There is now increasing collaborative activity by governments, academic institutions, biotechnology companies, and the pharmaceutical industry to investigate the range of possible treatments for COVID-19 and vaccines to prevent infection from SARS-CoV-2 [1]. Current approaches are drawing on previous studies on severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome (MERS-CoV) [1]. For example, studies have shown that SARS-CoV and SARS-CoV-2 have structural similarities within their respective receptor-binding domains (RBDs) of the S1 spike protein subunit that mediate strong multi-point binding to the extracellular globular domain of angiotensin-converting enzyme-2 (ACE2), which may involve neurological expression [2–9]. Within the lung, widespread expression of ACE2 by alveolar epithelia and capillary cells facilitates viral infection via internalization and replication, leading to severe respiratory disease [2,3]. Recent evidence of co-morbid neurological sequelae of SARS-CoV-2 infection has been reported in the presence or absence of severe respiratory disease where patients have presented with symptoms of nausea, vomiting, anosmia, loss of taste, impaired consciousness, agitation and confusion, corticospinal tract signs, and cerebrovascular diseases, including encephalopathy [5–7].