EBV DNA was highly prevalent in the CSF of treatment-naïve neuro-Behçet's disease patients (71.43%, versus 35.29% in MS), was linked to type II latency gene expression, an IFN-γ/IFN-α and Th1/Th17 signature with reduced FOXP3, and parenchymal disease occurred exclusively in EBV-positive patients, suggesting EBV may contribute to NBD pathophysiology by promoting a pro-inflammatory intrathecal microenvironment.
EBV DNA was detected in the CSF of 71.43% of NBD patients, significantly more than in MS patients (35.29%).
Other neurotropic herpesviruses were rarely detected in the CSF.
EBV presence in CSF was not associated with a specific intrathecal humoral response.
LMP1 and EBNA1 latent genes were expressed concurrently in CSF of NBD patients, indicating a type II latency program.
EBV-positive NBD patients had significantly elevated IFN-γ and IFN-α in CSF.
EBV-positive patients showed reduced FOXP3 expression, reflecting a Th17/Treg imbalance.
Parenchymal forms of NBD were observed exclusively in EBV-positive patients.
The authors propose EBV as a potential biomarker and therapeutic target in NBD.
This study looked at whether Epstein-Barr virus (EBV), a common virus known to be linked to multiple sclerosis, might also play a role in neuro-Behçet's disease, a rare inflammatory condition affecting the nervous system. Researchers tested blood and spinal fluid from patients who had not yet received treatment. They found EBV DNA in the spinal fluid of about 71% of neuro-Behçet's patients, compared with about 35% of people with multiple sclerosis. Other herpesviruses were rarely found. The virus did not appear to trigger a specific antibody response in the spinal fluid, which the authors interpret as the virus mostly being dormant and kept in check by cellular immunity. However, EBV-positive patients showed signs of an active inflammatory environment: higher interferon levels, a shift toward Th1/Th17 immune cells, and lower FOXP3, a marker of regulatory T cells that help calm immune responses. Notably, forms of the disease affecting the brain tissue itself (parenchymal forms) occurred only in EBV-positive patients. This research suggests EBV may contribute to inflammation in neuro-Behçet's disease and could eventually serve as a biomarker or treatment target. The findings show association rather than proof of cause, and the patient groups were likely small, so further studies are needed to confirm them.
Ben Laamari R, Saied Z, Maghrebi O, Bahrini K, Bekir J, Stiti A, et al.. (2026). Epstein-Barr virus shapes intrathecal Th1/Th17 immunity and parenchymal involvement in neuro-Behçet's disease.. Frontiers in immunology. https://doi.org/10.3389/fimmu.2026.1921667