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進入《TAIPEI TIMES》NHRI researchers unveil study into COVID-19 deaths
National Health Research Institute researcher Hsieh Shie-liang poses for a photograph with members of his team at the Ministry of Health and Welfare in Taipei on Monday. Photo: CNA
Staff writer, with CNA
A new study by the National Health Research Institute （NHRI） has identified a link between CLEC2, a C-type lectin-like type II transmembrane receptor, and thromboinflammation, the major cause of morbidity and mortality in COVID-19 patients.
The new findings, which shed light on the molecular mechanism of SARS-CoV-2-induced thromboinflammation, were presented on Monday at a news conference by research team leader Hsieh Shie-liang （謝世良） of the NHRI’s Immunology Research Center.
Although COVID-19 has ravaged the world for more than three years, the mechanisms that contribute to SARS-CoV-2-induced platelet activation and immunothrombosis have been poorly understood, Hsieh said.
In addition to their involvement in blood coagulation, studies have indicated that platelets are also immune cells with receptors that interact with various viruses.
Hsieh said the team found that CLEC2 interacts with the SARS-CoV-2 spike RBD （receptor binding domain） to release cytokines and induce the formation of neutrophil extracellular traps （NETs）.
Describing the lungs as one of the organs that produces platelets, Hsieh said that when neutrophils, platelets and SARS-CoV-2 are bound together they form structurally adhesive NETs that result in a pulmonary embolism.
However, platelets with no CLEC2 do not form NETs when they encounter SARS-CoV-2, he said.
The team used gene recombination technology to produce the CLEC2.Fc fusion protein, which effectively binds to the spike protein of various subvariants of the virus such as Omicron, Hsieh said.
The experiment conducted on laboratory mice confirmed that the CLEC2.Fc protein can reduce embolisms by 60 to 80 percent, and no side effects have been detected, Academia Sinica Genomics Research Center researcher Sung Pei-shan （宋佩珊） said.
It is hoped that CLEC2.Fc can be used to protect people from SARS-CoV-2-induced lung damage, Hsieh said, adding that because CLEC2.Fc has only been produced in a laboratory setting, further testing needs to be conducted on humans.
Domestic pharmaceutical firms have already approached the team to discuss the possibility of a technology transfer with the goal of possibly developing a therapeutic drug, he said.
The NHRI team’s study on the subject, titled “Inhibition of SARS-CoV-2-mediated thromboinflammation by CLEC2.Fc,” was published by the open-access peer-reviewed medical journal EMBO Molecular Medicine in May.
新聞來源：TAIPEI TIMES
