tetano
Editor, Senior Moderator
Front Immunol
. 2021 Jul 27;12:697329.
doi: 10.3389/fimmu.2021.697329. eCollection 2021.
SARS-CoV-2 Poorly Replicates in Cells of the Human Blood-Brain Barrier Without Associated Deleterious Effects
Orianne Constant[SUP] 1 [/SUP], Jonathan Barthelemy[SUP] 1 [/SUP], Karine Bolloré[SUP] 1 [/SUP], Edouard Tuaillon[SUP] 1 [/SUP], Fabien Gosselet[SUP] 2 [/SUP], Christine Chable-Bessia[SUP] 3 [/SUP], Peggy Merida[SUP] 4 [/SUP], Delphine Muriaux[SUP] 3 4 [/SUP], Philippe Van de Perre[SUP] 1 5 [/SUP], Sara Salinas[SUP] 1 [/SUP], Yannick Simonin[SUP] 1 [/SUP]
Affiliations
Abstract
Various neurological symptoms have been associated to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection including headache, fever, anosmia, ageusia, but also, encephalitis, Guillain-Barre syndrome and ischemic stroke. Responsible for the current coronavirus disease (COVID-19) pandemic, SARS-CoV-2 may access and affect the central nervous system (CNS) by several pathways such as axonal retrograde transport or through interaction with the blood-brain barrier (BBB) or blood-cerebrospinal fluid (CSF) barrier. Here, we explored the molecular and cellular effects of direct SARS-CoV-2 infection of human BBB cells. We observed low replication of SARS-CoV-2 that was accompanied by very moderate inflammatory response. Using a human in vitro BBB model, we also described low replication levels without strong inflammatory response or modulation of endothelium integrity. Finally, using serum samples from COVID-19 patients, we highlighted strong concentrations of pro-inflammatory factors that did not perturb BBB integrity after short term exposure. Altogether, our results show that the main mechanism of brain access following SARS-CoV-2 infection does not seem to be directed by brain infection through endothelial cells.
Keywords: COVID-19; SARS-CoV-2; blood-brain barrier; central nervous system; inflammation.
. 2021 Jul 27;12:697329.
doi: 10.3389/fimmu.2021.697329. eCollection 2021.
SARS-CoV-2 Poorly Replicates in Cells of the Human Blood-Brain Barrier Without Associated Deleterious Effects
Orianne Constant[SUP] 1 [/SUP], Jonathan Barthelemy[SUP] 1 [/SUP], Karine Bolloré[SUP] 1 [/SUP], Edouard Tuaillon[SUP] 1 [/SUP], Fabien Gosselet[SUP] 2 [/SUP], Christine Chable-Bessia[SUP] 3 [/SUP], Peggy Merida[SUP] 4 [/SUP], Delphine Muriaux[SUP] 3 4 [/SUP], Philippe Van de Perre[SUP] 1 5 [/SUP], Sara Salinas[SUP] 1 [/SUP], Yannick Simonin[SUP] 1 [/SUP]
Affiliations
- PMID: 34386007
- PMCID: PMC8353323
- DOI: 10.3389/fimmu.2021.697329
Abstract
Various neurological symptoms have been associated to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection including headache, fever, anosmia, ageusia, but also, encephalitis, Guillain-Barre syndrome and ischemic stroke. Responsible for the current coronavirus disease (COVID-19) pandemic, SARS-CoV-2 may access and affect the central nervous system (CNS) by several pathways such as axonal retrograde transport or through interaction with the blood-brain barrier (BBB) or blood-cerebrospinal fluid (CSF) barrier. Here, we explored the molecular and cellular effects of direct SARS-CoV-2 infection of human BBB cells. We observed low replication of SARS-CoV-2 that was accompanied by very moderate inflammatory response. Using a human in vitro BBB model, we also described low replication levels without strong inflammatory response or modulation of endothelium integrity. Finally, using serum samples from COVID-19 patients, we highlighted strong concentrations of pro-inflammatory factors that did not perturb BBB integrity after short term exposure. Altogether, our results show that the main mechanism of brain access following SARS-CoV-2 infection does not seem to be directed by brain infection through endothelial cells.
Keywords: COVID-19; SARS-CoV-2; blood-brain barrier; central nervous system; inflammation.