Histopathological impact of SARS-CoV-2 on the liver: Cellular damage and long-term complications

Figure 1 Mechanisms of viral entry and receptor expression in liver tissue. The severe acute respiratory syndrome coronavirus 2 virus enters the host cell using its spike protein (S protein) which binds to the angiotensin I converting enzyme 2 receptor. The S protein gets cleaved by furin and cathepsin L, then with the help of transmembrane serine protease 2 the S protein gets activated to facilitate viral entry. These cells are transduced by the virus, which enters the cell through endocytosis, where lysosomal Phosphatidylinositol 3-phosphate 5-kinase aids in endosome formation and permits fusion of viral and host membranes. ACE2: Angiotensin-converting enzyme 2; CTSL: Cathepsin L; TMPRSS2: Transmembrane serine protease 2; SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2.

Figure 2 Direct coronavirus disease 2019 liver injury is observed through various histopathological changes. After analyzing several cohorts of liver biopsies, the most common findings associated with severe acute respiratory syndrome coronavirus 2 hepatic infection were reported and described. I: Centrilobular areas of confluent necrosis. II: The inflammatory infiltrate surrounding necrosis showed lymphoplasmacytic infiltrate with histiocytes, few eosinophils, and neutrophils. III: Periportal fibrosis and presence of both micro and macrovesicular steatosis. IV: Ballooning degeneration shown by swelling and rounding up of hepatocytes. V: Canalicular cholestasis with discrete ductular reaction, predominantly in zone 3. VI: Chronic venous congestion, endotheliitis, portal vein thrombosis and platelet-fibrin thrombi in hepatic sinusoids.