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. 2020 Aug 5:1–10. doi: 10.1080/07391102.2020.1803139

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This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with 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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Figure 2. — Pathophysiology of ARDS in SARS-CoV-2 inducing COVID-19 patients with severe symptoms. Once SARS-CoV-2 gets into the body, it uses its S-spike type, as a key to enter the cells by binding to angiotensin-converting enzyme (ACE2). The virus use the mainly pneumocytes 2 components for its own proliferation. The infected cells secret a high amount of specific inflammatory mediators that enhance macrophages to release cytokines Tumor Necrosis Factor alpha (TNFα) and interleukins (IL-1 and IL-6). These cytokines lead to the disruption of the alveolar-capillary membrane integrity and increased the vascular permeability. The disrupted integrity of the alveolar-capillary allow the plasma leakage into the alveoli and the lungs interstitial spaces. The formation of protein rich edema, known as exudate, in the interstitium and alveolar spaces leads to alveolar flooding making it very difficult to breathe and lead to hypoxemia. Driven by IL-1, IL-6 and TNFα, PMNs invade the alveoli and release reactive oxygen species (ROS), neutrophil extracellular traps (NETs) and proteases that damage the vascular and the alveoli components that exacerbates the hypoxemia, the alveoli collapsing and lead to a worse situation: alveolar consolidation.