[No authors listed]
Infection by the severe acute respiratory syndrome (SARS) coronavirusâ2 (SARSâCoVâ2) is the cause of the new viral infectious disease (coronavirus disease 2019; COVIDâ19). Emerging evidence indicates that COVIDâ19 may be associated with a wide spectrum of neurological symptoms and complications with central nervous system (CNS) involvement. It is now wellâestablished that entry of SARSâCoVâ2 into host cells is facilitated by its spike proteins mainly through binding to the angiotensinâconverting enzyme 2 (ACEâ2). Preclinical studies have suggested that neuropilinâ1 (NRP1), which is a transmembrane receptor that lacks a cytosolic protein kinase domain and exhibits high expression in the respiratory and olfactory epithelium, may also be implicated in COVIDâ19 by enhancing the entry of SARSâCoVâ2 into the brain through the olfactory epithelium. In the present study, we expand on these findings and demonstrate that the NRP1 is also expressed in the CNS, including olfactoryârelated regions such as the olfactory tubercles and paraolfactory gyri. This furthers supports the potential role of NRP1 as an additional SARSâCoVâ2 infection mediator implicated in the neurologic manifestations of COVIDâ19. Accordingly, the neurotropism of SARSâCoVâ2 via NRP1âexpressing cells in the CNS merits further investigation.
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