COVID-19 pandemic is a severe viral sepsis characterized by the occurrence of Acute respiratory distress syndrome (ARDS) whose pathophysiology is little described

The new Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) epidemic started on December 2019 in China and spreaded in worldwide. The Coronavirus disease 2019 (COVID-19) is responsible of case of severe pneumonia whose the major risk is the development to ARDS. Concerning the pathophysiology, there appear to be hemostasis abnormalities including thrombocytopenia and coagulopathy. In recent studies, this thrombocytopenia is described as a risk factor to develop severe COVID-19 infection. Sepsis is associated with a major systemic inflammatory response with an increased production of pro-inflammatory cytokines. Since their discovery, inflammasomes have an important role during inflammatory response following an aggression. There are intracytoplasmic multiprotein complex activated by cellular stress or infections and is responsible for the release of pro-inflammatory cytokines, including IL-1β. Most studies have analysed inflammasomes in nucleated cells, nevertheless, little is known about inflammasomes in platelets.

Thus, the present work aims to study the activation of the platelet NLRP3 inflammasome and the platelet functions and coagulation during a SARS-CoV-2 viral pneumonia according to different levels of severity

Inclusion Criteria:

• Patients suffering from COVID-19, hospitalized in intensive care unit and in standard care unit.

Exclusion Criteria:

• Patients suffering from malignant blood disease, cryopyrinopathy, sickle cell disease, rheumatoid arthritis and Crohn's disease

Patients suffering from COVID-19, hospitalized in intensive care unit and in standard care unit.