Integrative Bioinformatics Analysis Reveals Convergent Immune Dysregulation in Th17 Cell Differentiation and JAK-STAT Signaling Pathways in Cytomegalovirus Infection and Guillain-Barré Syndrome

Guillain-Barré Syndrome (GBS) is a post-infectious autoimmune neuropathy and the leading cause of acute flaccid paralysis worldwide, frequently triggered by preceding infections including Campylobacter jejuni and cytomegalovirus (CMV). Unlike C. jejuni -associated GBS, the immunopathogenic mechanisms underlying CMV-associated GBS remain poorly defined. Using an integrative immunoinformatic approach, we separately analyzed disease-associated genes from DisGeNET and publicly available PBMC transcriptomic datasets from CMV-infected and GBS patients from the Gene Expression Omnibus. Differentially expressed genes (DEGs), protein–protein interaction networks, and pathway enrichment analyses were performed to identify shared immune signatures. We identified 245 common DEGs, with hub genes including TNF, IL-1β, IL-6, IL-10, TLR4, and ICAM-1. Pathway analyses revealed significant enrichment of Th17 cell differentiation, JAK–STAT signaling, cytokine–cytokine receptor interaction, and chemokine signaling in both diseases. Despite convergence on shared pathways, key immune genes were predominantly downregulated in CMV infection but upregulated in GBS, suggesting context-dependent pathway regulation across the transition from acute viral infection to post-infectious autoimmunity. These findings provide a mechanistic framework linking CMV-induced immune perturbation and autoimmune neuropathy, and highlight Th17 differentiation and JAK-STAT signaling as central dysregulated pathways in CMV-associated GBS warranting experimental validation.