Abstract
The coronaviruses that cause notable diseases, namely, severe acute respiratory syndrome (SARS), middle east respiratory syndrome (MERS) and coronavirus disease 2019 (COVID-19), exhibit remarkable similarities in genomic components and pathogenetic mechanisms. Although coronaviruses have widely been studied as respiratory tract pathogens, their effects on the hepatobiliary system have seldom been reported. Overall, the manifestations of liver injury caused by coronaviruses typically involve decreased albumin and elevated aminotransferase and bilirubin levels. Several pathophysiological hypotheses have been proposed, including direct damage, immune-mediated injury, ischemia and hypoxia, thrombosis and drug hepatotoxicity. The interaction between pre-existing liver disease and coronavirus infection has been illustrated, whereby coronaviruses influence the occurrence, severity, prognosis and treatment of liver diseases. Drugs and vaccines used for treating and preventing coronavirus infection also have hepatotoxicity. Currently, the establishment of optimized therapy for coronavirus infection and liver disease comorbidity is of significance, warranting further safety tests, animal trials and clinical trials.
Highlights
Coronavirus (CoV) is a family of viruses that display crown-like structures under electron microscopy, with an outer envelope and positive-stranded RNA as the genomic material [1]
During the acute phase of middle east respiratory syndrome (MERS)-CoV infection, the levels of IFN-γ, tumor necrosis factor (TNF)-α, IL-15, and IL-17 in the serum of patients were dramatically elevated [77]. These results suggest that the systemic inflammatory reaction syndrome (SIRS) and cytokine storms caused by coronavirus infection may be critical mechanisms of liver injury [68, 120, 121]
These results indicate that coronavirus infection and viral hepatitis interact; exploring the underlying mechanism will be meaningful for optimizing treatment guidance for COVID-19
Summary
Coronavirus (CoV) is a family of viruses that display crown-like structures under electron microscopy, with an outer envelope and positive-stranded RNA as the genomic material [1]. Similar to the observations for SARS and COVID-19 patients, the pathological changes in MERS patients include moderate portal tract infection, lobular lymphocytic inflammation, and hydropic degeneration of hepatic parenchymal cells [48, 76]. SARS-CoV and SARS-CoV-2 can cause liver function abnormality through binding to the ACE2 receptors of bile duct cells, viral inclusions were not observed in the liver biopsies of COVID-19 patients [46]. These results indicate that liver injury in patients with coronavirus infection may be the result of bile duct epithelium damage rather than hepatocyte changes [90]. Liver cells in patients with severe coronavirus infection show various inflammatory changes, such as swelling and steatosis in hepatocytes, proliferation in liver sinus cells, hyperplasia in Kupffer cells and infiltration in immune cells [40, 46, 116]
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