[The Epoch Times, September 14, 2022](Reported by Epoch Times reporter Xu Cuiling from Taipei, Taiwan)Academia SinicaThe research team of Xie Shiliang, a distinguished researcher at the Genome Research Center, found that COVID-19 (CCP Pneumonia) pathogen SARS-CoV-2 (CCP virus), which activates platelets to amplify the inflammatory response, which in turn produces blood clots. As long as the two receptors CLEC5A and TLR2 on the surface of neutrophils are blocked, thrombosis symptoms can be relieved, intravascular coagulation and inflammation can be reduced. The research results have been published in the Journal of Biomedical Science.
SARS-CoV-2 mainly infects the respiratory tract, but some infected people develop symptoms of blood clots, which can be fatal in severe cases. Recently published data show that COVID-19 (CCP Pneumonia) causes almost nine times the number of blood clots as the flu, and can have a lifelong impact; even after an infected person recovers,pulmonary embolismthe probability of respiratory symptoms is still 1 times higher than that of uninfected people.
Song Peishan, the first author of this article and a postdoctoral researcher at the Genome Research Center, said that when collecting blood samples from patients in the acute phase of COVID-19 (covid-19), it was found that the blood contained a high amount of extracellular vesicles (EVs), and these cells Most of the outer vesicles are derived from platelets, which is obviously related to the activation of platelets after encountering viruses. After platelet activation, a large number of extracellular thylakoids are released to stimulate neutrophils, resulting in a large number of neutrophil extracellular traps (NETs) and suicide cell death (NETosis).
Song Peishan mentioned that although past reports have pointed out that the formation of NETs is helpful for the clearance of bacteria, many recent COVID-19 studies have shown that excessive neutrophilic extracellular network structures in patients can cause immune thrombosis, and even Severe endovascular embolism, the blockage of these microvascular pulmonary vessels, can cause systemic damage by depriving the lungs and other organs of oxygen.
The research team took extracellular vesicles from healthy subjects and COVID-19 patients for mass spectrometry analysis, and found that the extracellular vesicles caused by SARS-CoV-2 infection showed a large number of platelets Related proteins, and there are a variety of proteins associated with leukocyte degranulation and platelet activation and aggregation, showing that platelets are vigorously activated in the blood of COVID-19 (covid-19) patients.
The research team further studied and found that extracellular vesicles in the healthy control group could not induce the formation of NETs, but extracellular vesicles in the COVID-19 (COVID-19) induced powerful NETs formation, while blocking CLEC5A and TLR2 could inhibit the formation of COVID-19 ( NETs formation by extracellular vesicles.
In animal experiments, it was also found that mice infected with SARS-CoV-2 (CCP virus) had a large number of NETs and severe cell infiltration in the lungs 3 to 5 days after infection; in contrast, mice with CLEC5A and TLR2 gene knockout, Inflammation and cellular infiltration were greatly reduced.
The Genome Research Center pointed out that these experimental data confirmed that the value of extracellular vesicles in platelets is closely related to SARS-CoV-2 (coronavirus) infection and thromboembolism, and inhibition of platelet activation may be a future method for reducing the virus-induced lung inflammation. new strategy.
Xie Shiliang said that CLEC5A and TLR2 are promising therapeutic targets for reducing the incidence of acute sequelae of COVID-19 (covid-19), which can reduce thrombotic inflammation in the future and reduce the incidence of post-acute sequelae of COVID-19 (covid-19) risk. Blocking CLEC5A and TLR2 opens a new direction for the treatment of thrombotic complications of COVID-19 (covid-19), and the research team will continue to explore and find more new treatments along the line.
Responsible editor: Tang Yin