Integrative Bioinformatics Analysis Reveals Convergent Immune Dysregulation in Th17 Cell Differentiation and JAK-STAT Signaling Pathways in Cytomegalovirus Infection and Guillain-Barré Syndrome
4 affiliations
- 1Gut-Brain Axis Laboratory, Infectious Diseases Division, icddr,b, Dhaka, Bangladesh
- 2Department of Medical Microbiology and Infectious Diseases, University Medical Center, Erasmus MC, Rotterdam, The Netherlands
- 3Department of Biotechnology, School of Life Sciences BRAC University, Dhaka, Bangladesh
- 4Department of Genetic Engineering and Biotechnology, Jashore University of Science and Technology, Jashore, Bangladesh
Abstract
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.
Related
- Integrative Multi-Database Bioinformatics Characterization of FANCE in Hepatocellular Carcinoma: Prognostic, Epigenetic, Immune, and ncRNA Associations
- Convergent Immunopathology in Influenza-Associated Encephalopathy: CD3+ CD4+ T Cell Depletion, IL-6-Mediated Inflammation, and Complement C3 Dysregulation
- Integrative bioinformatics analysis of Lianmei granules in diabetic nephropathy : Epidemiological and molecular insights
- Identification of SLC15A3 as a shared prognostic biomarker for AML and COVID-19 via integrative bioinformatics, machine learning and Mendelian randomization
- GSTP1 as a senescence-associated diagnostic candidate in prostate cancer: integrative bioinformatics and functional validation
BibTeX
@article{ahmed2026integrative,
title = {{Integrative Bioinformatics Analysis Reveals Convergent Immune Dysregulation in Th17 Cell Differentiation and JAK-STAT Signaling Pathways in Cytomegalovirus Infection and Guillain-Barré Syndrome}},
author = {Jigishu Ahmed and Israt Jahan and Pritha Promita Biswas and Syed Akib Hossain and Rasel Ahmed and Sarah Khurshid and Avizit Das and Asaduzzaman Asad and Zhahirul Islam},
journal = {Bioinformatics and Biology Insights},
year = {2026},
month = sep,
doi = {10.1177/11779322261489938},
url = {https://doi.org/10.1177/11779322261489938},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Integrative Bioinformatics Analysis Reveals Convergent Immune Dysregulation in Th17 Cell Differentiation and JAK-STAT Signaling Pathways in Cytomegalovirus Infection and Guillain-Barré Syndrome
AU - Jigishu Ahmed
AU - Israt Jahan
AU - Pritha Promita Biswas
AU - Syed Akib Hossain
AU - Rasel Ahmed
AU - Sarah Khurshid
AU - Avizit Das
AU - Asaduzzaman Asad
AU - Zhahirul Islam
PY - 2026
DA - 2026/09/22
JO - Bioinformatics and Biology Insights
DO - 10.1177/11779322261489938
UR - https://doi.org/10.1177/11779322261489938
AB - 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.
SN - 1177-9322
ER -