Fig. 3.

Fig. 3. Schematic representation of the lung damage induced by SARS-CoV-2 infection. In the human airway epithelium, SARS-CoV-2 infection induces the formation of syncytia and unique cytopathic effects (CPEs) associated with the clinical symptom of pneumonia. Interaction of the S protein on the cell surface of SARS-CoV-2-infected cells with ACE2 on the cell surface of adjacent cells is a cause of syncytia formation and cell fusion. In the meantime, SARS-CoV-2 infection causes mitochondrial damage, including depolarization of mitochondrial membrane potential (ΔΨm), opening of mitochondrial permeability transition pores, and increasing ROS release, ultimately disrupting mitochondrial homeostasis. Viral proteins, including the S protein and an accessory protein encoded in ORF8, can also induce cellular ER stress modulating innate immunity and inflammatory responses associated with immune evasion.

© J. Microbiol. Biotechnol.