Impairment in selenocysteine synthesis as a candidate mechanism of inducible coagulopathy in COVID-19 patients

Coagulopathy has recently been recognized as a recurring complication of COVID-19, most typically associated with critical illness. There are epidemiological, mechanistic and transcriptomic evidence that link Selenium with SARS-CoV-2's intracellular latency. Taking into consideration the vital role of selenoproteins in maintaining an adequate immune response, endothelial homeostasis and a non-prothrombotic platelet activation status, we propose that impairment in selenocysteine synthesis, via perturbations in the aforementioned physiological functions, potentially constitutes a mechanism of coagulopathy in COVID 19 patients other than those developed in critical illness.

Automated summary

Recent findings suggest that coagulopathy in COVID-19 patients may be linked to selenium deficiency, impacting selenoprotein synthesis and potentially leading to impairment in immune response and platelet activation status. This provides a new perspective on the mechanism of coagulopathy in COVID-19 beyond critical illness-related complications.