MOG Antibody–Associated Disease Presenting as Encephalitis With Concurrent EBV Findings: A Case

08 May 20264 min read0 viewsJournal Feed

GIST

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an autoimmune disorder affecting the central nervous system (CNS), characterized by the presence of autoantibodies against MOG (MOG-IgG) in serum or cerebrospinal fluid (CSF). While Epstein-Barr virus (EBV) is implicated in multiple sclerosis (MS), its role in MOGAD remains unclear.

Here, we report five cases of newly diagnosed MOGAD manifesting as encephalitis, in whom concurrent EBV-related laboratory findings were detected. All patients tested positive for serum MOG-IgG by live cell-based assay (CBA).

Regarding therapeutic response, three patients exhibited transient improvement in CSF parameters following initial antiviral therapy. However, clinical recovery was observed only after administration of corticosteroids (either high- or low-dose).

In refractory cases, additional interventions with intravenous immunoglobulin (IVIG) or tocilizumab were applied. In conclusion, this case series suggests that EBV-associated immune activation may coexist with some MOGAD patients presenting as encephalitis, which requires validation in larger prospective and mechanistic studies in the future.

Clinical Editorial

Emergent clinical pattern and design: Context and scope

Concurrent laboratory indicators suggestive of Epstein-Barr virus (EBV) involvement were detected.

This case-series summarizes five individuals with newly diagnosed MOG antibody–associated disease presenting as encephalitis, all testing positive for serum MOG-IgG by live cell-based assay.

Population and diagnostic framework

Patients were identified as having MOGAD with encephalitic presentation.
EBV-related laboratory findings were observed alongside MOG-IgG positivity.

Interventions and therapeutic sequence

Initial antiviral therapy yielded transient improvements in cerebrospinal fluid (CSF) parameters for three patients.
True clinical recovery emerged following corticosteroid treatment, with either high- or low-dose regimens.
For cases unresponsive to steroids, additional measures included intravenous immunoglobulin (IVIG) or tocilizumab.

Major signal and interpretation

The series notes a pattern where EBV-associated immune activation may coexist with MOGAD presenting as encephalitis.
Corticosteroids appear pivotal for clinical recovery after an initial antiviral response.

Limitations and need for further study

The authors emphasize that conclusions require validation in larger prospective cohorts and mechanistic studies to clarify the relationship between EBV activation and MOGAD.