TY - JOUR
T1 - Does COVID-19 contribute to development of neurological disease?
AU - Mahalakshmi, Arehally M.
AU - Ray, Bipul
AU - Tuladhar, Sunanda
AU - Bhat, Abid
AU - Paneyala, Shasthara
AU - Patteswari, Duraisamy
AU - Sakharkar, Meena Kishore
AU - Hamdan, Hamdan
AU - Ojcius, David M.
AU - Bolla, Srinivasa Rao
AU - Essa, Musthafa Mohamed
AU - Chidambaram, Saravana Babu
AU - Qoronfleh, M. Walid
N1 - Publisher Copyright:
© 2020 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd
PY - 2021/3
Y1 - 2021/3
N2 - Background: Although coronavirus disease 2019 (COVID-19) has been associated primarily with pneumonia, recent data show that the causative agent of COVID-19, the coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can infect a large number of vital organs beyond the lungs, such as the heart, kidneys, and the brain. Thus, there is evidence showing possible retrograde transmission of the virus from the olfactory epithelium to regions of the brain stem. Methods: This is a literature review article. The research design method is an evidence-based rapid review. The present discourse aim is first to scrutinize and assess the available literature on COVID-19 repercussion on the central nervous system (CNS). Standard literature and database searches were implemented, gathered relevant material, and extracted information was then assessed. Results: The angiotensin-converting enzyme 2 (ACE2) receptors being the receptor for the virus, the threat to the central nervous system is expected. Neurons and glial cells express ACE2 receptors in the CNS, and recent studies suggest that activated glial cells contribute to neuroinflammation and the devastating effects of SARS-CoV-2 infection on the CNS. The SARS-CoV-2-induced immune-mediated demyelinating disease, cerebrovascular damage, neurodegeneration, and depression are some of the neurological complications discussed here. Conclusion: This review correlates present clinical manifestations of COVID-19 patients with possible neurological consequences in the future, thus preparing healthcare providers for possible future consequences of COVID-19.
AB - Background: Although coronavirus disease 2019 (COVID-19) has been associated primarily with pneumonia, recent data show that the causative agent of COVID-19, the coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can infect a large number of vital organs beyond the lungs, such as the heart, kidneys, and the brain. Thus, there is evidence showing possible retrograde transmission of the virus from the olfactory epithelium to regions of the brain stem. Methods: This is a literature review article. The research design method is an evidence-based rapid review. The present discourse aim is first to scrutinize and assess the available literature on COVID-19 repercussion on the central nervous system (CNS). Standard literature and database searches were implemented, gathered relevant material, and extracted information was then assessed. Results: The angiotensin-converting enzyme 2 (ACE2) receptors being the receptor for the virus, the threat to the central nervous system is expected. Neurons and glial cells express ACE2 receptors in the CNS, and recent studies suggest that activated glial cells contribute to neuroinflammation and the devastating effects of SARS-CoV-2 infection on the CNS. The SARS-CoV-2-induced immune-mediated demyelinating disease, cerebrovascular damage, neurodegeneration, and depression are some of the neurological complications discussed here. Conclusion: This review correlates present clinical manifestations of COVID-19 patients with possible neurological consequences in the future, thus preparing healthcare providers for possible future consequences of COVID-19.
KW - ACE2
KW - COVID-19
KW - glial cells
KW - immune mediated demyelination
KW - memory impairment
KW - neurodegeneration
KW - neuroinflammation
KW - neurological circuits
KW - neurology
KW - SARS-CoV-2
UR - http://www.scopus.com/inward/record.url?scp=85097677426&partnerID=8YFLogxK
U2 - 10.1002/iid3.387
DO - 10.1002/iid3.387
M3 - Review article
C2 - 33332737
AN - SCOPUS:85097677426
SN - 2050-4527
VL - 9
SP - 48
EP - 58
JO - Immunity, Inflammation and Disease
JF - Immunity, Inflammation and Disease
IS - 1
ER -