Virus antibody responses in patients with myelin oligodendrocyte glycoprotein antibody-associated disease and multiple sclerosis

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an antibody-mediated inflammatory disorder of the central nervous system, which is characterized by demyelination targeting the optic nerve, brain, and spinal cord. The etiology of MOGAD still remains to be elucidated. Here we performed a retrospective study comparing virus antibody levels of monophasic MOGAD patients to relapsing-remitting multiple sclerosis patients (RRMS) and healthy controls (HCs).

We enrolled 19 patients with monophasic MOGAD (F:M 13:6, mean 41 years) and 30 patients with RRMS (F:M 21:9, mean 41 years) referred to the Department of Neurology at Rigshospitalet Glostrup, Denmark. Moreover, 15 HCs (F:M 8:7, mean 43 years) were included. Patients and HCs were matched according to age and gender when possible. Antibody levels to Epstein-Barr virus (EBV) Epstein-Barr nuclear antigen (EBNA)1, human herpes virus (HHV) 6A polymerase processivity factor, John Cunningham virus (JCV) major capsid protein 1, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein and cytomegalovirus (CMV) phosphoprotein 52 were measured by enzyme-linked immunosorbent assay.

No differences in antibody levels to HHV6, CMV, and JCV proteins were observed between MOGAD patients and HCs. Similarly, no significant differences in antibody levels to SARS-CoV-2, HHV6, CMV, and JCV were found between MOGAD patients and RRMS patients. However, RRMS patients presented with significantly increased EBV EBNA1 IgG levels in when compared to MOGAD patients and HCs.

Our findings suggest that development of MOGAD is neither associated with SARS-CoV-2, HHV6, CMV nor JCV alone. Furthermore, results presented indicate that EBV serology is different in MOGAD patients compared to RRMS, confirming a role of EBV in the development of MS and suggesting that the etiology of MOGAD is different from MS.