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Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis
Published on: September 7, 2022
Severe post-EBV encephalopathy associated with myelin oligodendrocyte glycoprotein-specific immune response
Samantha Jilek1, Jens Kuhle, Pascal Meylan
1Divisions of Immunology and Allergy, Centre Hospitalier Universitaire Vaudois, Rue du Bugnon, 1011 Lausanne, Switzerland.
Abstract:
The mechanisms leading to CNS disorders after EBV infections are unclear. We report the case of a patient who developed a severe, but reversible, encephalopathy following an infectious mononucleosis. We detected no EBV DNA in the blood or in the cerebrospinal fluid (CSF) and no EBV-specific antibodies in the CSF. However, we found a potent MOG-specific cellular and humoral immune response. Interestingly, MOG-specific cellular immune response rapidly decreased, paralleling the improvement of clinical condition. In conclusion, this detailed study shows that acute EBV infection can trigger a potent auto-inflammatory response in the CNS, without evidence of an overt infection.
Insights
Acute Epstein-Barr virus (EBV) infection can trigger central nervous system (CNS) autoimmunity. This case study reveals a reversible encephalopathy linked to a MOG-specific immune response, not direct EBV infection.
Area of Science:
- Neuroimmunology
- Infectious Diseases
- Neurology
Background:
- Central nervous system (CNS) disorders following Epstein-Barr virus (EBV) infections lack clear mechanistic understanding.
- Investigating the link between EBV and neurological sequelae is crucial for understanding CNS autoimmunity.
Observation:
- A patient presented with severe, yet reversible, encephalopathy after infectious mononucleosis.
- No EBV DNA or EBV-specific antibodies were detected in the patient's blood or cerebrospinal fluid (CSF).
Findings:
- A significant MOG-specific (myelin oligodendrocyte glycoprotein) cellular and humoral immune response was identified.
- The MOG-specific cellular immune response diminished as the patient's clinical condition improved.
Implications:
- Acute EBV infection can initiate CNS autoimmunity without overt viral presence.
- This suggests EBV may act as a trigger for autoimmune responses targeting CNS myelin.
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