Evidence map›Paper›PMID 36429047›Full record

ArticleCells2022

Epstein-Barr Virus-Induced Genes and Endogenous Retroviruses in Immortalized B Cells from Patients with Multiple Sclerosis.

Lisa Wieland, Tommy Schwarz, Kristina Engel, Ines Volkmer, Anna Krüger, Alexander Tarabuko, Jutta Junghans, Malte E Kornhuber, Frank Hoffmann, Martin S Staege and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 22 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

11 authors at 2 institutions in 1 country.

Lisa WielandDepartment of Neurology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.ORCID 0000-0002-0951-9285
Tommy SchwarzDepartment of Neurology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.
Kristina EngelDepartment of Surgical and Conservative Pediatrics and Adolescent Medicine, Medical Faculty, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.
Ines VolkmerDepartment of Surgical and Conservative Pediatrics and Adolescent Medicine, Medical Faculty, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.
Anna KrügerDepartment of Surgical and Conservative Pediatrics and Adolescent Medicine, Medical Faculty, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.
Alexander TarabukoDepartment of Neurology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.
Jutta JunghansDepartment of Neurology, Martha-Maria Hospital Halle-Dölau, 06120 Halle (Saale), Germany.
Malte E KornhuberDepartment of Neurology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.
Frank HoffmannDepartment of Neurology, Martha-Maria Hospital Halle-Dölau, 06120 Halle (Saale), Germany.
Martin S StaegeDepartment of Surgical and Conservative Pediatrics and Adolescent Medicine, Medical Faculty, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.
Alexander EmmerDepartment of Neurology, Medical Faculty, Martin Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany.ORCID 0000-0003-4272-8887
Martin Luther University Halle-Wittenberg · DEMartha-Maria Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune pathogenesis of multiple sclerosis (MS) is thought to be triggered by environmental factors in individuals with an unfavorable genetic predisposition. Epstein-Barr virus (EBV) infection is a major risk factor for subsequent development of MS. Human endogenous retroviruses (HERVs) can be activated by EBV, and might be a missing link between an initial EBV infection and the later onset of MS. In this study, we investigated differential gene expression patterns in EBV-immortalized lymphoblastoid B cell lines (LCL) from MS-affected individuals (MSLCL) and controls by using RNAseq and qRT-PCR. RNAseq data from LCL mapped to the human genome and a virtual virus metagenome were used to identify possible biomarkers for MS or disease-relevant risk factors, e.g., the relapse rate. We observed that lytic EBNA-1 transcripts seemed to be negatively correlated with age leading to an increased expression in LCL from younger PBMC donors. Further, HERV-K (HML-2) GAG was increased upon EBV-triggered immortalization. Besides the well-known transactivation of HERV-K18, our results suggest that another six HERV loci are up-regulated upon stimulation with EBV. We identified differentially expressed genes in MSLCL, e.g., several HERV-K loci, ERVMER61-1 and ERV3-1, as well as genes associated with relapses. In summary, EBV induces genes and HERV in LCL that might be suitable as biomarkers for MS or the relapse risk.

Indexed as

Endogenous RetrovirusesEpstein-Barr Virus InfectionsMultiple SclerosisHerpesvirus 4, HumanHumansLeukocytes, MononuclearRecurrencebiomarkersEpstein-Barr virushuman endogenous retroviruslymphoblastoid cell linesmultiple sclerosis

Identifiers

PMID36429047
PMCPMC9688211
OpenAlexW4309152904

What Socratic 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 Socratic graph.