Mary Wilson
Well-known member
Published: October 12, 2022
DOI: https://doi.org/10.1016/j.celrep.2022.111573
Danielle Beckman, Alyssa Bonillas, Giovanne B. Diniz, Sean Ott, Jamin W. Roh, Sonny R. Elizaldi, Brian A. Schmidt, Rebecca L. Sammak, Koen K.A. Van Rompay, Smita S. Iyer, John H. Morrison
Highlights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of coronavirus disease 2019 (COVID-19), can induce a plethora of neurological complications in some patients. However, it is still under debate if SARS-CoV-2 directly infects the brain or if CNS sequelae result from systemic inflammatory responses triggered in the periphery. Using high-resolution microscopy, we investigated whether SARS-CoV-2 reaches the brain and how viral neurotropism can be modulated by aging in a non-human primate model of COVID-19. Seven days after infection, SARS-CoV-2 was detected in the olfactory cortex and interconnected regions, accompanied by robust neuroinflammation and neuronal damage exacerbated in aged diabetic animals. Our study provides an initial framework for identifying the molecular and cellular mechanisms underlying SARS-CoV-2 neurological complications, which will be essential to reducing both the short- and long-term burden of COVID-19.
https://www.cell.com/action/showPdf?pii=S2211-1247(22)01434-6
DOI: https://doi.org/10.1016/j.celrep.2022.111573
Danielle Beckman, Alyssa Bonillas, Giovanne B. Diniz, Sean Ott, Jamin W. Roh, Sonny R. Elizaldi, Brian A. Schmidt, Rebecca L. Sammak, Koen K.A. Van Rompay, Smita S. Iyer, John H. Morrison
Highlights
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In macaques, SARS-CoV-2 is found in olfactory brain areas at 7 days post-infection - •
Neurons are initially the primary target of SARS-CoV-2 productive infection - •
Neurocovid is accompanied by robust neuroinflammation and vascular disruption - •
SARS-CoV-2 brain pathology is worsened by aging and diabetes in infected monkeys
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of coronavirus disease 2019 (COVID-19), can induce a plethora of neurological complications in some patients. However, it is still under debate if SARS-CoV-2 directly infects the brain or if CNS sequelae result from systemic inflammatory responses triggered in the periphery. Using high-resolution microscopy, we investigated whether SARS-CoV-2 reaches the brain and how viral neurotropism can be modulated by aging in a non-human primate model of COVID-19. Seven days after infection, SARS-CoV-2 was detected in the olfactory cortex and interconnected regions, accompanied by robust neuroinflammation and neuronal damage exacerbated in aged diabetic animals. Our study provides an initial framework for identifying the molecular and cellular mechanisms underlying SARS-CoV-2 neurological complications, which will be essential to reducing both the short- and long-term burden of COVID-19.
https://www.cell.com/action/showPdf?pii=S2211-1247(22)01434-6