key: cord-1019901-kcpt1d4e
authors: Tanasescu, Radu; Reindl, Markus
title: Guilty by association? SARS‐CoV‐2 antibodies and myelin oligodendrocyte glycoprotein antibody‐associated disease
date: 2022-04-03
journal: Eur J Neurol
DOI: 10.1111/ene.15335
sha: d01d37e68f5322040420c77dd5c97066af1e843b
doc_id: 1019901
cord_uid: kcpt1d4e

nan

samples from patients sent for myelin oligodendrocyte glycoprotein (MOG)-immunoglobulin G (IgG) testing for the presence of SARS-CoV-2 antibodies, to elucidate whether there is a correlation between COVID-19 and MOG antibody-associated disease (MOGAD) [2] . They report that SARS-CoV-2 IgG is more common in MOGAD than in controls and suggest that their findings provide preliminary data on the role of SARS-CoV-2 infection as a potential trigger of MOGAD.

The study is interesting for a number of reasons. It is the first study to date to look systematically into such a possible correlation in a larger group of MOGAD patients. By the nature of the study, the results raise to another level the debate on COVID-19 as a trigger for MOGAD, which is at this time still at the stage of case reports [3] .

The limitations are several (single centre, short follow-up, and still too small a sample size to infer a definite conclusion; other potential confounders such as the impact of other viral infections; lack of information on timing of occurrence of MOG antibodies after infection, which is key in discussing causation). Furthermore, the control group is not well selected, because it is not fully matched by clinical presentation and it is unclear how both the COVID-19 pandemic and increasing awareness of MOGAD among neurologists [4] might have influenced these results.

This study reports, in a group of newly diagnosed people with MOGAD, that SARS-CoV-2 IgG was twice more commonly found than in controls. This difference does not pass the threshold for significance of a Fisher test, but with such low numbers, the p-values may not be meaningful. The odds ratio is 2.67, but its 95% confidence interval crosses 1 (0.85-9.17). A power calculation shows the study is underpowered (39% power) and a sample size of at least 81 subjects in each group is needed to reach significance. The main value of this study therefore lies in providing pilot data to calculate estimations of effect sizes, which can allow future studies with a sample size adapted to a proper power. However, another recent study indicated that MOG-IgG-seropositive acute disseminated encephalomyelitis associated with SARS-CoV-2 infection is a rare finding [5] which should also be considered when planning future epidemiological studies. 

Do cross-reactive antibodies cause neuropathology in COVID-19?

Is there a correlation between MOGAD and SARS-CoV-2 infection?

SARS-CoV-2-related myelin oligodendrocyte glycoprotein antibody-associated disease: a case report and literature review

Myelinoligodendrocyte glycoprotein antibody-associated disease

Acute disseminated encephalomyelitis and acute hemorrhagic leukoencephalitis following COVID-19: systematic review and meta-synthesis

MOG antibody-associated disease after vaccination with ChAdOx1 nCoV-19

Neuromyelitis optica spectrum disorder after presumed coronavirus (COVID-19) infection: a case report