The Relationship between Anti-Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease and the Rubella Virus

Choi, Seok Jin; Oh, Dan A; Chun, Woochang; Kim, Sung Min

doi:10.3988/jcn.2018.14.4.598

Cited by 5 publications

(4 citation statements)

References 13 publications

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“…57 Because our multiple sclerosis patients were universally positive for IgG antibodies against Epstein-Barr virus nuclear antigen compared with only 29% of MOGAD patients, it appears that this is a key distinction between the 2 disorders and that the pathogen required for the aberrant immune response in MOGAD is not Epstein-Barr virus. Several studies have linked rubella, SARS-CoV-2, and even Pseudomonas to eventual MOG antibody positivity, 55,58,59 but a definitive link remains unascertained. With this in mind, the substantial trend toward increased day care attendance in the MOGAD group is noteworthy in that it may play a role in catalyzing the early childhood viral exposures that provoke the aberrant immune response noted in MOGAD patients.…”

Section: Discussionmentioning

confidence: 99%

Socioeconomic, Clinical, and Laboratory Parameters Differentiating Pediatric Patients With MOG Antibody–Associated Disease and Multiple Sclerosis

Florenzo

Brenton

2023

J Child Neurol

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Studies indicate differences in the clinical phenotypes and neuroimaging of children with myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD) compared to multiple sclerosis; however, there are limited data assessing the socioeconomic and paraclinical differences between these distinct disorders. This retrospective study identified patients aged <18 years at time of diagnosis with MOGAD or multiple sclerosis. Demographics, birth history, socioeconomic factors (insurance type, median income, parental education level), and paraclinical features (clinical manifestations, laboratory evaluation) were recorded for eligible participants. Seventy-eight patients (28 MOGAD, 50 multiple sclerosis) met inclusion criteria. Mothers of MOGAD children were more likely to have attended college compared to the mothers of children with multiple sclerosis (80% vs 49%; P = .02). Though MOGAD patients had greater rates of day care attendance (81% vs 57%), lower rates of birth complications (7% vs 21%), and higher rates of being breastfed (65% vs 46%), these findings did not meet predefined statistical significance. Clinically, children with MOGAD exhibited a lower body mass index percentile at presentation (58th ± 27th percentile vs 83rd ± 20th percentile; P = .0001) and were younger (7.6 ± 4.1 vs 14.8 ± 1.6 years; P < .0001) and more likely to exhibit an infectious prodrome (57% vs 10%; P < .0001). MOGAD patients were less likely to have evidence of remote Epstein-Barr virus infection (29% vs 100%; P < .0001) and less likely to have ≥3 unique oligoclonal bands in the cerebrospinal fluid (5% vs 87%; P < .001). Compared with multiple sclerosis, children with MOGAD exhibit lower body mass index percentiles at presentation, are more likely to have mothers with higher education levels, and are less likely to have had prior Epstein-Barr virus infection. Our data confirm that MOGAD patients are younger, more likely to exhibit infectious prodrome, and are less likely to exhibit intrathecal synthesis of oligoclonal bands. These features provide new insights into the differentiating pathobiology of MOGAD and may be helpful in differentiating these children from multiple sclerosis early in the diagnostic evaluation.

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Section: Discussionmentioning

confidence: 99%

Socioeconomic, Clinical, and Laboratory Parameters Differentiating Pediatric Patients With MOG Antibody–Associated Disease and Multiple Sclerosis

Florenzo

Brenton

2023

J Child Neurol

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“…MOG-associated disorders may emerge in the setting of infections (mainly viral) and, extremely rarely, vaccination. Although the overall proportion of postinfectious cases is not known, MOG-associated disorders have been associated with a wide variety of infectious organisms, including influenza, 22 Epstein-Barr virus, 23 herpes simplex virus, 24 severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), 25 human herpes virus 6, 26,27 Borrelia , 27 measles, 28 Zika virus, 29 Mycoplasma pneumoniae , 30 and unspecified infections 18 . That the disease can arise in the aftermath of such diverse microorganisms argues against the sole mechanism being molecular mimicry and may instead suggest an epiphenomenon associated with robust immune activation and/or disruption of the blood-brain barrier.…”

Section: Epidemiology and Clinical Course Of Myelin Oligodendrocyte G...mentioning

confidence: 99%

Myelin Oligodendrocyte Glycoprotein–Associated Disorders

Longbrake¹

2022

CONTINUUM: Lifelong Learning in Neurology

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PURPOSE OF REVIEW: Anti-myelin oligodendrocyte glycoprotein (MOG) autoantibodies have become a recognized cause of a pathophysiologically distinct group of central nervous system (CNS) autoimmune diseases. MOG-associated disorders can easily be confused with other CNS diseases such as multiple sclerosis or neuromyelitis optica, but they have a distinct clinical phenotype and prognosis.RECENT FINDINGS: Most patients with MOG-associated disorders exhibit optic neuritis, myelitis, or acute disseminated encephalomyelitis (ADEM) alone, sequentially, or in combination; the disease may be either monophasic or relapsing. Recent case reports have continued to expand the clinical spectrum of disease, and increasingly larger cohort studies have helped clarify its pathophysiology and natural history. SUMMARY: Anti-MOG-associated disorders comprise a substantial subset of patients previously thought to have other seronegative CNS diseases. Accurate diagnosis is important because the relapse patterns and prognosis for MOG-associated disorders are unique. Immunotherapy appears to successfully mitigate the disease, although not all agents are equally effective. The emerging large-scale data describing the clinical spectrum and natural history of MOG-associated disorders will be foundational for future therapeutic trials. UNLABELED USE OF PRODUCTS/INVESTIGATIONAL USE DISCLOSURE:Dr Longbrake discusses the unlabeled/investigational use of immunomodulators, none of which is approved for the treatment of myelin oligodendrocyte glycoprotein-associated disorders.

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“…In addition, in a Chinese cohort, there was an association between pediatric-onset MOGAD for DQB1*05:02-DRB1*16:02, but not for adult MOGAD ( 46 ). Moreover, in some cases, a viral infection preceded MOGAD diagnosis: Epstein–Barr virus, herpes simplex virus 1, rubella, varicella zoster virus, and severe acute respiratory syndrome–coronavirus-2 ( 47 48 49 50 51 52 ). A rare paraneoplastic incidence of MOGAD has also been described ( 53 ).…”

Section: T- and B-cell Mediated Pathogenesis Of Myelin Oligodendrocyt...mentioning

confidence: 99%

The Potential Pathogenicity of Myelin Oligodendrocyte Glycoprotein Antibodies in the Optic Pathway

Lerch

Bauer²,

Reindl³

2022

Journal of Neuro-Ophthalmology

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Background: Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an acquired inflammatory demyelinating disease with optic neuritis (ON) as the most frequent clinical symptom. The hallmark of the disease is the presence of autoantibodies against MOG (MOG-IgG) in the serum of patients. Whereas the role of MOG in the experimental autoimmune encephalomyelitis animal model is well-established, the pathogenesis of the human disease and the role of human MOG-IgG is still not fully clear. Evidence Acquisition: PubMed was searched for the terms “MOGAD,” “optic neuritis,” “MOG antibodies,” and “experimental autoimmune encephalomyelitis” alone or in combination, to find articles of interest for this review. Only articles written in English language were included and reference lists were searched for further relevant papers. Results: B and T cells play a role in the pathogenesis of human MOGAD. The distribution of lesions and their development toward the optic pathway is influenced by the genetic background in animal models. Moreover, MOGAD-associated ON is frequently bilateral and often relapsing with generally favorable visual outcome. Activated T-cell subsets create an inflammatory environment and B cells are necessary to produce autoantibodies directed against the MOG protein. Here, pathologic mechanisms of MOG-IgG are discussed, and histopathologic findings are presented. Conclusions: MOGAD patients often present with ON and harbor antibodies against MOG. Furthermore, pathogenesis is most likely a synergy between encephalitogenic T and antibody producing B cells. However, to which extent MOG-IgG are pathogenic and the exact pathologic mechanism is still not well understood.

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The Relationship between Anti-Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease and the Rubella Virus

Cited by 5 publications

References 13 publications

Socioeconomic, Clinical, and Laboratory Parameters Differentiating Pediatric Patients With MOG Antibody–Associated Disease and Multiple Sclerosis

Socioeconomic, Clinical, and Laboratory Parameters Differentiating Pediatric Patients With MOG Antibody–Associated Disease and Multiple Sclerosis

Myelin Oligodendrocyte Glycoprotein–Associated Disorders

The Potential Pathogenicity of Myelin Oligodendrocyte Glycoprotein Antibodies in the Optic Pathway

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