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Article: Long-term effects of SARS-CoV-2 infection on human brain and memory

TitleLong-term effects of SARS-CoV-2 infection on human brain and memory
Authors
Issue Date29-Jun-2023
PublisherSpringer Nature
Citation
Cell Death Discovery, 2023, v. 9, n. 1 How to Cite?
Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants have caused several waves of outbreaks. From the ancestral strain to Omicron variant, SARS-CoV-2 has evolved with the high transmissibility and increased immune escape against vaccines. Because of the multiple basic amino acids in the S1-S2 junction of spike protein, the widespread distribution of angiotensin-converting enzyme 2 (ACE2) receptor in human body and the high transmissibility, SARS-CoV-2 can infect multiple organs and has led to over 0.7 billion infectious cases. Studies showed that SARS-CoV-2 infection can cause more than 10% patients with the Long-COVID syndrome, including pathological changes in brains. This review mainly provides the molecular foundations for understanding the mechanism of SARS-CoV-2 invading human brain and the molecular basis of SARS-CoV-2 infection interfering with human brain and memory, which are associated with the immune dysfunction, syncytia-induced cell death, the persistence of SARS-CoV-2 infection, microclots and biopsychosocial aspects. We also discuss the strategies for reducing the Long-COVID syndrome. Further studies and analysis of shared researches will allow for further clarity regarding the long-term health consequences.


Persistent Identifierhttp://hdl.handle.net/10722/338211
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDing, Qiulu-
dc.contributor.authorZhao, HanJun-
dc.date.accessioned2024-03-11T10:27:06Z-
dc.date.available2024-03-11T10:27:06Z-
dc.date.issued2023-06-29-
dc.identifier.citationCell Death Discovery, 2023, v. 9, n. 1-
dc.identifier.urihttp://hdl.handle.net/10722/338211-
dc.description.abstract<p>The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants have caused several waves of outbreaks. From the ancestral strain to Omicron variant, SARS-CoV-2 has evolved with the high transmissibility and increased immune escape against vaccines. Because of the multiple basic amino acids in the S1-S2 junction of spike protein, the widespread distribution of angiotensin-converting enzyme 2 (ACE2) receptor in human body and the high transmissibility, SARS-CoV-2 can infect multiple organs and has led to over 0.7 billion infectious cases. Studies showed that SARS-CoV-2 infection can cause more than 10% patients with the Long-COVID syndrome, including pathological changes in brains. This review mainly provides the molecular foundations for understanding the mechanism of SARS-CoV-2 invading human brain and the molecular basis of SARS-CoV-2 infection interfering with human brain and memory, which are associated with the immune dysfunction, syncytia-induced cell death, the persistence of SARS-CoV-2 infection, microclots and biopsychosocial aspects. We also discuss the strategies for reducing the Long-COVID syndrome. Further studies and analysis of shared researches will allow for further clarity regarding the long-term health consequences.<br></p>-
dc.languageeng-
dc.publisherSpringer Nature-
dc.relation.ispartofCell Death Discovery-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleLong-term effects of SARS-CoV-2 infection on human brain and memory-
dc.typeArticle-
dc.identifier.doi10.1038/s41420-023-01512-z-
dc.identifier.scopuseid_2-s2.0-85163739586-
dc.identifier.volume9-
dc.identifier.issue1-
dc.identifier.eissn2058-7716-
dc.identifier.isiWOS:001021070100001-
dc.identifier.issnl2058-7716-

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