Abstract
COVID-19 follows a rather stereotyped and reproducible course. While the first events are mediated by direct viral toxicity, resolution of the infection relies on a finely tuned immune response. In patients with severe forms, defects of the initial immune response have been reported, including insufficient type 1 interferon production or signaling, attenuated or skewed adaptative immune response, sometimes due to viral immune escape properties. These defects induce an hyperinflammatory state featuring hypersecretion of pro-inflammatory cytokines, excessive recruitment of immune cells in the lungs and parenchymal lesions, responsible for COVID-19 acute respiratory distress syndrome. Thus, COVID-19 is successively a viral and an inflammatory disease. Clarifying the chronology of these viral and immunological mechanisms allows us to identify a therapeutic logic, which sometimes involves contradictory treatments
