Abstract
Substantial gaps in knowledge regarding the evolution and pathogenesis of COVID-19 remain after 1 year of the SARS-CoV-2 pandemic. At the start of the pandemic, a biphasic model to explain the physiopathology of COVID-19 became popular. This model divided the disease course into an initial viral response phase, followed by the inflammatory response phase.1,2 In the inflammatory response phase, the virus is thought to have a minor role, and host inflammatory responses are the predominant mediators of pathophysiology, by triggering tissue damage leading to acute respiratory distress syndrome.
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