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World J Virol. Jan 25, 2023; 12(1): 44-52
Published online Jan 25, 2023. doi: 10.5501/wjv.v12.i1.44
Table 1 Events in the liver from a broad perspective of severe acute respiratory syndrome coronavirus 2 infection
Effect
Mechanism
Result
Outcomes and morphological changes
SARS-CoV-2 virusGenomic translations and replicationMore viruses in circulationInflammation features. Usually, the biliary intrahepatic tree and bile duct did not show any significant histological alteration. Actin smooth muscle antibodies existed in pericytes which were in portal vein walls and adventitial areas
Viral proteins of SARS-CoV-2 SIRS -> stimulate cytokine stormIncreased TNF-α, IL-6, IL-1β, IL-2, IL-8, CCL2, CCL3, CCL5, CXCL10 levels. Decreased (CD4+) T cell and NK cell countsIncrease in the number of portal vein branches associated with lumen massive dilatation and focal periportal abnormal vessels. Portal vein endotheliitis (fragmented smooth muscle layer). Scattered portal and lobular lymphocytes. Extremely activated Kupffer cells with large cytoplasm containing necrotic debris
HypoxiaHypoxic ischemic injury of all organs and also liverDecreased SpO2 levels, mitochondrial dysfunction, and hypoxic hepatocytes express higher ACE-2 levelsPartial or complete luminal thrombosis of the portal and sinusoidal vessels, focal portal vein parietal fibrosis, enlarged and fibrotic vessels. A diffuse network of sinusoids decorated by CD34 suggests a disturbed circulation of blood within the liver
Drugs (antivirals, immune stimulants)Liver damageIncrease in ALT, AST, LDH, CRP, D-dimer, ferritin, and bilirubin levels and a decrease in albumin levelsPortal fibrosis, lobular and mild portal inflammation
Drugs and viral proteinsThe cytopathic effect, oxidative imbalanceApoptosis and steatosis Small and/or large droplets of steatosis in hepatocytes