COVID-19 is frequently accompanied by a hypercoagulable inflammatory state with microangiopathic pulmonary changes that can lead to the diffuse alveolar damage characteristic of typical acute respiratory distress syndrome (ARDS), as seen in other severe lung pathogenic infections. Accumulating evidence supports that COVID-19 is associated with a marked increase in the risk for venous and arterial thromboembolic events in hospitalized patients, which is associated with dysfunction of vascular barrier, edema, endotheliitis, thrombosis, and inflammatory cell infiltration. These clots may also form in multiple places in the body, besides the lungs. This unusual clotting may cause different complications, including organ damage, heart attacks and stroke.
In severe COVID-19, endothelial and platelet activation markers are significantly increased compared to healthy controls. In addition to the lung epithelial cells, SARS-CoV-2 viral load is detected in the kidneys, liver, heart, and brain, which are highly vascularized organs. Research has indicated that the coagulation may be triggered by the high levels of inflammation, caused by the SARS-CoV-2 infection. A high level of inflammation can affect multiple organs and result in severe disease. Many human host receptors reportedly interact with SARS-CoV-2 spike protein to infect and replicate in lung epithelial and other cells, such as monocytes. Researchers have also proposed various drug targets and unique signaling pathways in different cells through various omics approaches. Although a body of literature supports that COVID-19 is an endothelial disease, direct infection of endothelial cells remains controversial.
On the other hand, a small population may develop a clotting disorder after receiving a COVID-19 vaccine, this is termed as vaccine-induced immune thrombotic thrombocytopenia (VITT). Scientists have proposed that perhaps impurities remaining in the vaccine from the manufacturing process, such as snippets of DNA in the solution, or proteins in the broth used to grow the virus, are interacting with Platelet Factor 4 (PF4) to induce the aggregates that are then targeted by antibodies. But we are still unclear about the exact mechanisms that trigger VITT. Studies have demonstrated that antiphospholipid antibodies target endothelial cells to induce thrombo-inflammatory responses.
This article collection aims to highlight research across the vast area of COVID-19- associated coagulopathy (CAC). This special issue will cover the recent advancements in the understanding COVID-19 pathology, molecular pharmacology, animal models, and treatment options in relation to thrombo-inflammation in COVID-19.
Potential areas of research within this area include, but are not limited to, the following topics:
1) Blood cell interactions with the vessel wall in COVID-19.
2) Role of Platelets in COVID-19.
3) Endothelial cells in COVID-19.
4) NETs formation in COVID-19.
5) Vaccines-induced blood clots in COVID-19.
6) Monocytes and COVID-19.
7) Hyperinflammation in CAC.
8) Drug targets for COVID-19 and CAC.
9) Signaling receptors and COVID-19.
10) Anticoagulant effects and COVID-19.
11) The impact of concomitant conditions on CAC.
12) Autoantibodies in COVID-19.
13) Animal models for COVID-19 studies of thrombo-inflammation.
COVID-19 is frequently accompanied by a hypercoagulable inflammatory state with microangiopathic pulmonary changes that can lead to the diffuse alveolar damage characteristic of typical acute respiratory distress syndrome (ARDS), as seen in other severe lung pathogenic infections. Accumulating evidence supports that COVID-19 is associated with a marked increase in the risk for venous and arterial thromboembolic events in hospitalized patients, which is associated with dysfunction of vascular barrier, edema, endotheliitis, thrombosis, and inflammatory cell infiltration. These clots may also form in multiple places in the body, besides the lungs. This unusual clotting may cause different complications, including organ damage, heart attacks and stroke.
In severe COVID-19, endothelial and platelet activation markers are significantly increased compared to healthy controls. In addition to the lung epithelial cells, SARS-CoV-2 viral load is detected in the kidneys, liver, heart, and brain, which are highly vascularized organs. Research has indicated that the coagulation may be triggered by the high levels of inflammation, caused by the SARS-CoV-2 infection. A high level of inflammation can affect multiple organs and result in severe disease. Many human host receptors reportedly interact with SARS-CoV-2 spike protein to infect and replicate in lung epithelial and other cells, such as monocytes. Researchers have also proposed various drug targets and unique signaling pathways in different cells through various omics approaches. Although a body of literature supports that COVID-19 is an endothelial disease, direct infection of endothelial cells remains controversial.
On the other hand, a small population may develop a clotting disorder after receiving a COVID-19 vaccine, this is termed as vaccine-induced immune thrombotic thrombocytopenia (VITT). Scientists have proposed that perhaps impurities remaining in the vaccine from the manufacturing process, such as snippets of DNA in the solution, or proteins in the broth used to grow the virus, are interacting with Platelet Factor 4 (PF4) to induce the aggregates that are then targeted by antibodies. But we are still unclear about the exact mechanisms that trigger VITT. Studies have demonstrated that antiphospholipid antibodies target endothelial cells to induce thrombo-inflammatory responses.
This article collection aims to highlight research across the vast area of COVID-19- associated coagulopathy (CAC). This special issue will cover the recent advancements in the understanding COVID-19 pathology, molecular pharmacology, animal models, and treatment options in relation to thrombo-inflammation in COVID-19.
Potential areas of research within this area include, but are not limited to, the following topics:
1) Blood cell interactions with the vessel wall in COVID-19.
2) Role of Platelets in COVID-19.
3) Endothelial cells in COVID-19.
4) NETs formation in COVID-19.
5) Vaccines-induced blood clots in COVID-19.
6) Monocytes and COVID-19.
7) Hyperinflammation in CAC.
8) Drug targets for COVID-19 and CAC.
9) Signaling receptors and COVID-19.
10) Anticoagulant effects and COVID-19.
11) The impact of concomitant conditions on CAC.
12) Autoantibodies in COVID-19.
13) Animal models for COVID-19 studies of thrombo-inflammation.