Sarah J. Medina
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Sarah J. Medina has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Babu V. Sajesh
Cancer Care Manitoba Research Institute—CCMRI, Winnipeg, MB R3E 0V9, Canada
1 shared publication - Bryce M. Warner
Special Pathogens Program, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada
1 shared publication - Darwyn Kobasa
Special Pathogens Program, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Canada
1 shared publication - Heidi Wood
National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, Manitoba, Canada
1 shared publication - Jessy A. Slota
Public Health Agency of Canada
1 shared publication - Kathy Frost
Mycobacteriology, Vector-Borne and Prion Diseases Division, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg, MB R3E 3R2, Canada
1 shared publication
Latest Publications
- Open Access
Non-Productive Infection of Glial Cells with SARS-CoV-2 in Hamster Organotypic Cerebellar Slice Cultures
The numerous neurological syndromes associated with COVID-19 implicate an effect of viral pathogenesis on neuronal function, yet reports of direct SARS-CoV-2 infection in the brain are conflicting. We used a well-established organotypic brain slice culture to determine the permissivity of hamster brain tissues to SARS-CoV-2 infection. We found levels of live virus waned after inoculation and observed no evidence of cell-to-cell spread, indicating that SARS-CoV-2 infection was non-productive. Nonetheless, we identified a small number of infected cells with glial phenotypes; however, no evidence of viral infection or replication was observed in neurons. Our data corroborate several clinical studies that have assessed patients with COVID-19 and their association with neurological involvement.
Open AccessNon-Productive Infection of Glial Cells with SARS-CoV-2 in Hamster Organotypic Cerebellar Slice Cultures
The numerous neurological syndromes associated with COVID-19 implicate an effect of viral pathogenesis on neuronal function, yet reports of direct SARS-CoV-2 infection in the brain are conflicting. We used a well-established organotypic brain slice culture to determine the permissivity of hamster brain tissues to SARS-CoV-2 infection. We found levels of live virus waned after inoculation and observed no evidence of cell-to-cell spread, indicating that SARS-CoV-2 infection was non-productive. Nonetheless, we identified a small number of infected cells with glial phenotypes; however, no evidence of viral infection or replication was observed in neurons. Our data corroborate several clinical studies that have assessed patients with COVID-19 and their association with neurological involvement.