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. 2021 Dec 17;23:e24. doi: 10.1017/erm.2021.30

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© The Author(s) 2021

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means subject to acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Fig. 3. — Schematic diagram of cytokine storm in COVID-19. (1) SARS-CoV-2 infects lung bronchial, alveolar type I and type II epithelial cells. (2) Immune cells, including macrophages, recognise viruses and produce cytokines. (3) Cytokines attract more immune cells, such as neutrophils, T cells, monocyte and DCs, which in turn produce more cytokines, creating a cycle of inflammation that damages the lung cells. (4) Persistent inflammation lead to tissue damage, leucocytes infiltration and fluid leakage from the blood vessel, causing respiratory failure. (5) Excessive deposit of fibrin in the lungs.