Abstract
Our understanding of the hepatic consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and its resultant coronavirus disease 2019 (COVID-19) has evolved rapidly since the onset of the pandemic. In this Review, we discuss the hepatotropism of SARS-CoV-2, including the differential expression of viral receptors on liver cell types, and we describe the liver histology features present in patients with COVID-19. We also provide an overview of the pattern and relevance of abnormal liver biochemistry during COVID-19 and present the possible underlying direct and indirect mechanisms for liver injury. Furthermore, large international cohorts have been able to characterize the disease course of COVID-19 in patients with pre-existing chronic liver disease. Patients with cirrhosis have particularly high rates of hepatic decompensation and death following SARS-CoV-2 infection and we outline hypotheses to explain these findings, including the possible role of cirrhosis-associated immune dysfunction. This finding contrasts with outcome data in pharmacologically immunosuppressed patients after liver transplantation who seem to have comparatively better outcomes from COVID-19 than those with advanced liver disease. Finally, we discuss the approach to SARS-CoV-2 vaccination in patients with cirrhosis and after liver transplantation and predict how changes in social behaviours and clinical care pathways during the pandemic might lead to increased liver disease incidence and severity.
Highlights
Abstract | Our understanding of the hepatic consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and its resultant coronavirus disease 2019 (COVID-19) has evolved rapidly since the onset of the pandemic. In this Review, we discuss the hepatotropism of SARS-CoV-2, including the differential expression of viral receptors on liver cell types, and we describe the liver histology features present in patients with COVID-19
The hepatic consequences of SARS-CoV-2 infection are recognized as an important component of COVID-19
This aspect is most clinically relevant in patients with pre-existing cirrhosis who are at remarkably high risk of severe COVID-19 and death
Summary
Patients with cirrhosis have high rates of hepatic decompensation, acute-on-chronic liver failure and death from respiratory failure following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and should be prioritized for coronavirus disease 2019 (COVID-19) vaccination. Expression profiles of SARS-CoV-2 entry receptors vary across different in vitro and in vivo liver models; evidence of specific viral hepatotropism is limited. Liver injury and inflammation could potentiate SARS-CoV-2 hepatotropism by modulating viral receptor expression, with ACE2 being identified as an interferon-inducible gene in human respiratory epithelia[23,24]. Among hospitalized patients with COVID-19, elevations of serum AST levels positively correlate with levels of ALT but not with markers of muscle breakdown (such as creatinine kinase) or systemic inflammation (such as C-reactive protein (CRP) and ferritin)[50] These findings imply that elevated liver enzymes in COVID-19 result from direct hepatic injury, COVID-19associated rhabdomyolysis is rarely reported[51]. As with many other infections, SARS-CoV-2 is associated with systemic inflammation that could contribute www.nature.com/nrgastro a Hepatoma cell lines
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