What is the pathogenesis of lung injury in coronavirus disease 2019 (COVID-19)?

Updated: Jan 12, 2021
  • Author: Setu K Patolia, MD, MPH; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
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The RBD of the S protein of SARS-CoV-2 specifically recognizes the host angiotensin-converting enzyme 2 (ACE2) receptor. It is optimized for binding to the human receptor ACE2.

Similarly to SARS-CoV-2, SARS-CoV also binds with the ACE2 receptor to gain entry into human cells. Upon binding, host serine protease TMPRSS2 cleaves the S protein and results in the fusion of the viral and cellular membranes. The S protein of SARS-CoV-2 and SARS-CoV have almost identical three-dimensional structures, and, given this, researchers hypothesize that SARS-CoV-2 likely uses a similar mechanism.

The ACE2 receptor is expressed in type 2 alveolar epithelial cells in the lungs, heart, kidney, and gastrointestinal tract. However, the lungs seem to be particularly vulnerable to SARS-CoV-2 because of their large surface area and because alveolar epithelial type 2 cells seemingly act as a reservoir for virus replication. Direct injury to the lung tissue from a viral infection–mediated local inflammatory response is one of the proposed mechanisms behind the pulmonary manifestations of COVID-19. [6]

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