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Epstein-Barr virus infection of human brain microvessel endothelial cells: a novel role in multiple sclerosis
Costanza Casiraghi1, Katerina Dorovini-Zis, Marc S Horwitz
1Department of Microbiology and Immunology, The University of British Columbia, Vancouver, British Columbia, Canada.
Abstract:
Multiple sclerosis (MS) is an inflammatory neurological disease that is widely regarded as the outcome of complex interactions between a genetic predisposition and an environmental trigger. Epstein-Barr virus (EBV) has recently been associated with the onset of MS, yet understanding how it elicits autoimmunity remains elusive. Neuroinflammation, including the entry of autoreactive T cells, likely follows a breach of the blood-brain barrier (BBB) leading to CNS lesions in MS. We show that EBV can infect human BBB cells leading to increased production of pro-inflammatory mediators that result in immune cell adherence thus modeling a key step in MS pathogenesis.
Insights
Epstein-Barr virus (EBV) infects human blood-brain barrier cells, increasing inflammation and immune cell adherence. This finding models a key step in multiple sclerosis (MS) pathogenesis, linking EBV to the autoimmune disease.
Area of Science:
- Neurology
- Immunology
- Virology
Background:
- Multiple sclerosis (MS) is an inflammatory neurological disease.
- MS pathogenesis involves genetic and environmental factors.
- Epstein-Barr virus (EBV) is linked to MS onset, but mechanisms are unclear.
Purpose of the Study:
- To investigate how EBV contributes to MS pathogenesis.
- To model the initial steps of neuroinflammation in MS.
Main Methods:
- Infection of human blood-brain barrier (BBB) cells with EBV.
- Analysis of pro-inflammatory mediator production.
- Assessment of immune cell adherence to infected BBB cells.
Main Results:
- EBV successfully infected human BBB cells.
- Infection led to increased production of pro-inflammatory mediators.
- EBV-infected BBB cells showed enhanced immune cell adherence.
Conclusions:
- EBV infection of BBB cells promotes neuroinflammation.
- This process models a critical step in MS pathogenesis.
- EBV may play a direct role in initiating MS autoimmunity.
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