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De novo onset or relapse of optic neuritis in vaccinated individuals infected with SARS-CoV-2

In this study, the Chinese author investigated the prevalence of seropositivity for anti-myelin oligodendrocyte glycoprotein antibodies (MOG-Abs) and anti-aquaporin-4 antibodies (AQP4-Abs) in vaccinated individuals with de novo onset or relapse of optic neuritis (ON) after the infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 

The neuromyelitis optica spectrum disorder (NMOSD) is a rare chronic, relapsing, demyelinating, autoantibody-mediated disease of the central nervous system (CNS). It is also called Devic disease. The classical manifestation of this disease encompasses transverse myelitis, optic neuritis (ON), brainstem syndrome, and area postrema syndrome, which manifests as episodes of intractable vomiting and hiccoughs. Approximately 75% of patients have antibodies against AQP4, a water channel expressed on astrocytes. 

Although the etiology is still unknown, ON is believed to be an immune-mediated inflammation. Many pathogens, such as varicella-zoster, herpes simplex virus, Mycoplasma, and Mycobacterium tuberculosis can trigger a post-infectious immune-mediated ON and induce the production of anti-MOG and anti-AQP4 antibodies. Previous studies reported cases diagnosed with ON after the SARS-CoV-2 infection who were positive for anti-MOG-Abs and anti-AQP4-Abs. This indicates that SARS-CoV-2 can trigger ON and production of these antibodies.  



About the study

The author used a cell-based indirect immunofluorescence assay to determine the prevalence of seropositivity for anti-MOG-Abs and anti-AQP4-Abs in patients with de novo onset or relapse of ON after the infection with SARS-CoV-2. A reverse transcription‐polymerase chain reaction of nasopharyngeal swab for SARS-CoV-2 confirmed the infection.  The exclusion criteria were the presence of positive IgM or IgG antibodies against other pathogens, including Treponema pallidum, Mycobacterium tuberculosis, herpes viruses, hepatitis viruses, or HIV, as well as other ocular diseases that may have an impact on the evaluation of ON.

The mean follow-up period was 7.6 weeks, ranging from 8 to 16 weeks.

All patients underwent a complete ophthalmic examination, color fundus photography, and visual field testing. 29 cases had an orbital or brain magnetic resonance imaging (MRI). The serum samples were tested for anti-AQP4-Abs and anti-MOG-Abs and antibodies against other pathogens, such as Treponema pallidum, Mycobacterium tuberculosis, herpes viruses, hepatitis viruses, and HIV. In addition, the sera were tested for antinuclear antibodies, anti-double-stranded DNA, anti-Sjogren syndrome A or B antibodies, and anticardiolipin antibodies.

All 35 cases with confirmed ON diagnosis received at least two doses of the inactivated vaccine (Sinovac).




This prospective study included 35 individuals (46 eyes) with confirmed ON diagnosis and SARS-CoV-2 infection. In 24 cases, ON occurred unilaterally, whereas 11 cases had bilaterally ON.

In 29 cases, the viral infection occurred on average 12.3 days before the onset of ON and vision loss. In only two cases, the systemic symptoms of viral infection occurred on average 11.5 days after the onset of ON and vision loss. Six patients had a previous medical history of ON, three of them were positive for anti-AQP4-Abs and were treated with low-dose prednisone or immunosuppressive (azathioprine) therapy. The remaining three cases with a history of ON had discontinued their medical treatment months or years before the relapse of ON and were negative for anti-AQP4-Abs and anti-MOG-Abs. 

The mean age of the patients was 38.2 years (6-69 years), 17 were female. 

Orbital or cranial MRI was performed in 29 cases and showed an enlarged optic nerve. 

In 21 of 35 patients with confirmed ON, immunofluorescence findings demonstrated negative anti-MOG-Abs and anti-AQP4-Abs. Ten patients with ON were found to be positive for anti-MOG-Abs. 

All 35 cases were negative for IgM or IgG antibodies against pathogens such as Treponema pallidum, Mycobacterium tuberculosis, herpes viruses, hepatitis viruses, or HIV. Three ON cases were positive for anti-β2-glycoprotein IgM antibodies, two for anticardiolipin IgM, two for antinuclear antibodies, one for anti-Ro-52 antibodies, and one for Sjogren’s syndrome antibodies.



The author stated that the mechanism responsible for the production of anti-MOG-Abs after the SARS-CoV-2 infection can be molecular mimicry or the exposure of the MOG protein to antigen-presenting cells during inflammation induced by SARS-CoV-2. Also, the SARS-CoV-2 can compromise the blood-brain barrier. The neuroinvasion of SAR-CoV-2 or its antigens may lead to the release of CNS antigens such as AQP-4 into the systemic circulation, triggering the bystander immune response.

This study has shown that SARS-CoV-2 infection can trigger an initial onset or a relapse of optic neuritis. Further studies are needed to clarify the relationship between SARS-CoV-2 infection and the production of ati-MOG-Abs.


This article was published in Frontiers in Immunology.


Journal Reference

Sun C. Prevalence of serum MOG antibody and AQP4 antibody in optic neuritis after SARS-CoV-2 infection. Front. Immunol. 20 November 2023, Vol 14.
Sec. Autoimmune and Autoinflammatory Disorders: Autoimmune Disorders



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