SARS-CoV-2 infects neurons and induces neuroinflammation in a non-human primate model of COVID-19

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

Research output: Contribution to journalArticlepeer-review

39 Scopus citations

Abstract

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.

Original languageEnglish
Article number111573
JournalCell Reports
Volume41
Issue number5
DOIs
StatePublished - 1 Nov 2022
Externally publishedYes

Keywords

  • CP: Microbiology
  • CP: Neuroscience
  • NHP
  • astrocytes
  • coronavirus
  • macaque
  • microglia
  • neurotropism
  • rhesus

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