Evidence map›Paper›PMID 31776268›Full record

ArticleJournal of virology2020

Human Papillomavirus E7 Oncoprotein Subverts Host Innate Immunity via SUV39H1-Mediated Epigenetic Silencing of Immune Sensor Genes.

Irene Lo Cigno, Federica Calati, Cinzia Borgogna, Alessandra Zevini, Silvia Albertini, Licia Martuscelli, Marco De Andrea, John Hiscott, Santo Landolfo, Marisa Gariglio

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

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 67 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Irene Lo Cigno *University of Piemonte Orientale Medical School, Department of Translational Medicine, Molecular Virology Unit, Novara, Italy.
Federica Calati *University of Piemonte Orientale Medical School, Department of Translational Medicine, Molecular Virology Unit, Novara, Italy.
Cinzia BorgognaUniversity of Piemonte Orientale Medical School, Department of Translational Medicine, Molecular Virology Unit, Novara, Italy.ORCID 0000-0001-9973-2620
Alessandra ZeviniIstituto Pasteur-Fondazione Cenci Bolognetti, Rome, Italy.
Silvia AlbertiniUniversity of Piemonte Orientale Medical School, Department of Translational Medicine, Molecular Virology Unit, Novara, Italy.
Licia MartuscelliUniversity of Piemonte Orientale Medical School, Department of Translational Medicine, Molecular Virology Unit, Novara, Italy.
Marco De AndreaCenter for Translational Research on Autoimmune and Allergic Disease-CAAD, Novara, Italy.ORCID 0000-0002-3188-5783
John HiscottIstituto Pasteur-Fondazione Cenci Bolognetti, Rome, Italy.
Santo LandolfoUniversity of Turin Medical School, Department of Public Health and Pediatric Sciences, Viral Pathogenesis Unit, Turin, Italy.ORCID 0000-0002-3153-2865
Marisa GariglioUniversity of Piemonte Orientale Medical School, Department of Translational Medicine, Molecular Virology Unit, Novara, Italy marisa.gariglio@med.uniupo.it.ORCID 0000-0002-5187-0140
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITIstituto Pasteur · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subversion of innate immunity by oncoviruses, such as human papillomavirus (HPV), favors carcinogenesis because the mechanism(s) of viral immune evasion can also hamper cancer immunosurveillance. Previously, we demonstrated that high-risk (hr) HPVs trigger simultaneous epigenetic silencing of multiple effectors of innate immunity to promote viral persistence. Here, we expand on those observations and show that the HPV E7 oncoprotein upregulates the H3K9-specific methyltransferase, whose action shuts down the host innate immune response. Specifically, we demonstrate that SUV39H1 contributes to chromatin repression at the promoter regions of the viral nucleic acid sensors RIG-I and cGAS and the adaptor molecule STING in HPV-transformed cells. Inhibition of SUV39H1 leads to transcriptional activation of these genes, especially RIG-I, followed by increased beta interferon (IFN-β) and IFN-λ

Indexed as

Cell LineCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDEAD Box Protein 58Epigenesis, GeneticHEK293 CellsHeLa CellsHost-Pathogen InteractionsHumansImmune EvasionImmunity, InnateInterferon-betaKeratinocytesMembrane ProteinsMethyltransferasesNucleotidyltransferasesOncogene Proteins, ViralcGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDEAD Box Protein 58Interferon-betaMembrane ProteinsMethyltransferasesNucleotidyltransferasesOncogene Proteins, ViralPapillomavirus E7 ProteinsReceptors, ImmunologicRepressor ProteinsRIGI protein, humanSTING1 protein, humanSTING ProteinSUV39H1 protein, humanepigeneticsHPVinnate immunityRIG-ISUV39H1

Identifiers

PMID31776268
PMCPMC6997746
OpenAlexW2991171227

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.