English: Inflammatory responses during severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection. SARS-CoV-2 attaches to the ACE2 receptor, and the spike protein is cleaved by the type II transmembrane serine protease (TMPRSS2), resulting in viral replication. Mature viruses are released from the cell by exocytosis. In the dysfunctional immune response, cells may undergo pyroptosis and release adenosine triphosphate (ATP), nucleic acids, and ASC oligomer. These impaired-associated molecular forms can be detected by the neighboring epithelial cells and other alveolar macrophages. In response, the pro-inflammatory cytokines are released along with chemokines, including IL-6, IP-10, macrophage inflammatory protein 1α (MIP1β), MCP1, and MIP1α. These released proteins draw the monocytes, T cells, and lymphocytes to the inflammatory site, causing exaggerated inflammation at the site of action. This exaggerated response damages the lung’s infrastructure. This cytokine storm can move to other organs and may damages the other organs as well.