ArticleFunctional & integrative genomics2026
EBV-informed multi-omics target prioritization and structure-based drug repurposing reveal potential therapeutic strategies for multiple sclerosis.
Article in Functional & integrative genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Multiple sclerosis (MS) is a chronic neuroinflammatory disorder characterized by progressive neurodegeneration, demyelination, and genetic susceptibility. Epstein-Barr virus (EBV) infection has been implicated as a major environmental risk factor in MS pathogenesis. Despite the availability of disease-modifying therapies, effective targeted interventions for progressive disease remain limited. In this study, an EBV-informed integrative computational framework combining MS transcriptomic datasets, EBV-associated transcriptional signatures, GWAS susceptibility genes, and network analyses was employed to identify molecular targets associated with immune dysregulation in MS. RNA-sequencing datasets related to MS and EBV infection were obtained from the GEO database, whereas MS susceptibility genes were retrieved from the GWAS Catalog. Differential expression analysis identified 275, 200, and 773 significant DEGs in CD4⁺ T cells, CD8⁺ T cells, and CD14⁺ monocytes, respectively, along with 8,633 EBV-associated DEGs. Integrative overlap and enrichment analyses revealed convergence at the pathway level, particularly involving B-cell receptor signaling, Fc receptor activation, antigen presentation, complement activation, and inflammatory immune signaling. Hub gene analysis identified IL6, CD86, CD28, and PTPN11 as central regulatory nodes. Based on biological relevance and structural tractability, PTPN11/SHP2 was selected as the final therapeutic target. Structure-based drug repurposing identified Gusperimus as the top-ranked ligand, exhibiting a favorable docking score (- 9.287 kcal/mol) and a broader interaction profile within the SHP2 allosteric pocket relative to the reference inhibitor SHP099 (- 7.915 kcal/mol). Molecular dynamics simulations supported stable occupancy of the SHP2 allosteric pocket by Gusperimus over a 100 ns trajectory. Collectively, these findings highlight SHP2 as a potential therapeutic target and identify Gusperimus as a candidate for further investigation in MS-associated immune dysregulation.
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