Neurological manifestations of SARS-CoV-2: complexity, mechanism and associated disorders

被引:30
作者
Tyagi, Kritika [1 ]
Rai, Prachi [1 ]
Gautam, Anuj [1 ]
Kaur, Harjeet [1 ]
Kapoor, Sumeet [2 ]
Suttee, Ashish [3 ]
Jaiswal, Pradeep Kumar [4 ]
Sharma, Akanksha [1 ,5 ]
Singh, Gurpal [5 ]
Barnwal, Ravi Pratap [1 ]
机构
[1] Panjab Univ, Dept Biophys, Chandigarh, India
[2] Indian Inst Technol, Ctr Biomed Engn, New Delhi, India
[3] Lovely Profess Univ, Sch Pharmaceut Sci, Phagwara, India
[4] Texas A&M Univ, Dept Biochem & Biophys, College Stn, TX 77843 USA
[5] Panjab Univ, Univ Inst Pharmaceut Sci, Chandigarh, India
关键词
SARS-CoV-2; COVID; Blood-brain barrier; Central nervous system; Neuroinvasion; ACE-2; Cerebrovascular disease; RESPIRATORY SYNDROME CORONAVIRUS; BLOOD-BRAIN-BARRIER; CLATHRIN-MEDIATED ENDOCYTOSIS; VIRAL-INFECTION; COVID-19; ENTRY; VIRUS; RECEPTOR; CAVEOLAE; IMPACT;
D O I
10.1186/s40001-023-01293-2
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background Coronaviruses such as Severe Acute Respiratory Syndrome coronavirus (SARS), Middle Eastern Respiratory Syndrome (MERS) and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) are associated with critical illnesses, including severe respiratory disorders. SARS-CoV-2 is the causative agent of the deadly COVID-19 illness, which has spread globally as a pandemic. SARS-CoV-2 may enter the human body through olfactory lobes and interact with the angiotensin-converting enzyme2 (ACE2) receptor, further facilitating cell binding and entry into the cells. Reports have shown that the virus can pass through the blood-brain barrier (BBB) and enter the central nervous system (CNS), resulting in various disorders. Cell entry by SARS-CoV-2 largely relies on TMPRSS2 and cathepsin L, which activate S protein. TMPRSS2 is found on the cell surface of respiratory, gastrointestinal and urogenital epithelium, while cathepsin-L is a part of endosomes. Aim The current review aims to provide information on how SARS-CoV-2 infection affects brain function.. Furthermore, CNS disorders associated with SARS-CoV-2 infection, including ischemic stroke, cerebral venous thrombosis, Guillain-Barre syndrome, multiple sclerosis, meningitis, and encephalitis, are discussed. The many probable mechanisms and paths involved in developing cerebrovascular problems in COVID patients are thoroughly detailed. Main body There have been reports that the SARS-CoV-2 virus can cross the blood-brain barrier (BBB) and enter the central nervous system (CNS), where it could cause a various illnesses. Patients suffering from COVID-19 experience a range of neurological complications, including sleep disorders, viral encephalitis, headaches, dysgeusia, and cognitive impairment. The presence of SARS-CoV-2 in the cerebrospinal fluid (CSF) of COVID-19 patients has been reported. Health experts also reported its presence in cortical neurons and human brain organoids. The possible mechanism of virus infiltration into the brain can be neurotropic, direct infiltration and cytokine storm-based pathways. The olfactory lobes could also be the primary pathway for the entrance of SARS-CoV-2 into the brain. Conclusions SARS-CoV-2 can lead to neurological complications, such as cerebrovascular manifestations, motor movement complications, and cognitive decline. COVID-19 infection can result in cerebrovascular symptoms and diseases, such as strokes and thrombosis. The virus can affect the neural system, disrupt cognitive function and cause neurological disorders. To combat the epidemic, it is crucial to repurpose drugs currently in use quickly and develop novel therapeutics.
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页数:25
相关论文
共 151 条
[1]   Phenotypic heterogeneity of the endothelium II. Representative vascular beds [J].
Aird, William C. .
CIRCULATION RESEARCH, 2007, 100 (02) :174-190
[2]   Blood-brain barrier: emerging trends on transport models and new-age strategies for therapeutics intervention against neurological disorders [J].
Alajangi, Hema Kumari ;
Kaur, Mandeep ;
Sharma, Akanksha ;
Rana, Sumedh ;
Thakur, Shipali ;
Chatterjee, Mary ;
Singla, Neha ;
Jaiswal, Pradeep Kumar ;
Singh, Gurpal ;
Barnwal, Ravi Pratap .
MOLECULAR BRAIN, 2022, 15 (01)
[3]   Guillain-Barre syndrome related to COVID-19 infection [J].
Alberti, Paola ;
Beretta, Simone ;
Piatti, Marco ;
Karantzoulis, Aristotelis ;
Piatti, Maria Luisa ;
Santoro, Patrizia ;
Vigano, Martina ;
Giovannelli, Ginevra ;
Pirro, Fiammetta ;
Montisano, Danilo Antonio ;
Appollonio, Ildebrando ;
Ferrarese, Carlo .
NEUROLOGY-NEUROIMMUNOLOGY & NEUROINFLAMMATION, 2020, 7 (04)
[4]   Brain MRI in SARS-CoV-2 pneumonia patients with newly developed neurological manifestations suggestive of brain involvement [J].
Alonazi, Batil ;
Farghaly, Ahmed M. ;
Mostafa, Mohamed A. ;
Al-Watban, Jehad A. ;
Zindani, Salah A. ;
Altaimi, Feras ;
Fagiry, Moram A. ;
Mahmoud, Mustafa Z. .
SCIENTIFIC REPORTS, 2021, 11 (01)
[5]   SARS-CoV-2 mediated neuroinflammation and the impact of COVID-19 in neurological disorders [J].
Amruta, Narayanappa ;
Chastain, Wesley H. ;
Paz, Meshi ;
Solch, Rebecca J. ;
Murray-Brown, Isabel C. ;
Befeler, Jaime B. ;
Gressett, Timothy E. ;
Longo, Michele T. ;
Engler-Chiurazzi, Elizabeth B. ;
Bix, Gregory .
CYTOKINE & GROWTH FACTOR REVIEWS, 2021, 58 :1-15
[6]   Vitamin D and multiple sclerosis [J].
Ascherio, Alberto ;
Munger, Kassandra L. ;
Simon, K. Claire .
LANCET NEUROLOGY, 2010, 9 (06) :599-612
[7]   The blood-brain barrier: an overview - Structure, regulation, and clinical implications [J].
Ballabh, P ;
Braun, A ;
Nedergaard, M .
NEUROBIOLOGY OF DISEASE, 2004, 16 (01) :1-13
[8]   Characteristics of compounds that cross the blood-brain barrier [J].
Banks, William A. .
BMC NEUROLOGY, 2009, 9
[9]   Caveola-dependent endocytic entry of amphotropic murine leukemia virus [J].
Beer, C ;
Andersen, DS ;
Rojek, A ;
Pedersen, L .
JOURNAL OF VIROLOGY, 2005, 79 (16) :10776-10787
[10]   Ligand-induced clathrin-mediated endocytosis of the keratinocyte growth factor receptor occurs independently of either phosphorylation or recruitment of eps15 [J].
Belleudi, F ;
Visco, V ;
Ceridono, M ;
Leone, L ;
Muraro, R ;
Frati, L ;
Torrisi, MR .
FEBS LETTERS, 2003, 553 (03) :262-270