SARS-CoV-2 ORF7a and SARS-CoV ORF7a share the same ER retention motif (C-terminal KRKTE sequence), suggesting that SARS-CoV-2 ORF7a may be incorporated into the viral envelope as SARS-CoV ORF7a . Viruses bind to bacteria or directly bind to free Lipopolysaccharide(LPS), enhancing their attachment to the ACE2 receptor on the host cell surface. This interaction significantly increases viral infectivity and promotes hypercytokineemia 127 . Therefore, LPS makes the virus spread more efficiently. In addition, SARS-COV-2 virus protein synthesized and transported LPS, which activated monocytes or phagocytes through CD14 receptors. When LPS increased, the number of activated phagocytes increased significantly. The swallowed behavior for red blood cell and iron by activated phagocytes was enhanced. There were more heme and iron in phagocytes. ROS damage theory 128 believes that the SARS-COV-2 virus parasitizes in the vesicles or lysosomes of phagocytes. After the virus binds to the heme in the vesicles or lysosomes, it is more aggressive. It attacks the phagocytes' lysosome membrane by generating ROS. The lysosomal membrane ruptures after being damaged by ROS to release hydrolase. The phagocytes will die and rupture due to autophagy reaction and released virus particles. The nearby phagocytes swallows the virus particles again and continues a vicious circle. The surrounding tissues will therefore produce a robust inflammatory response and fibrosis.