SARS-CoV-2 and neurotropism: evidence, gaps and reflections.

Abstract

Coronavirus disease 2019 (COVID-19) patients may present with a wide clinical spectrum, including extrapulmonary involvement, such as neurological damage. Although the pathogenesis of neurological COVID-19 still remains unclear, some studies have discussed the potential association between tissue injury and severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) infection in the central nervous system (CNS) and/or immune imbalance. These two mechanisms are non-mutually exclusive; however, exacerbated inflammatory-response-induced neurological damage appears to be more aligned with COVID-19 pathogenesis, whereas SARS-CoV-2 infection/replication in the CNS remains widely discussed. Herein, we dissect this last issue, highlighting some evidence on SARS-CoV-2 neuroinvasion, as well as discussing gaps that should be addressed for a better understanding of its potential neurotropism, specifically in the CNS. Finally, we propose some deeper reflections on the SARS-CoV-2 neurotropic potential.