Evidence map›Paper›PMID 38806670›Full record

ArticleNature microbiology2024

Multiple sclerosis patient-derived spontaneous B cells have distinct EBV and host gene expression profiles in active disease.

Samantha S Soldan, Chenhe Su, Maria Chiara Monaco, Leena Yoon, Toshitha Kannan, Urvi Zankharia, Rishi J Patel, Jayaraju Dheekollu, Olga Vladimirova, Jack W Dowling and 12 more

Abstract read
In one paragraph

Article in Nature microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed.

  1. Article
  2. Article
  3. CD4Science translational medicine · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. EBV Genome Variations and Association With Diseases.Journal of medical virology · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Toward a global research agenda for preventing multiple sclerosis.Multiple sclerosis (Houndmills, Basingstoke, England) · 2026
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors.

Samantha S SoldanThe Wistar Institute, Philadelphia, PA, USA.
Chenhe SuThe Wistar Institute, Philadelphia, PA, USA.
Maria Chiara MonacoNeuroimmunology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, USA.
Leena YoonThe Wistar Institute, Philadelphia, PA, USA.
Toshitha KannanThe Wistar Institute, Philadelphia, PA, USA.ORCID http://orcid.org/0009-0007-7775-6585
Urvi ZankhariaThe Wistar Institute, Philadelphia, PA, USA.
Rishi J PatelThe Wistar Institute, Philadelphia, PA, USA.ORCID http://orcid.org/0009-0007-2238-9511
Jayaraju DheekolluThe Wistar Institute, Philadelphia, PA, USA.
Olga VladimirovaThe Wistar Institute, Philadelphia, PA, USA.
Jack W DowlingThe Wistar Institute, Philadelphia, PA, USA.
Simon ThebaultPerelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Natalie BrownThe Wistar Institute, Philadelphia, PA, USA.ORCID http://orcid.org/0000-0002-1691-3213
Annaliese ClauzeNeuroimmunology Clinic, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, USA.
Frances AndradaNeuroimmunology Clinic, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, USA.
Andries FederDivision of Infectious Diseases, Children's Hospital of Philadelphia, Philadelphia, PA, USA.ORCID http://orcid.org/0009-0000-3448-6342
Paul J PlanetDivision of Infectious Diseases, Children's Hospital of Philadelphia, Philadelphia, PA, USA.ORCID http://orcid.org/0000-0003-0543-0539
Andrew KossenkovThe Wistar Institute, Philadelphia, PA, USA.
Daniel E SchäfferThe Wistar Institute, Philadelphia, PA, USA.ORCID http://orcid.org/0000-0003-3608-152X
Joan OhayonNeuroimmunology Clinic, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, USA.
Noam AuslanderThe Wistar Institute, Philadelphia, PA, USA.ORCID http://orcid.org/0000-0002-2037-1517
Steven JacobsonNeuroimmunology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, USA.
Paul M LiebermanThe Wistar Institute, Philadelphia, PA, USA. lieberman@wistar.org.ORCID http://orcid.org/0000-0002-3935-9921

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Aaron Robert Goldman · 1985 to 2026
$75.9M
Regulation of Epstein-Barr Virus LatencyR01CA093606 · NCI · WISTAR INSTITUTE · PI LIEBERMAN, PAUL M. · 2002 to 2022
$6.7M
Epigenetic Regulation of Epstein-Barr Virus Latency ProgramsR01DE017336 · NIDCR · WISTAR INSTITUTE · PI PAUL M. LIEBERMAN · 2005 to 2026
$6.5M
Drugging EBNA1 to Treat EBV-Associated Cancers - Diversity SupplementR01CA259171 · NCI · WISTAR INSTITUTE · PI MESSICK, TROY E · 2021 to 2025
$3.3M
Regulation of EBV Latency by Purine Metabolism and SignalingR01AI153508 · NIAID · WISTAR INSTITUTE · PI TEMPERA, ITALO · 2021 to 2025
$2.3M
Integrative Approach to Comprehensive Analysis of High Throughput Data on a Cancer Center LevelR50CA211199 · NCI · WISTAR INSTITUTE · PI Andrew V Kossenkov · 2016 to 2026
$1.6M
Computational methods for discovery of disease-modulating microbial genesR01LM014503 · NLM · WISTAR INSTITUTE · PI Noam Auslander · 2024 to 2026
$1.2M
NCI NIH HHS P30 CA010815NCI NIH HHS R01 CA093606NCI NIH HHS R01 CA259171NCI NIH HHS R50 CA211199NIAID NIH HHS R01 AI153508NIDCR NIH HHS R01 DE017336NLM NIH HHS R01 LM014503U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) RO1 CA093606U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR) RO1 DE017336
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) is an aetiologic risk factor for the development of multiple sclerosis (MS). However, the role of EBV-infected B cells in the immunopathology of MS is not well understood. Here we characterized spontaneous lymphoblastoid cell lines (SLCLs) isolated from MS patients and healthy controls (HC) ex vivo to study EBV and host gene expression in the context of an individual's endogenous EBV. SLCLs derived from MS patient B cells during active disease had higher EBV lytic gene expression than SLCLs from MS patients with stable disease or HCs. Host gene expression analysis revealed activation of pathways associated with hypercytokinemia and interferon signalling in MS SLCLs and upregulation of forkhead box protein 1 (FOXP1), which contributes to EBV lytic gene expression. We demonstrate that antiviral approaches targeting EBV replication decreased cytokine production and autologous CD4

Indexed as

B-LymphocytesEpstein-Barr Virus InfectionsHerpesvirus 4, HumanMultiple SclerosisAdultCD4-Positive T-LymphocytesCell LineCytokinesFemaleForkhead Transcription FactorsGene Expression ProfilingGene Expression Regulation, ViralHost-Pathogen InteractionsHumansMaleTranscriptomeCytokinesForkhead Transcription Factors

Identifiers

PMID38806670
PMCPMC11900839

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.