Guillain-Barré syndromes (GBSs) comprise a spectrum of polyneuropathies characterized by acute (within 1–4 weeks) ascending motor weakness, mild or moderate sensory abnormalities, occasional cranial nerve involvement, and muscle or radicular pain. According to the degree of involvement of the motor or sensory nerves, myelin sheath, axon, or cranial nerve predominance, the most common subtypes are the acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and the Miller Fisher syndrome (MFS) characterized by acute ophthalmoplegia, gait ataxia, and areflexia.1 GBS is one of the prototypic viral-triggered autoimmune neurologic diseases as approximately 70% of the patients have a preceding by 1–3 weeks, flu-like, viral illness.1–3 Among the infectious agents associated with triggering sporadic GBS are viruses, including influenza, enteroviruses, cytomegalovirus, Epstein–Barr virus, herpes simplex virus, hepatitis, or HIV, and bacteria, such as Campylobacter jejuni, Mycoplasma pneumoniae, and Haemophilus influenzae.1 GBS outbreaks have been also associated with viral epidemics or pandemics, including H1N1, swine flu A/New Jersey influenza strain, arthropod-borne flaviviruses, such as the West Nile virus, chikungunya, or Zika, and with coronaviruses, including the Middle East respiratory syndrome (MERS)-CoV and SARS-CoV.1–3