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How does COVID-19 increase clotting risk?

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A detailed review article describing coronavirus disease 2019 (COVID-19)-related coagulopathy was recently published in the journal. nature review immunology.

Perspective: Understanding COVID-19-related coagulopathy. Image Credit: NIAIDperspective: Understanding COVID-19-related coagulopathyImage Credit: NIAID

Background

Hyperinflammation and hypercoagulation are two key features of COVID-19, a novel disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In his severely ill COVID-19 patients, coagulopathy has been found to be associated with multiple organ damage or failure, which increases the risk of death.

Complex interactions between the innate immune system, coagulation and fibrinolytic pathways, and vascular endothelial cells are responsible for COVID-19-related coagulopathy.

Alveolar vascular dysfunction in COVID-19

The vascular endothelium functions as an antithrombotic system by secreting various molecules that prevent platelet activation and clotting. In COVID-19, a dysregulated vascular antithrombotic system is believed to be responsible for the life-threatening conditions hypercoagulability and angiopathy.

SARS-CoV-2 infects type II pneumocytes in the lung and causes damage to the alveolar vasculature. In some cases, viruses have also been observed to directly infect endothelial cells and induce vascular endothelial dysfunction. Collectively, these conditions cause abnormal immune and inflammatory responses.

It is well established that SARS-CoV-2 infects respiratory epithelial cells by interacting with the plasma membrane receptor angiotensin-converting enzyme 2 (ACE2). Under normal physiological conditions, ACE2 regulates the renin-angiotensin and kallikrein-kinin systems. Kinins are vasoactive peptides that increase vascular permeability.

The interaction of SARS-CoV-2 and ACE2 reduces the cell surface expression of ACE2 at sites of infection. This further leads to activation of the kallikrein-kinin system, induction of vascular permeability, fluid accumulation, and organ damage.

COVID-19 and the blood-brain barrier

In addition to respiratory illness, COVID-19 is associated with a wide range of neurological symptoms. Autopsy analyzes of COVID-19 patients have observed microthrombi and microinfarcts in the brain.

Several studies suggest that SARS-CoV-2 directly infects brain tissue and induces neurological effects. However, the majority of studies emphasize the involvement of indirect mechanisms.According to these studies, viral proteins such as SARS-CoV-2 spike proteincrosses the blood-brain barrier and triggers an innate immune response and hyperinflammation of brain microvascular endothelial cells.

The major protease of SARS-CoV-2 contributes to neuropathology by cleaving the endothelial cell NF-κB essential modulator (NEMO), leading to vascular endothelial dysfunction. Taken together, all these factors contribute to hypercoagulability, thrombosis, and brain pathology in her COVID-19 patients.

hyperinflammation and coagulopathy

Neutrophils are important components of the innate immune system. These phagocytic immune cells contribute to early-stage viral clearance by forming neutrophil extracellular traps, net-like structures composed of antimicrobial proteins, oxidases, clotting agents, and complement factors. increase. In COVID-19, increased levels of neutrophil extracellular traps have been found to be associated with hypercoagulability and thrombosis.

Overactivation of the complement system induced by SARS-CoV-2 leads to hypercoagulability and hyperinflammation through a positive feedback loop between complement, neutrophils, neutrophil extracellular traps, and coagulation. can cause it.

Platelet dysfunction, hypercoagulability, and protein C dysregulation in COVID-19-associated coagulopathy

COVID-19 is associated with platelet activation and increased platelet-neutrophil and platelet-monocyte aggregation. Platelet-neutrophil aggregates readily adhere to the vessel wall and release prothrombotic and pro-inflammatory mediators, whereas platelet-monocyte aggregates inhibit clotting by increasing the expression of monocyte tissue factor. Promote hyperactivity.

Platelet transcriptome alterations by SARS-CoV-2 may be responsible for platelet hyperactivity in COVID-19. However, it is unknown whether transcriptomic alterations are associated with direct viral infection of platelets or virus-induced hyperinflammation.

COVID-19 is associated with increased coagulation pathway activity and decreased fibrinolytic pathway activity. These two processes may collectively contribute to coagulopathy. Genes encoding coagulation and fibrinolytic proteins show differential expression in COVID-19 patients.

It is becoming increasingly clear that low protein C levels are associated with severity and mortality in hospitalized COVID-19 patients. Endothelial thrombomodulin shedding has been observed to be associated with dysregulation of the protein C pathway, leading to hyperinflammation and hypercoagulation.

COVID-19 animal models to study coagulopathy

A mouse-adapted SARS-CoV-2 was developed to infect wild-type mice expressing mouse ACE2. This mouse model recapitulates some features of coagulopathy observed in COVID-19 patients and may therefore serve as a useful tool for deciphering mechanisms and identifying new therapeutics.

Transgenic mice expressing human ACE2 were developed to mimic the clinical course of COVID-19. This mouse model provides an excellent platform for studying neural invasion and subsequent neuropathology, including meningoencephalitis, thrombosis, hemorrhage, and vasculitis.

Other suitable animal models for studying COVID-19-related coagulopathy include hamsters, non-human primates, rhesus monkeys, and African green monkeys.

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