Identification of key signaling pathways induced by SARS‐CoV2 that underlie thrombosis and vascular injury in COVID‐19 patients

The SARS‐CoV‐2 pandemic has led to hundreds of thousands of deaths and billions of dollars in economic damage. The immune response elicited from this virus is poorly understood. An alarming number of cases have arisen where COVID‐19 patients develop complications on top of the symptoms already associated with SARS, such as thrombosis, injuries of vascular system, kidney, and liver, as well as Kawasaki disease. In this review, a bioinformatics approach was used to elucidate the immune response triggered by SARS‐CoV‐2 infection in primary human lung epithelial and transformed human lung alveolar. Additionally, examined the potential mechanism behind several complications that have been associated with COVID‐19 and determined that a specific cytokine storm is leading to excessive neutrophil recruitment. These neutrophils are directly leading to thrombosis, organ damage, and complement activation via neutrophil extracellular trap release. Graphical SARS‐Cov‐2 induces a specific cytokine profile, which induces the excessive release of extracellular traps by various cell types and leads to a prothrombotic environment.