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Exploring the Link Between IL-6 rs1800795 G > C SNP and the Severity of Epstein-Barr Virus-Associated Multiple Sclerosis: Potential Impact on Cognitive Impairment

Tokka M. Hassan; Azza M. El Amir; Nahla Elsayed Nagy; Nashwa El-Khazragy
Molecular Neurobiology · Vol. 62, Issue 11 · pp. 14089-14100 · 2025

Abstract

Multiple Sclerosis (MS) is a chronic immune-mediated neurological disorder frequently accompanied by cognitive impairment, which affects up to 60% of patients and is associated with faster disease progression and greater disability. Interleukin-6 (IL-6), a key proinflammatory cytokine involved in neuroinflammation, has been implicated in MS pathogenesis, and the rs1800795 (−174 G>C) single nucleotide polymorphism (SNP) in the IL6 gene may influence disease susceptibility and clinical severity. This study investigated the association between the IL6 rs1800795 polymorphism and clinical outcomes in Epstein-Barr virus (EBV)-positive MS patients, with a particular focus on cognitive dysfunction. A case-control design was employed, including 300 participants: 150 EBV-positive MS patients and 150 matched healthy controls. Genotyping was performed using TaqMan-based PCR, and clinical data such as disability status, disease progression, and cognitive performance were analyzed. The CC genotype was significantly more frequent in MS patients and was associated with a higher risk of severe disability (OR = 6.11, p = 0.0004), faster disease progression, and increased likelihood of cognitive impairment. These findings suggest that the IL6 rs1800795 polymorphism, particularly the CC genotype, contributes to MS susceptibility and adverse clinical outcomes. IL6 genotyping may hold promise as a predictive tool for disease progression and cognitive decline in EBV-associated MS, offering insights for more personalized therapeutic strategies.

Bibliographic Information

JournalMolecular Neurobiology
PublisherSpringer
Publication Date2025-11-01
Publication Year2025
Volume62
Issue11
Pages14089-14100
Document TypeJournal Article
Print ISSN0893-7648
eISSN1559-1182
DOI10.1007/s12035-025-05211-x

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NARA Access Coverage1987-01-01~Current
Journal Homepagehttps://www.springer.com/journal/12035
Publisher PageOpen Publisher Page
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