Unraveling the SARS-CoV-2 spike protein long-term effect on neuro-PASC
The persistence or emergence of long-term symptoms following resolution of primary SARS-CoV-2 infection is referred to as long COVID or post-acute sequelae of COVID-19 (PASC). PASC predominantly affects the cardiovascular, neurological, respiratory, gastrointestinal, reproductive, and immune systems...
| Autores: | , , , , , , , |
|---|---|
| Formato: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2024 |
| País: | Brasil |
| Recursos: | Universidade de Brasília (UnB) |
| Repositorio: | Repositório Institucional da UnB |
| Idioma: | inglés |
| OAI Identifier: | oai:repositorio.unb.br:10482/52506 |
| Acesso em linha: | http://repositorio.unb.br/handle/10482/52506 https://doi.org/10.3389/fncel.2024.1481963 https://orcid.org/0009-0001-7830-0447 https://orcid.org/0000-0002-2724-369X https://orcid.org/0000-0002-1612-2411 https://orcid.org/0000-0002-7982-1789 https://orcid.org/0000-0003-1775-7176 https://orcid.org/0000-0002-1061-196X https://orcid.org/0000-0002-4359-7594 |
| Access Level: | acceso abierto |
| Palavra-chave: | Covid-19 - fisiopatologia SARS-CoV-2 Barreira hematoencefálica |
| Resumo: | The persistence or emergence of long-term symptoms following resolution of primary SARS-CoV-2 infection is referred to as long COVID or post-acute sequelae of COVID-19 (PASC). PASC predominantly affects the cardiovascular, neurological, respiratory, gastrointestinal, reproductive, and immune systems. Among these, the central nervous system (CNS) is significantly impacted, leading to a spectrum of symptoms, including fatigue, headaches, brain fog, cognitive impairment, anosmia, hypogeusia, neuropsychiatric symptoms, and peripheral neuropathy (neuro-PASC). However, the risk factors and pathogenic mechanisms responsible for neuro-PASC remain unclear. This review hypothesis discusses the leading hypotheses regarding the pathophysiological mechanisms involved in long COVID/PASC, focusing on neuro-PASC. We propose vascular dysfunction mediated by activation of astrocytes and pericytes followed by blood–brain barrier (BBB) disruption as underlying pathophysiological mechanisms of neurological manifestations. Additionally, we provide insights into the role of spike protein at the blood–brain interface. Finally, we explore the potential pathogenic mechanisms initiated by the interaction between the spike protein and cellular receptors at the brain endothelial and tissue levels. |
|---|