When severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects cells expressing the surface receptors angiotensin-converting enzyme 2 (ACE2) and TMPRSS2, the active replication and release of the virus cause the host cell to undergo pyroptosis and release damage-associated molecular patterns, including ATP, nucleic acids and ASC oligomers. These are recognized by neighbouring epithelial cells, endothelial cells and alveolar macrophages, triggering the generation of pro-inflammatory cytokines and chemokines (including IL-6, IP-10, macrophage inflammatory protein 1α (MIP1α), MIP1β and MCP1). These proteins attract monocytes, macrophages and T cells to the site of infection, promoting further inflammation (with the addition of IFNγ produced by T cells) and establishing a pro-inflammatory feedback loop. In a defective immune response (left side) this may lead to further accumulation of immune cells in the lungs, causing overproduction of pro-inflammatory cytokines, which eventually damages the lung infrastructure. The resulting cytokine storm circulates to other organs, leading to multi-organ damage. In addition, non-neutralizing antibodies produced by B cells may enhance SARS-CoV-2 infection through antibody-dependent enhancement (ADE), further exacerbating organ damage. Alternatively, in a healthy immune response (right side), the initial inflammation attracts virus-specific T cells to the site of infection, where they can eliminate the infected cells before the virus spreads. Neutralizing antibodies in these individuals can block viral infection, and alveolar macrophages recognize neutralized viruses and apoptotic cells and clear them by phagocytosis. Altogether, these processes lead to clearance of the virus and minimal lung damage, resulting in recovery. G-CSF, granulocyte colony-stimulating factor; TNF, tumour necrosis factor.