ReviewOpen forum infectious diseases2026
The Immunosuppression Paradox in Multiple Sclerosis: Are We Fueling the Fire by Suppressing Immunity in an Epstein-Barr Virus-Linked Disease?
Review in Open forum infectious diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Immune reconstitution and tolerance-inducing therapies as promising therapeutic approaches in multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies strongly implicate Epstein-Barr virus (EBV) as a necessary trigger for multiple sclerosis (MS). Longitudinal data show that EBV seroconversion precedes MS onset, while mechanistic studies identify molecular mimicry between EBV antigens and central nervous system proteins. Yet, MS treatments remain largely immunosuppressive, potentially impairing antiviral surveillance required to control EBV latency. Therapies that deplete T cells or impair lymphocyte trafficking have been linked to EBV-driven lymphoproliferative complications, potentially leading to EBV reactivation and exacerbation of MS. In contrast, B-cell-depleting therapies may reduce EBV reservoirs by targeting infected memory B cells and thus be more suited to treating EBV-associated MS. In this Review, we examine the paradox of treating an EBV-associated disease with immunosuppression, highlight data suggesting EBV reactivation under certain MS therapies, and propose that future MS management may require integration of EBV-targeted strategies, including vaccines and virus-directed immunotherapies, to address the underlying viral etiology.
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Registered trials
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.