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- Publisher Website: 10.1038/s41420-023-01512-z
- Scopus: eid_2-s2.0-85163739586
- WOS: WOS:001021070100001
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Article: Long-term effects of SARS-CoV-2 infection on human brain and memory
Title | Long-term effects of SARS-CoV-2 infection on human brain and memory |
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Authors | |
Issue Date | 29-Jun-2023 |
Publisher | Springer 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 Identifier | http://hdl.handle.net/10722/338211 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Ding, Qiulu | - |
dc.contributor.author | Zhao, HanJun | - |
dc.date.accessioned | 2024-03-11T10:27:06Z | - |
dc.date.available | 2024-03-11T10:27:06Z | - |
dc.date.issued | 2023-06-29 | - |
dc.identifier.citation | Cell Death Discovery, 2023, v. 9, n. 1 | - |
dc.identifier.uri | http://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.language | eng | - |
dc.publisher | Springer Nature | - |
dc.relation.ispartof | Cell Death Discovery | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.title | Long-term effects of SARS-CoV-2 infection on human brain and memory | - |
dc.type | Article | - |
dc.identifier.doi | 10.1038/s41420-023-01512-z | - |
dc.identifier.scopus | eid_2-s2.0-85163739586 | - |
dc.identifier.volume | 9 | - |
dc.identifier.issue | 1 | - |
dc.identifier.eissn | 2058-7716 | - |
dc.identifier.isi | WOS:001021070100001 | - |
dc.identifier.issnl | 2058-7716 | - |