[Epoch Times, September 22, 2022](Epoch Times reporter Lin Huizhen Hong Kong reported) Infection with COVID-19 can lead to the formation of blood clots in the lungs, which can be fatal in severe cases, and there is also the risk of serious sequelae. A study by the Academia Sinica in Taiwan found that the key cause of thrombosis in COVID-19 patients is that the COVID-19 pathogen SARS-CoV-2 activates platelets to amplify the inflammatory response, which in turn produces blood clots. Blocking two receptors on the surface of neutrophils, CLEC5A and TLR2, alleviates thrombotic symptoms and reduces intravascular coagulation and inflammation.
Song Peishan, the first author of the study and a postdoctoral researcher at the Genome Research Center, said that blood samples collected from patients in the acute phase of COVID-19 found that the blood contained a high amount of extracellular vesicles (EVs), most of which were derived from platelets. Apparently it is related to the activation of platelets after encountering the virus. When platelets are activated by the virus, they release a large number of extracellular thylakoids to stimulate neutrophils, resulting in a large number of neutrophil extracellular network structures (NETs) and suicide cell death (NETosis). Earlier studies have found that while the formation of NETs helps clear bacteria, too many NETs can trigger blood clots, which can lead to the blockage of microvessels in the lungs.
The research team took the extracellular vesicles of healthy subjects and COVID-19 patients for mass spectrometry analysis, and found that the extracellular vesicles caused by SARS-CoV-2 infection expressed a large number of platelet-related proteins, and had a variety of platelet-related proteins associated with leukocyte degranulation. The protein of platelet activation and aggregation, showing the vigorous activation of platelets in the blood of COVID-19 patients.
The research team further cultured extracellular vesicles from healthy people and COVID-19 patients with neutrophils. The results showed that the extracellular vesicles of the healthy control group could not induce the formation of NETs, but the extracellular vesicles of the COVID-19 patients induced the formation of NETs. The formation of robust NETs was inhibited by blocking two receptors on the surface of neutrophils, CLEC5A and TLR2.
In animal experiments, the researchers found that 3 to 5 days after mice were infected with SARS-CoV-2 virus, the lungs produced a large number of NETs and severe cellular infiltration; in CLEC5A and TLR2 knockout mice, inflammation and Cell infiltration was greatly reduced.
Xie Shiliang, a distinguished researcher at the Genome Research Center of Academia Sinica, pointed out that CLEC5A and TLR2 are promising therapeutic targets to reduce thrombotic inflammation and reduce the risk of developing COVID-19 sequelae in the future.
The research has been published in the Journal of Biomedical Science. @
Responsible editor: Chen Wenqi