SARS-CoV-2 infects neurons and induces neuroinflammation in a non-human primate model of COVID-19
Jun 25, 2024 21:47:12 GMT
Post by Nadica (She/Her) on Jun 25, 2024 21:47:12 GMT
SARS-CoV-2 infects neurons and induces neuroinflammation in a non-human primate model of COVID-19 - Published Nov 1, 2022
Highlights
•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
Summary
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 whether SARS-CoV-2 directly infects the brain or whether CNS sequelae result from systemic inflammatory responses triggered in the periphery. By 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 and was 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.
Graphical abstract
Highlights
•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
Summary
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 whether SARS-CoV-2 directly infects the brain or whether CNS sequelae result from systemic inflammatory responses triggered in the periphery. By 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 and was 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.
Graphical abstract