---
title: "EBV reactivation primes peripheral immune changes before multiple sclerosis relapse"
id: "nature-0-ebv-reactivation-priming-of-the-peripheral-immune-system-in-multiple-sclerosis"
canonical_url: "https://medichelpline.com/clinical-feed/nature-0-ebv-reactivation-priming-of-the-peripheral-immune-system-in-multiple-sclerosis"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "Nature Medicine"
source_url: "https://www.nature.com/articles/s41591-026-04665-3"
published_at: "2026-09-16T10:48:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# EBV reactivation primes peripheral immune changes before multiple sclerosis relapse
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/nature-0-ebv-reactivation-priming-of-the-peripheral-immune-system-in-multiple-sclerosis
- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** Nature Medicine
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41591-026-04665-3)
- **Published At:** 2026-09-16T10:48:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- This observational, longitudinal blood study mapped immune changes that precede clinical relapse in relapsing‑remitting **multiple sclerosis (MS)** using single‑cell RNA sequencing, bulk transcriptomics, multiparameter flow cytometry and targeted viral RT‑qPCR. - A reproducible **pre‑relapse transcriptional signature** was identified in monocytes and B cells emerging up to about 3 months before clinical symptom onset. - Pre‑relapse gene modules were enriched for host genes responsive to **Epstein–Barr virus (EBV)** lytic reactivation factors, implicating viral reactivation in the peripheral immune priming before relapse. - Targeted RT‑qPCR detected elevated EBV LMP‑1 transcripts in B cells isolated from the pre‑relapse period, supporting transcriptional evidence of EBV activity. - Flow cytometry showed expansion of **CD11c+ atypical B cells (ABCs)** in the pre‑relapse window; these cells displayed the EBV surface protein **gp350**. - The pre‑relapse transcriptional modules overlapped with **MS GWAS risk loci** and enhancers bound by the EBV nuclear antigen **EBNA‑2**, suggesting shared regulatory elements linking genetic susceptibility and EBV‑responsive programs. - The study did not establish how the observed peripheral activation relates temporally or causally to CNS lesion formation; that connection remains to be determined. - Overall, the findings support a model in which **EBV reactivation** occurring within a genetically susceptible peripheral immune environment is a proximal precursor to clinical MS relapse, but mechanistic and causal links to CNS pathology require further investigation.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [nature medicine](https://www.nature.com/nm) 3. [articles](https://www.nature.com/nm/articles?type=article) 4. article EBV reactivation priming of the peripheral immune system in multiple sclerosis relapse [ Download PDF ](https://www.nature.com/articles/s41591-026-04665-3.pdf) [ Download PDF ](https://www.nature.com/articles/s41591-026-04665-3.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 16 September 2026 # EBV reactivation priming of the peripheral immune system in multiple sclerosis relapse * [Devin A. King](https://www.nature.com/articles/s41591-026-04665-3#auth-Devin_A_-King-Aff1-Aff2-Aff3-Aff4) [ORCID: orcid.org/0009-0005-6485-2362](https://orcid.org/0009-0005-6485-2362)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3),[4](https://www.nature.com/articles/s41591-026-04665-3#Aff4), * [Shrishti Saxena](https://www.nature.com/articles/s41591-026-04665-3#auth-Shrishti-Saxena-Aff1-Aff2-Aff3) [ORCID: orcid.org/0000-0003-3429-5671](https://orcid.org/0000-0003-3429-5671)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3), * [Danielle Caefer](https://www.nature.com/articles/s41591-026-04665-3#auth-Danielle-Caefer-Aff1-Aff2-Aff3-Aff4) [ORCID: orcid.org/0000-0002-3100-4085](https://orcid.org/0000-0002-3100-4085)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3),[4](https://www.nature.com/articles/s41591-026-04665-3#Aff4), * [Kyle C. Downer](https://www.nature.com/articles/s41591-026-04665-3#auth-Kyle_C_-Downer-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3), * [Laura E. Saucier](https://www.nature.com/articles/s41591-026-04665-3#auth-Laura_E_-Saucier-Aff1-Aff2-Aff3-Aff4-Aff5)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3),[4](https://www.nature.com/articles/s41591-026-04665-3#Aff4),[5](https://www.nature.com/articles/s41591-026-04665-3#Aff5), * [Ethan Goodman](https://www.nature.com/articles/s41591-026-04665-3#auth-Ethan-Goodman-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3), * [Jonmichael Aracena](https://www.nature.com/articles/s41591-026-04665-3#auth-Jonmichael-Aracena-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3), * [Alena Zhirova](https://www.nature.com/articles/s41591-026-04665-3#auth-Alena-Zhirova-Aff1-Aff2-Aff3) [ORCID: orcid.org/0009-0008-4752-5142](https://orcid.org/0009-0008-4752-5142)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3), * [Anthilia Alchanat](https://www.nature.com/articles/s41591-026-04665-3#auth-Anthilia-Alchanat-Aff1-Aff2-Aff3) [ORCID: orcid.org/0009-0006-4529-9482](https://orcid.org/0009-0006-4529-9482)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3), * [Saoirse Nolan](https://www.nature.com/articles/s41591-026-04665-3#auth-Saoirse-Nolan-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3), * [Hrishikesh Lokhande](https://www.nature.com/articles/s41591-026-04665-3#auth-Hrishikesh-Lokhande-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3), * [Howard L. Weiner](https://www.nature.com/articles/s41591-026-04665-3#auth-Howard_L_-Weiner-Aff2-Aff3-Aff4-Aff5)[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3),[4](https://www.nature.com/articles/s41591-026-04665-3#Aff4),[5](https://www.nature.com/articles/s41591-026-04665-3#Aff5), * [Benjamin E. Gewurz](https://www.nature.com/articles/s41591-026-04665-3#auth-Benjamin_E_-Gewurz-Aff4-Aff6-Aff7) [ORCID: orcid.org/0000-0002-3965-3418](https://orcid.org/0000-0002-3965-3418)[4](https://www.nature.com/articles/s41591-026-04665-3#Aff4),[6](https://www.nature.com/articles/s41591-026-04665-3#Aff6),[7](https://www.nature.com/articles/s41591-026-04665-3#Aff7) & * … * [Tanuja Chitnis](https://www.nature.com/articles/s41591-026-04665-3#auth-Tanuja-Chitnis-Aff1-Aff2-Aff3-Aff4-Aff5) [ORCID: orcid.org/0000-0002-9897-4422](https://orcid.org/0000-0002-9897-4422)[1](https://www.nature.com/articles/s41591-026-04665-3#Aff1),[2](https://www.nature.com/articles/s41591-026-04665-3#Aff2),[3](https://www.nature.com/articles/s41591-026-04665-3#Aff3),[4](https://www.nature.com/articles/s41591-026-04665-3#Aff4),[5](https://www.nature.com/articles/s41591-026-04665-3#Aff5) Show authors [_Nature Medicine_](https://www.nature.com/nm) (2026) [Cite this article](https://www.nature.com/articles/s41591-026-04665-3#citeas) [ Save article ](https://www.nature.com/articles/s41591-026-04665-3/save-research?_csrf=7Of_alnDGUgZMCseCg7_WhsYJpTdaW6g) [ View saved research ](https://www.nature.com/saved-research) ## Abstract Despite decades of research, the cellular and molecular events preceding multiple sclerosis (MS) relapse remain incompletely understood. Here, in this observational study of longitudinal blood samples from patients with relapsing-remitting MS, we used single-cell RNA sequencing, bulk transcriptomics, multiparameter flow cytometry and targeted viral reverse transcription quantitative polymerase chain reaction (RT−qPCR) to construct a time-resolved atlas of immune perturbations surrounding relapse. A reproducible pre-relapse signature in monocytes and B cells, emerging up to 3 months before clinical onset, was enriched for host genes responsive to Epstein−Barr virus (EBV) lytic reactivation factors. RT−qPCR confirmed elevated EBV _LMP-1_ transcripts in pre-relapse B cells, and flow cytometry demonstrated expansion of CD11c+ atypical B cell populations displaying EBV surface protein gp350. Pre-relapse transcriptional modules overlapped with MS genome-wide association study (GWAS) risk loci and EBNA-2-bound enhancers, suggesting that inherited MS susceptibility and EBV-responsive programs operate through shared regulatory elements. How this peripheral activation relates to central nervous system lesion formation remains to be established. These findings nonetheless suggest that EBV reactivation, when occurring within a genetically predisposed peripheral immune environment, is a proximal precursor of MS relapse. ### Explore related subjects Discover the latest articles and news in related subjects. * [Multiple sclerosis](https://www.nature.com/subjects/multiple-sclerosis) * [Neuroimmunology](https://www.nature.com/subjects/neuroimmunology) * [Neurology](https://www.nature.com/subjects/neurology) ## Main Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) and a leading cause of neurologic disability in young adults, affecting approximately 2.9 million people worldwide[1](https://www.nature.com/articles/s41591-026-04665-3#ref-CR1 "Walton, C. et al. Rising prevalence of multiple sclerosis worldwide: insights from the Atlas of MS, third edition. Mult. Scler. 26, 1816–1821 \(2020\)."). The disease course, particularly in early stages, is characterized by symptomatic flare-ups separated by periods of remission whose timing is highly variable and difficult to predict. A central challenge in identifying the triggers of relapse is uncertainty in the timing of molecular events that precede clinical symptoms. Multiple inflammatory processes participate in relapse pathophysiology, many of which are transient. In viral meningitis, for example, neutrophilic pleocytosis in the cerebrospinal fluid may be detectable for only hours after infection, whereas lymphocytic dominance persists weeks later[2](https://www.nature.com/articles/s41591-026-04665-3#ref-CR2 "Jaijakul, S., Salazar, L., Wootton, S. H., Aguilera, E. & Hasbun, R. The clinical significance of neutrophilic pleocytosis in cerebrospinal fluid in patients with viral central nervous system infections. Int. J. Infect. Dis. 59, 77–81 \(2017\)."). In MS, the inability to sample immune activity during such short-lived presymptomatic windows has limited efforts to capture the molecular events that initiate relapses. A growing body of evidence supports serum neurofilament light chain (NfL) as a useful biomarker of disease activity in MS[3](https://www.nature.com/articles/s41591-026-04665-3#ref-CR3 "Thebault, S. et al. Serum neurofilament light chain predicts long term clinical outcomes in multiple sclerosis. Sci. Rep. 10, 10381 \(2020\)."),[4](https://www.nature.com/articles/s41591-026-04665-3#ref-CR4 "Canto, E. et al. Association between serum neurofilament light chain levels and long-term disease course among patients with multiple sclerosis followed up for 12 years. JAMA Neurol. 76, 1359–1366 \(2019\)."),[5](https://www.nature.com/articles/s41591-026-04665-3#ref-CR5 "Chitnis, T. et al. Neurofilament light chain serum levels correlate with 10-year MRI outcomes in multiple sclerosis. Ann. Clin. Transl. Neurol. 5, 1478–1491 \(2018\)."). Moreover, proteomic studies have identified elevated cytokines that accompany relapse[6](https://www.nature.com/articles/s41591-026-04665-3#ref-CR6 "Akesson, J. et al. Proteomics reveal biomarkers for diagnosis, disease activity and long-term disability outcomes in multiple sclerosis. Nat. Commun. 14, 6903 \(2023\)."),[7](https://www.nature.com/articles/s41591-026-04665-3#ref-CR7 "Chitnis, T. et al. Inflammatory and neurodegenerative serum protein biomarkers increase sensitivity to detect clinical and radiographic disease activity in multiple sclerosis. Nat. Commun. 15, 4297 \(2024\)."). However, these markers reflect tissue damage that has already occurred and an inflammatory process already underway, rather than the upstream factors that instigate relapse. In parallel, B cell dysregulation has emerged as a central feature of MS relapse biology. Since B cell depletion was shown to reduce relapse rates[8](https://www.nature.com/articles/s41591-026-04665-3#ref-CR8 "Hauser, S. L. et al. B-cell depletion with rituximab in relapsing-remitting multiple sclerosis. N. Engl. J. Med. 358, 676–688 \(2008\)."), experimental and human studies have demonstrated that B cells function not only as antibody producers but also as antigen-presenting cells and sources of inflammatory cytokines that activate pathogenic T cell programs[9](https://www.nature.com/articles/s41591-026-04665-3#ref-CR9 "Ramesh, A. et al. A pathogenic and clonally expanded B cell transcriptome in active multiple sclerosis. Proc. Natl Acad. Sci. USA 117, 22932–22943 \(2020\)."),[10](https://www.nature.com/articles/s41591-026-04665-3#ref-CR10 "Lanz, T. V. et al. Clonally expanded B cells in multiple sclerosis bind EBV EBNA1 and GlialCAM. Nature 603, 321–327 \(2022\)."). Among B cell subsets, CD11c+T-bet+ atypical memory B cells (ABCs) expand in autoimmune diseases and chronic viral infections, including Epstein–Barr virus (EBV), HIV and hepatitis C[11](https://www.nature.com/articles/s41591-026-04665-3#ref-CR11 "Jenks, S. A. et al. Distinct effector B cells induced by unregulated Toll-like receptor 7 contribute to pathogenic responses in systemic lupus erythematosus. Immunity 49, 725–739 \(2018\)."),[12](https://www.nature.com/articles/s41591-026-04665-3#ref-CR12 "Portugal, S., Obeng-Adjei, N., Moir, S., Crompton, P. D. & Pierce, S. K. Atypical memory B cells in human chronic infectious diseases: an interim report. Cell Immunol. 321, 18–25 \(2017\)."),[13](https://www.nature.com/articles/s41591-026-04665-3#ref-CR13 "SoRelle, E. D., Reinoso-Vizcaino, N. M., Horn, G. Q. & Luftig, M. A. Epstein-Barr virus perpetuates B cell germinal center dynamics and generation of autoimmune-associated phenotypes in vitro. Front. Immunol. 13, 1001145 \(2022\)."). In MS, ABCs accumulate in blood and CNS-adjacent compartments, display elevated expression of interferon-stimulated genes and antigen presentation machinery[14](https://www.nature.com/articles/s41591-026-04665-3#ref-CR14 "Jelcic, I. et al. T-bet+ CXCR3+ B cells drive hyperreactive B-T cell interactions in multiple sclerosis. Cell Rep. Med. 6, 102027 \(2025\)."),[15](https://www.nature.com/articles/s41591-026-04665-3#ref-CR15 "Claes, N. et al. Age-associated B cells with proinflammatory characteristics are expanded in a proportion of multiple sclerosis patients. J. Immunol. 197, 4576–4583 \(2016\)."),[16](https://www.nature.com/articles/s41591-026-04665-3#ref-CR16 "SoRelle, E. D. et al. Early multiple sclerosis activity associated with TBX21+CD21loCXCR3+ B cell expansion resembling EBV-induced phenotypes. JCI Insight 10, e188543 \(2025\).") and are less effectively depleted by anti-CD20 therapies[17](https://www.nature.com/articles/s41591-026-04665-3#ref-CR17 "El Mahdaoui, S. et al. CD11c+ B cells in relapsing-remitting multiple sclerosis and effects of anti-CD20 therapy. Ann. Clin. Transl. Neurol. 11, 926–937 \(2024\)."). Whether ABCs expand before relapse and whether they contribute to the inflammatory cascade remain undetermined. MS is further shaped by host genetics. Genome-wide association studies (GWASs) have identified more than 200 independent risk loci, many mapping to regulators of immune activation, B cell differentiation and antigen presentation[18](https://www.nature.com/articles/s41591-026-04665-3#ref-CR18 "International Multiple Sclerosis Genetics Consortium. Multiple sclerosis genomic map implicates peripheral immune cells and microglia in susceptibility. Science 365, eaav7188 \(2019\)."). _HLA-DRB1_ *15:01 confers the largest individual risk effect[19](https://www.nature.com/articles/s41591-026-04665-3#ref-CR19 "Hollenbach, J. A. & Oksenberg, J. R. The immunogenetics of multiple sclerosis: a comprehensive review. J. Autoimmun. 64, 13–25 \(2015\)."), and additional non-HLA loci are concentrated in B cell and innate immunoregulatory pathways[20](https://www.nature.com/articles/s41591-026-04665-3#ref-CR20 "Smets, I. et al. Multiple sclerosis risk variants alter expression of co-stimulatory genes in B cells. Brain 141, 786–796 \(2018\)."),[21](https://www.nature.com/articles/s41591-026-04665-3#ref-CR21 "Cenit, M. C. et al. STAT3 locus in inflammatory bowel disease and multiple sclerosis susceptibility. Genes Immun. 11, 264–268 \(2010\)."),[22](https://www.nature.com/articles/s41591-026-04665-3#ref-CR22 "Parnell, G. P. & Booth, D. R. The multiple sclerosis \(MS\) genetic risk factors indicate both acquired and innate immune cell subsets contribute to MS pathogenesis and identify novel therapeutic opportunities. Front. Immunol. 8, 425 \(2017\)."),[23](https://www.nature.com/articles/s41591-026-04665-3#ref-CR23 "Skarlis, C., Papadopoulos, V., Raftopoulou, S., Mavragani, C. P. & Evangelopoulos, M. E. B-cell activating factor gene variants in multiple sclerosis: possible associations with disease susceptibility among females. Clin. Immunol. 257, 109847 \(2023\)."). Notably, the EBV nuclear antigen EBNA-2 binds prefe
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