe RibaldoneDepartment of Medical Sciences, Division of Gastroenterology, University of Turin, 10123 Turin, Italy.ORCID 0000-0002-9421-3087
Ilaria GallianoPediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94, 10126 Turin, Italy.ORCID 0000-0002-1273-3178
Gian Paolo CavigliaDepartment of Medical Sciences, Division of Gastroenterology, University of Turin, 10123 Turin, Italy.ORCID 0000-0002-0529-9481
Maddalena DiniPediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94, 10126 Turin, Italy.
Valentina VeglioDepartment of Medical Sciences, Division of Gastroenterology, University of Turin, 10123 Turin, Italy.
Cristina CalviPediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94, 10126 Turin, Italy.
Paola MontanariPediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94, 10126 Turin, Italy.
Demis PitoniDepartment of Medical Sciences, Division of Gastroenterology, University of Turin, 10123 Turin, Italy.
Simone FraraDepartment of Medical Sciences, Division of Gastroenterology, University of Turin, 10123 Turin, Italy.
Elisa TriboccoDepartment of Medical Sciences, Division of Gastroenterology, University of Turin, 10123 Turin, Italy.
Anxhela PoshnjariDepartment of Medical Sciences, Division of Gastroenterology, University of Turin, 10123 Turin, Italy.
Massimiliano BergalloPediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94, 10126 Turin, Italy.ORCID 0000-0002-9291-1332

Funding

Research Grant of the CRT bank BERM_CRT_24_01Research Grant of the University of Turin RIBD_RILO_22_01
6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) includes patients affected by Crohn's disease or ulcerative colitis. IBD is thought to be a chronic immune-mediated disease, but its origin remains elusive, and this limits new therapeutic approaches. Human endogenous retroviruses (HERVs) originate from ancestral infections and represent 8% of the human genome. HERVs are no longer infectious, but some retroviral sequences can be activated, and their aberrant expressions have been implicated in inflammatory and autoimmune disorders. HERV transcription is regulated by TRIM28 and SETDB1, which are also directly involved in epigenetic processes and modulation of the immune response. Using a PCR real-time Taqman amplification assay, we assessed, for the first time, the transcription levels of pol genes of HERV-H, -K, and -W families of env genes of syncytin 1 (SYN1), SYN2, and HERV-W, as well as of TRIM28 and SETDB1 in the whole blood of 48 patients with Crohn's disease (CD), 20 with ulcerative colitis (UC), and in healthy controls (HC) of comparable age. The transcriptional levels of HERV-H-pol (

Indexed as

Endogenous RetrovirusesInflammatory Bowel DiseasesTranscription, GeneticTripartite Motif-Containing Protein 28AdultAgedColitis, UlcerativeCrohn DiseaseDown-RegulationFemaleGene Products, envHistone-Lysine N-MethyltransferaseHumansMaleMiddle AgedPregnancy ProteinsGene Products, envHistone-Lysine N-MethyltransferasePregnancy ProteinsSETDB1 protein, humansyncytinTRIM28 protein, humanTripartite Motif-Containing Protein 28Crohn’s diseasehuman endogenous retrovirusesIBDpathogenesisSETDB1TRIM28ulcerative colitis

Identifiers

PMID39459904
PMCPMC11512322

What OpenQuestion holds

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Registered trials

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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.