SARS-CoV-2 infects neurons, astrocytes, choroid plexus epithelial cells and pericytes of the human central nervous system in vitro

Author:

Haverty Ruth1ORCID,McCormack Janet2,Evans Christopher1,Purves Kevin1ORCID,O'Reilly Sophie3,Gautier Virginie43,Rochfort Keith5,Fabre Aurelie62,Fletcher Nicola F.41ORCID

Affiliation:

1. Veterinary Sciences Centre, University College Dublin, Belfield, Dublin 4, Ireland

2. Research Pathology Core Facility, Conway Institute of Biomedical and Biomolecular Research, University College Dublin, Belfield, Dublin 4, Ireland

3. Centre for Experimental Pathogen Host Research, School of Medicine, University College Dublin, Belfield, Dublin 4, Ireland

4. Conway Institute of Biomedical and Biomolecular Research, University College Dublin, Belfield, Dublin 4, Ireland

5. School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland

6. Department of Histopathology, St. Vincent’s University Hospital, Dublin 4, Ireland

Abstract

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is associated with neurological sequelae including haemorrhage, thrombosis and ischaemic necrosis and encephalitis. However, the mechanism by which this occurs is unclear. Neurological disease associated with COVID-19 has been proposed to occur following direct infection of the central nervous system and/or indirectly by local or systemic immune activation. We evaluated the expression of angiotensin-converting enzyme-2 and transmembrane protease, serine 2 (TMPRSS2) in brain tissue from five healthy human donors and observed low-level expression of these proteins in cells morphologically consistent with astrocytes, neurons and choroidal ependymal cells within the frontal cortex and medulla oblongata. Primary human astrocytes, neurons, choroid plexus epithelial cells and pericytes supported productive SARS-CoV-2 infection with ancestral, Alpha, Delta and Omicron variants. Infected cells supported the full viral life cycle, releasing infectious virus particles. In contrast, primary brain microvascular endothelial cells and microglia were refractory to SARS-CoV-2 infection. These data support a model whereby SARS-CoV-2 can infect human brain cells, and the mechanism of viral entry warrants further investigation.

Funder

Ireland Funds

Publisher

Microbiology Society

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