Macrophage activation syndrome and COVID 19: Immune - Epigenetic programming in play

Idiopathic association of the ongoing COVID-19 pandemic with many diseases appears to be multifactorial. SARS-CoV-2 enters into host cells via ACE-II receptor and triggers the secretion of copious amount of IL-6;promote pulmonary fibrosis and Th2 / 17 programming of lungs, leading to severe lung pathology in COVID-19 patients. This virus interact and tweak all kind of cells like epithelium, macrophages, dendritic cells, and T cells and exploit them in a way that support its replication for progression of disease. Out of several patho-physiological manifestations, Macrophage activation syndrome is responsible for acute respiratory distress syndrome (ARDS) and subsequent death of COVID-19 patients. This is mainly accompanied by the increased infiltration of FCN1 + macrophages and other immune cells like neutrophils that contribute to Th2/Th17 programming of lung cells in COVID-19 patients. However, in view of durability and plasticity, macrophages are responsible for high-grade inflammatory response and mortality in patients.