SARS-CoV and SARS-CoV-2 could induce acute lung injury (ALI) and inflammation, which is mimicked by lipopolysaccharide (LPS), a bacterial endotoxin present on the outer membrane of Gram-negative bacteria [14], implicating SARS-CoV-2 and LPS through similar pathways of binding toll-like receptor-4 (TLR4) to activate angiotensin converting enzyme 2 (ACE2), to induce ALI and hyperinflammation [15, 16]. Here, ACE2 is linked to acute respiratory distress syndrome.