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

Med Hypotheses. 2021 Feb:147:110475. doi: 10.1016/j.mehy.2020.110475. Epub 2020 Dec 26.


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.

Keywords: Coagulopathy; Endothelium; Platelets; SARS-CoV-2; Selenium.

MeSH terms

  • Blood Coagulation Disorders / complications*
  • Blood Coagulation Disorders / virology
  • Blood Platelets / metabolism
  • COVID-19 / complications*
  • Critical Illness
  • Endothelium, Vascular / metabolism
  • Homeostasis
  • Humans
  • Immune System
  • Inflammation
  • Models, Theoretical
  • Oxidative Stress
  • Platelet Activation
  • SARS-CoV-2 / pathogenicity*
  • Selenium / chemistry
  • Selenocysteine / biosynthesis*
  • Selenocysteine / chemistry
  • Transcriptome


  • Selenocysteine
  • Selenium