Peer-review started: September 8, 2022
First decision: September 19, 2022
Revised: October 3, 2022
Accepted: November 21, 2022
Article in press: November 21, 2022
Published online: January 25, 2023
Processing time: 131 Days and 12.6 Hours
As the outbreak evolves, our understanding of the consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the resulting coronavirus disease 2019 (COVID-19) on the liver has grown. In this review, we discussed the hepatotropic nature of SARS-CoV-2 and described the distribution of receptors for SARS-CoV-2 (e.g., angiotensin-converting enzyme 2) in the vascular endothelium and cholangiocytes of the liver. Also, we proposed mechanisms for possible viral entry that mediate liver injury, such as liver fibrosis. Due to SARS-CoV-2-induced liver damage, many COVID-19 patients develop liver dysfunction, mainly characterized by moderately elevated serum aminotransferase levels. Patients with chronic liver disease (CLD), such as cirrhosis, hepatocellular carcinoma, nonalcoholic fatty liver disease, and viral hepatitis, are also sensitive to SARS-CoV-2 infection. We discussed the longer disease duration and higher mortality following SARS-CoV-2 infection in CLD patients. Correspondingly, relevant risk factors and possible mechanisms were proposed, including cirrhosis-related immune dysfunction and liver deco-mpensation. Finally, we discussed the potential hepatotoxicity of COVID-19-related vaccines and drugs, which influence the treatment of CLD patients with SARS-CoV-2 infection. In addition, we suggested that COVID-19 vaccines in terms of immunogenicity, duration of protection, and long-term safety for CLD patients need to be further researched. The diagnosis and treatment for liver injury caused by COVID-19 were also analyzed in this review.
Core Tip: In this review, we discussed the hepatotropic nature of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and described the distribution of receptors for SARS-CoV-2 in the vascular endothelium and cholangiocytes of the liver. We proposed mechanisms for possible viral entry that mediate liver injury, such as liver fibrosis. Due to SARS-CoV-2-induced liver damage, many coronavirus disease 2019 (COVID-19) patients develop liver dysfunction. We discussed the longer disease duration and higher mortality following SARS-CoV-2 infection in chronic liver disease patients. Correspondingly, relevant risk factors and possible mechanisms were proposed. Finally, we discussed the potential hepatotoxicity of COVID-19-related vaccines and drugs.