Last June, and article1 was published in the online digital version of this journal regarding the possible association between SARS-CoV-2 and Guillain-Barré syndrome (GBS). Through this letter we wish to reinforce the reality this binomial by conducting a bibliographic search of the cases published to this date.

Back in 1977, Peter Brian Medawar, an all-time greatest immunologists and Nobel Prize winner in Physiology said that a virus “is piece of bad news wrapped up in protein”. Although these words cannot be considered proper medical terminology per se, they do anticipate the catastrophic consequences of the person-to-person transmission of SARS-CoV-2 we have seen across the world.

The beta-coronavirus SARS-CoV-2 has the focus of attention of scientific publications over the last few months. However, we still do not know much about the underlying pathophysiological mechanism, virulence, and management of the infection caused by this virus.

In January 2020, China offered a new hypothesis to the international scientific community: GBS associated with SARS-CoV-2, ¿chance or coincidence?2

Six months have gone by since then. In a total of 14 countries (China, Switzerland, Spain, Morocco, Italy, France, Iran, Austria, Canada, The Netherlands, United States, Germany, Turkey, and United Kingdom) 39 clinical cases have been reportedly associated the virus with the syndrome, according to our bibliographic search (Annex 1 and 2, electronic supplementary data). Most cases reported are mild respiratory and abdominal symptoms prior to the appearance of neurological disorders in the SARS-CoV-2 infection setting. A total of 49% of the patients are > 60, and predominantly men (69%) as it has already been described in other series.3 The most prevalent clinical presentation has been acute inflammatory demyelinating polyradiculopathy (27 cases) followed by acute motor and sensory axonal neuropathy (4 cases). A total of 33% of the patients required respiratory support. The albuminocytologic dissociation, an important step to achieve the diagnosis,4 was confirmed in 21 patients while in 7 no lumbar puncture was performed. A total of 87% of the patients were treated with immunoglobulins and 10% with plasmapheresis. To this date, based on the data reported in the articles reviewed, 2 patients have died (5%), both of acute respiratory failure.

The medical literature searched and analyzed during this review is consistent with the existence of an etiological link between SARS-CoV-2 and GBS. Considering the high number of patients infected with this virus we conclude that the cases of post-infectious polyradiculopathies will exceed the annual incidence rate that is estimated in 0.6–4 cases/for every 100,000 inhabitants/per year.5 We will have to wait to see the response to therapy, the neurological sequelae occurred, and the lethality due to SARS-CoV-2-induced GBS.