Therapeutic Insights into Epstein-Barr Virus: Linking T-Cell Immunity to CNS Pathology in Correlation with Multiple Sclerosis and Alzheimer’s Disease

Epstein-Barr virus (EBV), a common gamma-herpesvirus, establishes lifelong latency in over 90% of the global population and has been implicated in the pathogenesis of several neurological disorders, including multiple sclerosis (MS) and Alzheimer’s disease (AD). Available evidence suggests a significant link between impaired EBV-specific T-cell immunity and the persistence of viral reservoirs within the central nervous system (CNS), which contributes to chronic neuroinflammation and neurodegeneration. This study investigates the molecular and cellular mechanisms underlying EBV-induced CNS pathology, and also studies immunotherapeutic techniques aimed at restoring antiviral immunity. Using data from four peer-reviewed studies, this study analyzes experimental models involving EBV-infected humanized mice and rabbits, peripheral blood mononuclear cell (PBMC) profiling, and flow cytometry assays to identify key immune dysfunctions. The figures evaluated include cytokine profiling in T-lymphocytes, CNS histopathology in humanized mice, and T-cell transcriptomics in MS patients. Findings show significant reductions in CD8+ T-cell function, increased CNS demyelination, and molecular markers for continuous T-cell use. Therapeutic implications point toward strategies such as B-cell depletion, EBV-specific cytotoxic T-cell restoration, and checkpoint inhibition. These approaches show promise in stopping EBV-mediated CNS damage and may form the basis for unified therapies for both neurological and oncological diseases with EBV involvement.