tetano
Editor, Senior Moderator
Neurobiol Dis
. 2022 Mar 29;168:105715.
doi: 10.1016/j.nbd.2022.105715. Online ahead of print.
Neurological sequela and disruption of neuron-glia homeostasis in SARS-CoV-2 infection
Masha G Savelieff[SUP] 1 [/SUP], Eva L Feldman[SUP] 2 [/SUP], Amro M Stino[SUP] 3 [/SUP]
Affiliations
Abstract
The coronavirus disease 2019 (COVID-19) pandemic is responsible for 267 million infections and over 5 million deaths globally. COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a single-stranded RNA beta-coronavirus, which causes a systemic inflammatory response, multi-organ damage, and respiratory failure requiring intubation in serious cases. SARS-CoV-2 can also trigger neurological conditions and syndromes, which can be long-lasting and potentially irreversible. Since COVID-19 infections continue to mount, the burden of SARS-CoV-2-induced neurologic sequalae will rise in parallel. Therefore, understanding the spectrum of neurological clinical presentations in SARS-CoV-2 is needed to manage COVID-19 patients, facilitate diagnosis, and expedite earlier treatment to improve outcomes. Furthermore, a deeper knowledge of the neurological SARS-CoV-2 pathomechanisms could uncover potential therapeutic targets to prevent or mitigate neurologic damage secondary to COVID-19 infection. Evidence indicates a multifaceted pathology involving viral neurotropism and direct neuroinvasion along with cytokine storm and neuroinflammation leading to nerve injury. Importantly, pathological processes in neural tissue are non-cell autonomous and occur through a concerted breakdown in neuron-glia homeostasis, spanning neuron axonal damage, astrogliosis, microgliosis, and impaired neuron-glia communication. A clearer mechanistic and molecular picture of neurological pathology in SARS-CoV-2 may lead to effective therapies that prevent or mitigate neural damage in patients contracting and developing severe COVID-19 infection.
Keywords: Astrocyte; Axon; COVID-19; Cytokine storm; Extracellular vesicles; Immune system; Microglia; Neuron; Oligodendrocyte.
. 2022 Mar 29;168:105715.
doi: 10.1016/j.nbd.2022.105715. Online ahead of print.
Neurological sequela and disruption of neuron-glia homeostasis in SARS-CoV-2 infection
Masha G Savelieff[SUP] 1 [/SUP], Eva L Feldman[SUP] 2 [/SUP], Amro M Stino[SUP] 3 [/SUP]
Affiliations
- PMID: 35364273
- PMCID: PMC8963977
- DOI: 10.1016/j.nbd.2022.105715
Abstract
The coronavirus disease 2019 (COVID-19) pandemic is responsible for 267 million infections and over 5 million deaths globally. COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a single-stranded RNA beta-coronavirus, which causes a systemic inflammatory response, multi-organ damage, and respiratory failure requiring intubation in serious cases. SARS-CoV-2 can also trigger neurological conditions and syndromes, which can be long-lasting and potentially irreversible. Since COVID-19 infections continue to mount, the burden of SARS-CoV-2-induced neurologic sequalae will rise in parallel. Therefore, understanding the spectrum of neurological clinical presentations in SARS-CoV-2 is needed to manage COVID-19 patients, facilitate diagnosis, and expedite earlier treatment to improve outcomes. Furthermore, a deeper knowledge of the neurological SARS-CoV-2 pathomechanisms could uncover potential therapeutic targets to prevent or mitigate neurologic damage secondary to COVID-19 infection. Evidence indicates a multifaceted pathology involving viral neurotropism and direct neuroinvasion along with cytokine storm and neuroinflammation leading to nerve injury. Importantly, pathological processes in neural tissue are non-cell autonomous and occur through a concerted breakdown in neuron-glia homeostasis, spanning neuron axonal damage, astrogliosis, microgliosis, and impaired neuron-glia communication. A clearer mechanistic and molecular picture of neurological pathology in SARS-CoV-2 may lead to effective therapies that prevent or mitigate neural damage in patients contracting and developing severe COVID-19 infection.
Keywords: Astrocyte; Axon; COVID-19; Cytokine storm; Extracellular vesicles; Immune system; Microglia; Neuron; Oligodendrocyte.