Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequences

Concerns for the long-term effects of COVID-19 infection have grown due to frequently reported persisting symptoms that can affect multiple systems for longer than 4 weeks after initial infection, a condition known as long-COVID-19 or post-acute COVID-19 syndrome (PACS). Even nonhospitalized survivo...

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Main Authors: Remy Martins-Gonçalves, Eugenio D. Hottz, Patricia T. Bozza
Format: Article
Language:English
Published: Elsevier 2023-01-01
Series:Current Research in Immunology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2590255523000045
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author Remy Martins-Gonçalves
Eugenio D. Hottz
Patricia T. Bozza
author_facet Remy Martins-Gonçalves
Eugenio D. Hottz
Patricia T. Bozza
author_sort Remy Martins-Gonçalves
collection DOAJ
description Concerns for the long-term effects of COVID-19 infection have grown due to frequently reported persisting symptoms that can affect multiple systems for longer than 4 weeks after initial infection, a condition known as long-COVID-19 or post-acute COVID-19 syndrome (PACS). Even nonhospitalized survivors have an elevated risk for the development of thromboinflammatory-associated events, such as ischemic stroke and heart failure, pulmonary embolism and deep vein thrombosis. Recent findings point to the persistence of many mechanisms of hypercoagulability identified to be associated with disease severity and mortality in the acute phase of the disease, such as sustained inflammation and endotheliopathy, accompanied by abnormal fibrin generation and impaired fibrinolysis. Platelets seem to be central to the sustained hypercoagulable state, displaying hyperreactivity to stimuli and increased adhesive capacity. Platelets also contribute to elevated levels of thromboinflammatory mediators and pro-coagulant extracellular vesicles in individuals with ongoing PACS. Despite new advances in the understanding of mechanisms sustaining thromboinflammation in PACS, little is known about what triggers this persistence. In this graphical review, we provide a schematic representation of the known mechanisms and consequences of persisting thromboinflammation in COVID-19 survivors and summarize the hypothesized triggers maintaining this prothrombotic state.
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spelling doaj.art-80b9b451424d44118da41ac6c44d12d32023-12-03T05:42:48ZengElsevierCurrent Research in Immunology2590-25552023-01-014100058Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequencesRemy Martins-Gonçalves0Eugenio D. Hottz1Patricia T. Bozza2Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz (IOC), Fundação Oswaldo Cruz (FIOCRUZ), Rio de Janeiro, Brazil; Programa de Imunologia e Inflamação, Universidade Federal do Rio de Janeiro, UFRJ, Rio de Janeiro, Rio de Janeiro, BrazilLaboratório de Imunotrombose, Departamento de Bioquímica, Universidade Federal de Juiz de Fora (UFJF), Juiz de Fora, Minas Gerais, BrazilLaboratório de Imunofarmacologia, Instituto Oswaldo Cruz (IOC), Fundação Oswaldo Cruz (FIOCRUZ), Rio de Janeiro, Brazil; Corresponding author.Concerns for the long-term effects of COVID-19 infection have grown due to frequently reported persisting symptoms that can affect multiple systems for longer than 4 weeks after initial infection, a condition known as long-COVID-19 or post-acute COVID-19 syndrome (PACS). Even nonhospitalized survivors have an elevated risk for the development of thromboinflammatory-associated events, such as ischemic stroke and heart failure, pulmonary embolism and deep vein thrombosis. Recent findings point to the persistence of many mechanisms of hypercoagulability identified to be associated with disease severity and mortality in the acute phase of the disease, such as sustained inflammation and endotheliopathy, accompanied by abnormal fibrin generation and impaired fibrinolysis. Platelets seem to be central to the sustained hypercoagulable state, displaying hyperreactivity to stimuli and increased adhesive capacity. Platelets also contribute to elevated levels of thromboinflammatory mediators and pro-coagulant extracellular vesicles in individuals with ongoing PACS. Despite new advances in the understanding of mechanisms sustaining thromboinflammation in PACS, little is known about what triggers this persistence. In this graphical review, we provide a schematic representation of the known mechanisms and consequences of persisting thromboinflammation in COVID-19 survivors and summarize the hypothesized triggers maintaining this prothrombotic state.http://www.sciencedirect.com/science/article/pii/S2590255523000045Post-acute COVID-19 syndrome (PACS)Platelet activationHypercoagulabilityThromboinflammation
spellingShingle Remy Martins-Gonçalves
Eugenio D. Hottz
Patricia T. Bozza
Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequences
Current Research in Immunology
Post-acute COVID-19 syndrome (PACS)
Platelet activation
Hypercoagulability
Thromboinflammation
title Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequences
title_full Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequences
title_fullStr Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequences
title_full_unstemmed Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequences
title_short Acute to post-acute COVID-19 thromboinflammation persistence: Mechanisms and potential consequences
title_sort acute to post acute covid 19 thromboinflammation persistence mechanisms and potential consequences
topic Post-acute COVID-19 syndrome (PACS)
Platelet activation
Hypercoagulability
Thromboinflammation
url http://www.sciencedirect.com/science/article/pii/S2590255523000045
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