An Important Marker that Determines Disease Severity in COVID-19: Immunothrombotic Dysregulation

It is known after observation and investigation that the severe cases of COVID-19 patients can lead to obstruction of blood vessels in the heart, lungs, and kidneys. Activated immune cells and blood platelets play a vital role in these pathologies. The virus basically affects the respiratory tract and in some worse cases, it results in lung failure. This leads to further complications like pulmonary embolisms or thrombosis in veins. It is still unclear if the respiratory failure caused by coronavirus is functionally related to the clot.

However, new research states that scientists have found a link between virus-induced changes in the blood vessels of the lung and an increase in the thrombotic risk level. In a post-mortem of a COVID-19 patient, many micro clots within the finest branches of the pulmonary vasculature were found. This was also the case with the heart and kidney. These clots were basically made up of platelets and activated immune cells, mostly neutrophils. Neutrophils fit into the innate immune system and their basic task is to fight the invading pathogens. After analyzing these clots, the researchers suggested that an activating interaction between platelets and neutrophils is responsible for promoting intravascular coagulation. In severely affected patients, the stimulation of clot formation affects the supply of blood to nearby tissues.

This leads to respiratory failure. These activated neutrophils extrude mesh-like complexes that are made up of DNA and cytoplasmic proteins known as neutrophil extracellular traps (NETs). These NET’s normally serve to destroy the bacterial and viral pathogens, but they also play a significant role in immunothrombosis by stabilizing thrombi. This process is localized in the lungs and hence results in a systemic thrombogenic state.

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