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. 2023 Apr 14;29(14):2064–2077. doi: 10.3748/wjg.v29.i14.2064

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©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

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Molecular mechanisms of liver damage during coronavirus disease 2019 infection. Hypoxia, ischemia, and cytokine storm significantly contribute to liver damage in coronavirus disease 2019-related comorbidities. This figure depicts how severe acute respiratory syndrome coronavirus 2 exponentially proliferates after entering hepatocytes. The steps occur: (1) Binding and viral entry via membrane fusion or endocytosis; (2) Translation of polypeptide; (3) Autoproteolysis and cotranslational polypeptide cleavage to generate non-structural proteins (nsps); (4) Sense subgenomic transcription and RNA replication; (5) + Sense subgenomic transcription and RNA replication; (6) Translation of subgenomic mRNA into structural and accessory proteins; (7) Nucleocapsid buds into ER-Golgi intermediate compartment studded with spike, envelope, and membrane proteins; (8) Formation of virion; and (9) Exocytosis. SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2; COVID-19: Coronavirus disease 2019; ERGIC: ER-Golgi intermediate compartment; DMV: Double-membrane vesicle.