Last update:
17-Jan-2023

COVID-19 was identified in late 2019 and spread rapidly to become a pandemic. The causative agent is the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA-virus, which affects mainly the respiratory tract. SARS-CoV-2 enters the host's alveolar lung cells through the angiotensin converting enzyme (ACE2) receptor. During infection, in addition to abnormal activation of the immune system, an acute decrease in the ACE2 expression level occurs, resulting in acute respiratory distress syndrome (ARDS) and acute lung damage. Histopathologically, diffuse alveolar damage is observed, and vascular injury appears to be very important, as the pulmonary vessels demonstrate extensive thrombosis with microangiopathy and endothelitis. The virus has also been shown to affect heart tissue, and some patients develop acute cardiovascular syndrome. Endothelitis has also been found in the heart, kidney, spleen, liver and small intestine, and thrombogenic angiopathy is observed in the skin. Vascular injury also affects the brain. In placentas from COVID-19 positive mothers, inflammation and infarcts have been observed. The aim of this literature review is to summarize emerging data on the pathophysiology of SARS-CoV-2 disease in the lungs and other target organs, with an emphasis on microscopic findings in the tissues. Progress in understanding the pathophysiology of COVID-19 is of great importance for comprehension of clinical condition and administration of optimal treatment.

Key words: COVID-19, Histopathology, SARS-CoV-2.