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Hamostaseologie 2021; 41(05): 379-385
DOI: 10.1055/a-1581-4355
Review Article

Platelets and COVID-19

Anne-Katrin Rohlfing
1   Department of Cardiology and Angiology, University Hospital Tübingen, Eberhard Karls Universtität Tübingen, Tübingen, Germany
,
Dominik Rath
1   Department of Cardiology and Angiology, University Hospital Tübingen, Eberhard Karls Universtität Tübingen, Tübingen, Germany
,
Tobias Geisler
1   Department of Cardiology and Angiology, University Hospital Tübingen, Eberhard Karls Universtität Tübingen, Tübingen, Germany
,
Meinrad Gawaz
1   Department of Cardiology and Angiology, University Hospital Tübingen, Eberhard Karls Universtität Tübingen, Tübingen, Germany
› Author Affiliations Funding This project was supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)—project number 374031971–TRR 240 (molecular aspects).
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Abstract

In 2019 first reports about a new human coronavirus emerged, which causes common cold symptoms as well as acute respiratory distress syndrome. The virus was identified as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and severe thrombotic events including deep vein thrombosis, pulmonary embolism, and microthrombi emerged as additional symptoms. Heart failure, myocardial infarction, myocarditis, and stroke have also been observed. As main mediator of thrombus formation, platelets became one of the key aspects in SARS-CoV-2 research. Platelets may also directly interact with SARS-CoV-2 and have been shown to carry the SARS-CoV-2 virus. Platelets can also facilitate the virus uptake by secretion of the subtilisin-like proprotein convertase furin. Cleavage of the SARS-CoV-2 spike protein by furin enhances binding capabilities and virus entry into various cell types. In COVID-19 patients, platelet count differs between mild and serious infections. Patients with mild symptoms have a slightly increased platelet count, whereas thrombocytopenia is a hallmark of severe COVID-19 infections. Low platelet count can be attributed to platelet apoptosis and the incorporation of platelets into microthrombi (peripheral consumption) and severe thrombotic events. The observed excessive formation of thrombi is due to hyperactivation of platelets caused by the infection. Various factors have been suggested in the activation of platelets in COVID-19, such as hypoxia, vessel damage, inflammatory factors, NETosis, SARS-CoV-2 interaction, autoimmune reactions, and autocrine activation. COVID-19 does alter chemokine and cytokine plasma concentrations. Platelet chemokine profiles are altered in COVID-19 and contribute to the described chemokine storms observed in severely ill COVID-19 patients.

Zusammenfassung

In 2019 wurden erste Berichte über ein neuartiges Coronavirus bekannt, welches bei Menschen Erkältungssymptome aber auch ein akutes Lungenversargen (ARDS) auslösen kann. Das Virus wurde als SARS-CoV-2 eingeordnet und schwere Thrombosen, wie z.B. tiefe Venenthrombosen und Lungenembolien, sowie Mikrothromben als zusätzliche Symptome identifiziert. Herzinfarkte, Myokarditis sowie Schlaganfälle wurden ebenfalls beobachtet. Als einer der Hauptmediatoren der Thrombusbildung wurden Thrombozyten schnell zu einem Fokus der SARS-CoV-2 Forschung. Blutplättchen können wahrscheinlich direkt mit SARS-CoV-2 interagieren und es wurde gezeigt das sich Viruspartikel im Zytosol von Thrombozyten befinden können. Thrombozyten können darüber hinaus die Aufnahme des Virus erleichtern, indem sie die subtilisin-like proprotein convertase furin sezernieren, welche das Spike Protein von SARS-CoV-2 Viren spaltet und dadurch die Bindungskapazität des Proteins an zelluläre Rezeptoren erhöht. Die Thrombozytenzahl wird durch eine Covid-19 Infektion beeinflusst. Patienten mit milden Symptomen zeigen leicht erhöhte Thrombozytenwerte, wohingegen eine Thrombozytopenie ein wichtiges Merkmal einer schweren Erkrankung ist. Diese geringe Thrombozytenzahl kann auf eine erhöhte Apoptose sowie den Einschluss von Thrombozyten in Mikrothromben (peripherer Verbrauch) oder massive Thrombosen zurückgeführt werden. Die beobachtete massive Bildung von Thromben erfolgt auf Grund einer Covid-19 induzierten Hyperaktivierung von Thrombozyten. Verschiedene Faktoren können Thrombozyten während einer Covid-19 Infektion aktivieren, dazu zählen Hypoxie, Gefäßschäden, Entzündungsmarker, NETosis, direkte SARS-CoV-2 Interaktionen, Autoimmunreaktionen sowie eine autokrine Aktivierung. Zudem verändert Covid-19 die Chemokin- und Zytokin-Konzentrationen im Blutplasma. Auch das Chemokin Profil von Thrombozyten ist in Covid-19 Patienten verändert und trägt stark zu dem in schwer kranken Patienten beobachteten Chemokinsturm bei.

Keywords

SARS-CoV-2 - COVID-19 - platelets - thrombosis - thrombocytopenia

Keywords (German)

SARS-CoV-2 - COVID-19 - Plättchen - Thrombose - Thrombozytopenie


Publication History

Received: 22 June 2021

Accepted: 11 August 2021

Article published online:
25 October 2021

© 2021. Thieme. All rights reserved.

Georg Thieme Verlag KG
Rüdigerstraße 14, 70469 Stuttgart, Germany

 

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