The ongoing enigma of SARS‐CoV‐2 and platelet interaction
Abstract Since the onset of the global pandemic of coronavirus disease 2019 (COVID‐19), there is an urgent need to understand the pathogenesis of the common inflammatory and thrombotic complications associated with this illness leading to multiorgan failure and mortality. It is well established that...
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Format: | Article |
Language: | English |
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Elsevier
2022-01-01
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Series: | Research and Practice in Thrombosis and Haemostasis |
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Online Access: | https://doi.org/10.1002/rth2.12642 |
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author | Younes Zaid Fadila Guessous |
author_facet | Younes Zaid Fadila Guessous |
author_sort | Younes Zaid |
collection | DOAJ |
description | Abstract Since the onset of the global pandemic of coronavirus disease 2019 (COVID‐19), there is an urgent need to understand the pathogenesis of the common inflammatory and thrombotic complications associated with this illness leading to multiorgan failure and mortality. It is well established that platelets are hyperactivated during COVID‐19. Data from independent studies reported an angiotensin‐converting enzyme (ACE2)‐dependent severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) platelet interaction, raising the concern whether ACE2 receptor is the “key receptor” in this process, while other platelet research groups demonstrated that thrombotic events occur via ACE2‐independent mechanisms, where the virus probably uses alternative pathways. In this study, we discuss the conflicting results and highlight the ongoing controversy related to SARS‐CoV‐2‐platelet interaction. |
first_indexed | 2024-03-12T09:23:59Z |
format | Article |
id | doaj.art-2cfe6a9cdf764e55b3794af1027100f4 |
institution | Directory Open Access Journal |
issn | 2475-0379 |
language | English |
last_indexed | 2024-03-12T09:23:59Z |
publishDate | 2022-01-01 |
publisher | Elsevier |
record_format | Article |
series | Research and Practice in Thrombosis and Haemostasis |
spelling | doaj.art-2cfe6a9cdf764e55b3794af1027100f42023-09-02T14:19:06ZengElsevierResearch and Practice in Thrombosis and Haemostasis2475-03792022-01-0161n/an/a10.1002/rth2.12642The ongoing enigma of SARS‐CoV‐2 and platelet interactionYounes Zaid0Fadila Guessous1Botany Laboratory Department of Biology Faculty of Sciences Mohammed V University Rabat MoroccoMicrobiology, Immunology and Cancer Biology School of Medicine University of Virginia Charlottesville Virginia USAAbstract Since the onset of the global pandemic of coronavirus disease 2019 (COVID‐19), there is an urgent need to understand the pathogenesis of the common inflammatory and thrombotic complications associated with this illness leading to multiorgan failure and mortality. It is well established that platelets are hyperactivated during COVID‐19. Data from independent studies reported an angiotensin‐converting enzyme (ACE2)‐dependent severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) platelet interaction, raising the concern whether ACE2 receptor is the “key receptor” in this process, while other platelet research groups demonstrated that thrombotic events occur via ACE2‐independent mechanisms, where the virus probably uses alternative pathways. In this study, we discuss the conflicting results and highlight the ongoing controversy related to SARS‐CoV‐2‐platelet interaction.https://doi.org/10.1002/rth2.12642ACE2coagulopathyCOVID‐19plateletsSARS‐CoV‐2 |
spellingShingle | Younes Zaid Fadila Guessous The ongoing enigma of SARS‐CoV‐2 and platelet interaction Research and Practice in Thrombosis and Haemostasis ACE2 coagulopathy COVID‐19 platelets SARS‐CoV‐2 |
title | The ongoing enigma of SARS‐CoV‐2 and platelet interaction |
title_full | The ongoing enigma of SARS‐CoV‐2 and platelet interaction |
title_fullStr | The ongoing enigma of SARS‐CoV‐2 and platelet interaction |
title_full_unstemmed | The ongoing enigma of SARS‐CoV‐2 and platelet interaction |
title_short | The ongoing enigma of SARS‐CoV‐2 and platelet interaction |
title_sort | ongoing enigma of sars cov 2 and platelet interaction |
topic | ACE2 coagulopathy COVID‐19 platelets SARS‐CoV‐2 |
url | https://doi.org/10.1002/rth2.12642 |
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