Evidence map›Paper›PMID 41873126›Full record

ArticleImmunity, inflammation and disease2026

Epstein-Barr Virus Transformed B Cells From Systemic Lupus Erythematosus and Multiple Sclerosis Patients Differ in EBV Lytic and Latency Marker Expression.

Ali Afrasiabi, Wade J Bocking, Stephen D Schibeci, Samantha P L Law, Nicole L Fewings, Ming-Wei Lin, Stephen J Sawcer, Maria Ban, Sanjay Swaminathan, Grant P Parnell

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. EBV Triggers a Distinct Antiviral Response in HMC3 Cells.bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
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.

Ali AfrasiabiEBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.
Wade J BockingEBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.
Stephen D SchibeciEBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.
Samantha P L LawEBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.
Nicole L FewingsCOVID-19 Research Lab, Centre for Virology Research, Westmead Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.
Ming-Wei LinDepartment of Clinical Immunology and Allergy, Westmead Hospital and Institute of Clinical Pathology & Medical Research (ICPMR), Westmead, New South Wales, Australia.
Stephen J SawcerDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Maria BanDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Sanjay SwaminathanEBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.
Grant P ParnellEBV Molecular Lab, Centre for Immunology and Allergy Research, Westmead Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.ORCID https://orcid.org/0000-0002-2898-0253

Funding

Australian Government Research Training ProgramMedical Research Council G0000648Multiple Sclerosis Research Australia 19-0640
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) is an important environmental risk factor in the development of several autoimmune conditions, with the mechanisms still to be fully elucidated. EBV primarily infects memory B cells, transitioning between lytic (active) and latent (dormant) phases of infection. Our group has previously proposed two molecular mechanisms linking EBV pathogenesis to autoimmunity: one indicates that EBV lytic switching contributes to systemic lupus erythematosus (SLE) pathogenesis, while another posits that latency III is more crucial in the development of multiple sclerosis (MS). In this study, we tested the proposed molecular model using a cohort of EBV-transformed lymphoblastoid cell lines derived from individuals with either SLE, MS or healthy controls. Measuring the expression levels of a panel of EBV genes, representing the different phases of the EBV lifecycle, we found compelling proof-of-concept evidence validating our proposed model. This discovery highlights promising signatures for further investigation, where the same approach can be explored across other EBV-associated immune conditions, deepening our understanding of the virus's lifecycle dysregulation in autoimmunity etiology and ultimately aiding in the design of new treatments.

Indexed as

B-LymphocytesEpstein-Barr Virus InfectionsHerpesvirus 4, HumanLupus Erythematosus, SystemicMultiple SclerosisVirus LatencyCell Line, TransformedCell Transformation, ViralFemaleGene Expression Regulation, ViralHumansEBVlatentLCLlyticMSSLE

Identifiers

PMID41873126
PMCPMC13097320

What OpenQuestion holds

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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.