tetano
Editor, Senior Moderator
J Neurosci Res
. 2020 Aug 31.
doi: 10.1002/jnr.24717. Online ahead of print.
Possible routes of SARS-CoV-2 invasion in brain: In context of neurological symptoms in COVID-19 patients
Ashutosh Kumar[SUP] 1 2 [/SUP], Vikas Pareek[SUP] 1 3 [/SUP], Pranav Prasoon[SUP] 1 4 [/SUP], Muneeb A Faiq[SUP] 1 5 [/SUP], Pavan Kumar[SUP] 1 6 [/SUP], Chiman Kumari[SUP] 1 7 [/SUP], Ravi K Narayan[SUP] 1 2 [/SUP]
Affiliations
Abstract
Manifestation of neurological symptoms in certain patients of coronavirus disease-2019 (COVID-19) has warranted for their virus-induced etiogenesis. SARS-CoV-2, the causative agent of COVID-19, belongs to the genus of betacoronaviruses which also includes SARS-CoV-1 and MERS-CoV; causative agents for severe acute respiratory syndrome (SARS) in 2002 and Middle East respiratory syndrome (MERS) in 2012, respectively. Studies demonstrating the neural invasion of SARS-CoV-2 in vivo are still scarce, although such characteristics of certain other betacoronaviruses are well demonstrated in the literature. Based on the recent evidence for the presence of SARS-CoV-2 host cell entry receptors in specific components of the human nervous and vascular tissue, a neural (olfactory and/or vagal), and a hematogenous-crossing the blood-brain barrier, routes have been proposed. The neurological symptoms in COVID-19 may also arise as a consequence of the "cytokine storm" (characteristically present in severe disease) induced neuroinflammation, or co-morbidities. There is also a possibility that, there may be multiple routes of SARS-CoV-2 entry into the brain, or multiple mechanisms can be involved in the pathogenesis of the neurological symptoms. In this review article, we have discussed the possible routes of SARS-CoV-2 brain entry based on the emerging evidence for this virus, and that available for other betacoronaviruses in literature.
Keywords: COVID-19; SARS-CoV-2; blood-brain barrier; neural invasion; neurological symptoms.
. 2020 Aug 31.
doi: 10.1002/jnr.24717. Online ahead of print.
Possible routes of SARS-CoV-2 invasion in brain: In context of neurological symptoms in COVID-19 patients
Ashutosh Kumar[SUP] 1 2 [/SUP], Vikas Pareek[SUP] 1 3 [/SUP], Pranav Prasoon[SUP] 1 4 [/SUP], Muneeb A Faiq[SUP] 1 5 [/SUP], Pavan Kumar[SUP] 1 6 [/SUP], Chiman Kumari[SUP] 1 7 [/SUP], Ravi K Narayan[SUP] 1 2 [/SUP]
Affiliations
- PMID: 32869376
- DOI: 10.1002/jnr.24717
Abstract
Manifestation of neurological symptoms in certain patients of coronavirus disease-2019 (COVID-19) has warranted for their virus-induced etiogenesis. SARS-CoV-2, the causative agent of COVID-19, belongs to the genus of betacoronaviruses which also includes SARS-CoV-1 and MERS-CoV; causative agents for severe acute respiratory syndrome (SARS) in 2002 and Middle East respiratory syndrome (MERS) in 2012, respectively. Studies demonstrating the neural invasion of SARS-CoV-2 in vivo are still scarce, although such characteristics of certain other betacoronaviruses are well demonstrated in the literature. Based on the recent evidence for the presence of SARS-CoV-2 host cell entry receptors in specific components of the human nervous and vascular tissue, a neural (olfactory and/or vagal), and a hematogenous-crossing the blood-brain barrier, routes have been proposed. The neurological symptoms in COVID-19 may also arise as a consequence of the "cytokine storm" (characteristically present in severe disease) induced neuroinflammation, or co-morbidities. There is also a possibility that, there may be multiple routes of SARS-CoV-2 entry into the brain, or multiple mechanisms can be involved in the pathogenesis of the neurological symptoms. In this review article, we have discussed the possible routes of SARS-CoV-2 brain entry based on the emerging evidence for this virus, and that available for other betacoronaviruses in literature.
Keywords: COVID-19; SARS-CoV-2; blood-brain barrier; neural invasion; neurological symptoms.