key: cord-1008173-aifsbm4l
authors: Hussain, Faraz S.; Eldeeb, Mohamed A.; Blackmore, Derrick; Siddiqi, Zaeem A.
title: Guillian Barré syndrome and COVID-19: Possible role of the cytokine storm()
date: 2020-10-22
journal: Autoimmun Rev
DOI: 10.1016/j.autrev.2020.102681
sha: a65259235cffa9feabd19205e2d9ecaa73fb3b3a
doc_id: 1008173
cord_uid: aifsbm4l

nan

The typical GBS is a heterogonous disease with considerable clinical and phenotypic variation.

The two major types included the acute inflammatory demyelinating polyneuropathy (AIDPdemyelinating) and acute motor axonal neuropathy (AMAN-axonal), where the immunologic processes target the myelin or the axons, respectively. In about 2/3rd of cases GBS is preceded by a bacterial or viral infection of the respiratory or gastrointestinal tract with Campylobacter jejuni (26-65%) [8] , cytomegalovirus (10-15%), Epstein-Barr virus (8-10%) being the most common preceding infections. Other agents include mycoplasma pneumonia, haemophilus influenzae, and influenza A virus [9] . Antecedent infection with hepatitis E virus (HEV) has been noted to be a potential trigger of GBS in up to 5 to10% patients [10, 11] . Outbreaks of the Zika virus resulted in an upsurge of GBS incidence that was more sever [12] . About 50-85% of patients with GBS or its variants have antiganglioside antibodies in their sera [13, 14] .

Gangliosides are sialylated glycosphingolipids found abundantly in various nervous tissues and the antibodies develop post-infection due to shared epitopes between the gangliosides and the infectious agent. In GBS, this phenomenon of molecular mimicry leads to binding of the antibody to nerves causing conduction blocks and axonal degeneration.

Recent case reports and case series show that GBS associated with COVID -19 has multiple distinctive features. As compared to the typical "post-infectious" course in the classical form, the GBS associated with COVID 19 presents as an "acute para-infection" as almost all reported cases have had acute onset within days of onset of viral infection, mostly within first few days. In COVID-19, the early CRS results in a surge of several cytokines include interleukin-1β (IL-1β), IL-6, IL-17, tumor necrosis factor-α (TNF-α), interferon-γ (IF-γ) along with other chemokines [16] , which are the mediators of the widespread and severe damage culminating in multi-organ failure and death primarily associated with acute respiratory distress syndrome [17] . 6. The COVID-19-mediated CRS causes a surge in the brain of IL-2, IL-7, interferon-γ, macrophage inflammatory protein 1-α, and TNF-α, leading to hyperinflammation, severe encephalopathy and stroke [23] . [24] likely, due to their ability to modulate a number of cytokines i.e. IL-1, IL-6, IL-8, IL-12 and TNFα. Low dose corticosteroids have also been previously used in the closely related SARS-CoV outbreaks [25, 26] . Till more data becomes available in patients with COVID-19 associated GBS, it may not be unreasonable to have concurrent steroids on board along with other conventional therapies.

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