Self-DNA-induced inflammation and related clinical manifestations: Lessons from coronavirus disease 2019

In 2020, the author proposed the hypothesis that free DNA present in the cytoplasm or circulating blood may induce severe coronavirus disease 2019 (COVID-19), which is consistent with multiple specific clinical phenotypes reported during the COVID-19 outbreak.At that time, only a few months after the pandemic was first reported, the majority of the proposed associations and mechanistic insights regarding DNA sensors, their pathways and related biomarkers in COVID-19 had not yet been published.To date, a large number of population-based and fundamental studies have indicated that DNA sensor-mediated immune responses are involved in disease progression.This review synthesizes recent evidence to support the author's hypothesis that the self-DNA axis acts as a common driver of many pathways promoting inflammatory responses and inducing multiple organ damage in COVID-19, thereby affecting disease prognosis.This work may modestly contribute to the improved understanding of the potential role of self-DNA in severe and sustained inflammation, and elucidate its association with relevant clinical manifestations in multiple fatal infectious diseases.