| Literature DB >> 33393420 |
Muhammad Ali Haidar1, Hussam Jourdi2, Zeinab Haj Hassan3, Ohanes Ashekyan1, Manal Fardoun4, Zena Wehbe4, Dina Maaliki5, Maya Wehbe6, Stefania Mondello7, Samar Abdelhady8, Shima Shahjouei9, Maya Bizri10, Yehia Mechref11, Mark S Gold12, Ghassan Dbaibo1,13,14, Hassan Zaraket13,15, Ali H Eid5,13, Firas Kobeissy1,16.
Abstract
SARS-CoV-2 infects cells through angiotensin-converting enzyme 2 (ACE2), a ubiquitous receptor that interacts with the virus' surface S glycoprotein. Recent reports show that the virus affects the central nervous system (CNS) with symptoms and complications that include dizziness, altered consciousness, encephalitis, and even stroke. These can immerge as indirect immune effects due to increased cytokine production or via direct viral entry into brain tissue. The latter is possible through neuronal access via the olfactory bulb, hematogenous access through immune cells or directly across the blood-brain barrier (BBB), and through the brain's circumventricular organs characterized by their extensive and highly permeable capillaries. Last, the COVID-19 pandemic increases stress, depression, and anxiety within infected individuals, those in isolation, and high-risk populations like children, the elderly, and health workers. This review surveys the recent updates of CNS manifestations post SARS-CoV-2 infection along with possible mechanisms that lead to them.Entities:
Keywords: ARDS; COVID-19; SARS; angiotensin; autoantibodies; encephalitis; inflammation; neurodegeneration; pandemic; stroke; viral infection
Year: 2021 PMID: 33393420 DOI: 10.1177/1073858420984106
Source DB: PubMed Journal: Neuroscientist ISSN: 1073-8584 Impact factor: 7.519