Autoimmunity of COVID-19–GBS: significance of sialic acids present in the coronaviruses and peripheral nerve myelin In 7/11 tested patients with COVID-19–GBS, the virus was not detected in the CSF, implying no direct root infection or intrathecal viral replication. The improvement of several patients with IVIg and the presence of GD1b antibodies in 1 tested patient suggest a postviral-triggered immune response similar to other postviral-induced GBS cases1–3 or other postviral autoimmune neurologic disorders.14 The reported GD1b ganglioside antibodies, however, although in contrast to GQ1b antibodies typically seen in MFS, are of very special interest. The SARS-CoV 3a protein contains oligosaccharides with direct evidence that sialic acids play a critical role in human coronavirus infection.15 It has been just shown that the attachment of coronaviruses to the surface of respiratory cells is mediated by the spike (S) viral protein, which binds not only to the angiotensin-converting enzyme 2 (ACE-2) receptor for entry16 but also to sialic acid–containing glycoproteins and gangliosides on cell surfaces.15 Such a dual receptor/attachment is proposed to be a reason for the increased transmissibility of COVID-19 compared with SARS-CoV that binds only to ACE-2 receptor.15,16 Of relevance to GBS is that various gangliosides, most commonly those containing either a disialosyl moiety, such as GD1b, GQ1b, and GT1b, or 2 gangliosides that share epitopes with GM2, or a combination of GM2 and GM1, GM1 and GD1b, can serve as antigens in patients with neuropathies.17 When IgM recognizes the Gal (pl-3) GalNAc moiety of GM1, which is found on the surface of motor neurons, there is clinically a motor neuropathy, but if recognizes epitopes containing disialosyl groups of GDlb, which is present on the dorsal root ganglionic neurons, there is sensory ataxic neuropathy.17 Immunization of rabbits with GDlb also causes sensory ataxic neuropathy mimicking the human disease.18 Of interest, the first described patient with sensory ataxic neuropathy and GDlb antibodies had also ophthalmoplegia,19 as seen in MFS and the present series.10 As COVID-19 spike interacts with the GalNAc residue of GM1 and ganglioside dimers for anchoring to cell surface gangliosides,15 cross-reactivity between epitopes within the COVID-19 spike-bearing gangliosides and signature sugar residues of surface peripheral nerve glycolipids is a very likely possibility. Such typical molecular mimicry has been shown between peripheral nerve glycolipids and Campylobacter jejuni or Zika virus that also trigger GBS.1–3 Accordingly, all GBS subtypes (AIDP, AMAN, and MFS) can be expected with COVID-19, necessitating screening for ganglioside antibodies to assess autoimmunity. An interesting therapeutic component in this association is the emerging data that chloroquine, an antimalarial drug under investigation for treating COVID-19, binds with high-affinity sialic acids and GM1 gangliosides and, in the presence of chloroquine, the SARS-CoV viral spike cannot bind gangliosides to infect the targeted cells.15 If benefit is confirmed and safety is established, chloroquine may be of added therapeutic value in future patients with COVID-19–triggered GBS in conjunction with IVIg.