Pulmonary pathology of infection by SARS-CoV-2, what we have learnt through post-mortem studies and pathophysiological considerations

Abstract

Background: Since the declaration of Coronavirus Disease 2019 (COVID-19) caused the by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as a pandemic, millions of people throughout the world have contracted the disease and more than 500,000 have died. While this terrible disease has brought devastation to many countries, it has also generated the fastest growing amount of research output that science has seen during the last decades. Objectives: The objectives of this work were to review the pulmonary pathology from post-mortem studies and case reports of patients who succumbed to COVID-19, perform clinicopathologic correlation and hypothesize about pathogenetic mechanisms, and translate this understanding into better prevention, management and outcomes in the battle against COVID-19. Method: I performed a literature search through PubMed. Results: The main histopathologic findings in COVID-19 pneumonia are diffuse alveolar damage, organizing pneumonia, acute fibrinous and organizing pneumonia, interstitial pneumonia, endotheliitis, thromboembolism that correlates with respiratory failure and manifestations of thrombotic microangiopathy and hypercoagulable state. Immunohistochemical and transmission electron microscopic studies demonstrate viral proteins and viral structures within epithelial and endothelial cells. Reverse transcriptase polymerase chain reaction demonstrates the presence of viral RNA in nasopharynx and lung tissue post-mortem. Conclusions: SARS-CoV-2 is a respiratory virus that infects cells by binding to angiotensin-converting enzyme II (ACE2) receptors, produces cell death and ACE2 downregulation, which, in conjunction with dysregulated immune response, orchestrates a proinflammatory and prothrombic state that results in respiratory and multiple organ failure.