Abstract

SARS-CoV-2 contains certain molecules that are related to the presence of immunothrombosis. Here, we review the pathogen and damage-associated molecular patterns. We also study the imbalance of different molecules participating in immunothrombosis, such as tissue factor, factors of the contact system, histones, and the role of cells, such as endothelial cells, platelets, and neutrophil extracellular traps. Regarding the pathogenetic mechanism, we discuss clinical trials, case-control studies, comparative and translational studies, and observational studies of regulatory or inhibitory molecules, more specifically, extracellular DNA and RNA, histones, sensors for RNA and DNA, as well as heparin and heparinoids. Overall, it appears that a network of cells and molecules identified in this axis is simultaneously but differentially affecting patients at different stages of COVID-19, and this is characterized by endothelial damage, microthrombosis, and inflammation.

Highlights

  • In December 2019, the infectious outbreak of a new human coronavirus (SARS-CoV-2)responsible for acute respiratory syndrome was detected in Wuhan, China [1]

  • Considering that one of the main characteristics of COVID-19 is hypercoagulability, and the increased risk of venous and arterial thrombosis, it is necessary to differentiate from Heparin-induced thrombocytopenia (HIT) [67,68,69], secondary to the use of vaccines [70]

  • HIT is characterized by a decrease in platelets >30–50% associated with thromboembolic complications in around 50% of patients with confirmed HIT

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Summary

Introduction

In December 2019, the infectious outbreak of a new human coronavirus (SARS-CoV-2). responsible for acute respiratory syndrome was detected in Wuhan, China [1]. SARS-CoV-2 has caused more than 235 million cases worldwide and more than 4 million deaths as of 5 October 2021 It could correspond to complement-mediated thrombotic microangiopathies [6,7]. Biomolecules 2021, 11, 1550 other hand, it could correspond to complement-mediated thrombotic microangiopathies [6,7]. In criteria the selection criteria for study and population, the general the frequency thrombosis variable. The sequence sequenceofofthese theseevents events in SARS-CoV-2 infection is related the actions of different cells and molecules To immune complexes SARS-CoV-2 platelet aggregates, complement-TF-NETs, and histones. To immune complexes SARS-CoV-2 spike/anti-spike spike/anti-spike IgG, anti-PF4/heparin IgG antibodies and antiphospholipid antibodies.

Factors of the Contact System
Tissue Factor
Neutrophil Extracellular Traps and Molecule Release
Heparin-Induced Thrombocytopenia
Key Findings
12 COVID-19 patients with HIT
Cytokine Storm Syndrome
Findings
Conclusions
Full Text
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