Evidence map›Paper›PMID 34696366›Full record

ArticleViruses2021

IFNα and β Mediated JCPyV Suppression through C/EBPβ-LIP Isoform.

Dana May, Anna Bellizzi, Workineh Kassa, John M Cipriaso, Maurizio Caocci, Hassen S Wollebo

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

Article in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.6field-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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. 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

6 authors at 2 institutions in 1 country.

Dana MayDepartment of Neuroscience, Center for Neurovirology-Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA 19140, USA.
Anna BellizziDepartment of Neuroscience, Center for Neurovirology-Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA 19140, USA.ORCID 0000-0002-2098-5236
Workineh KassaMayo Clinic Hospital and Health Care, 200 First St. S.W., Rochester, MN 55905, USA.
John M CipriasoDepartment of Neuroscience, Center for Neurovirology-Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA 19140, USA.
Maurizio CaocciDepartment of Neuroscience, Center for Neurovirology-Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA 19140, USA.
Hassen S WolleboDepartment of Neuroscience, Center for Neurovirology-Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA 19140, USA.ORCID 0000-0003-2285-3496
Temple University · USMayo Clinic Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polyomavirus JC (JCPyV) causes the demyelinating disease progressive multifocal leukoencephalopathy (PML). JCPyV infection is very common in childhood and, under conditions of severe immunosuppression, JCPyV may reactivate to cause PML. JC viral proteins expression is regulated by the JCPyV non-coding control region (NCCR), which contains binding sites for cellular transcriptional factors which regulate JCPyV transcription. Our earlier studies suggest that JCPyV reactivation occurs within glial cells due to cytokines such as TNF-α which stimulate viral gene expression. In this study, we examined interferon-α (IFNα) or β (IFNβ) which have a negative effect on JCPyV transcriptional regulation. We also showed that these interferons induce the endogenous liver inhibitory protein (LIP), an isoform of CAAT/enhancer binding protein beta (C/EBPβ). Treatment of glial cell line with interferons increases the endogenous level of C/EBPβ-LIP. Furthermore, we showed that the negative regulatory role of the interferons in JCPyV early and late transcription and viral replication is more pronounced in the presence of C/EBPβ-LIP. Knockdown of C/EBPβ-LIP by shRNA reverse the inhibitory effect on JCPyV viral replication. Therefore, IFNα and IFNβ negatively regulate JCPyV through induction of C/EBPβ-LIP, which together with other cellular transcriptional factors may control the balance between JCPyV latency and activation.

Indexed as

CCAAT-Enhancer-Binding Protein-betaCell Line, TumorDNA, ViralGene ExpressionGene Expression Regulation, ViralHumansInterferon-alphaInterferon-betaJC VirusLeukoencephalopathy, Progressive MultifocalNeurogliaProtein IsoformsVirus ReplicationCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanDNA, ViralInterferon-alphaInterferon-betaProtein IsoformsC/EBPβ-LIPCRISPR Cas9 STAT-1 knockoutinterferonα and β signalingpolyomavirus JCprogressive multifocal leukoencephalopathy

Identifiers

PMID34696366
PMCPMC8537971
OpenAlexW3203962294

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.