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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 fordoi:10.31219/osf.io/kwbhr fatcat:wc57p7t37jeyvblwmuwnjf2yri