Pathophysiological mechanisms of liver injury in COVID-19

Liver Int. 2021 Jan;41(1):20-32. doi: 10.1111/liv.14730. Epub 2020 Nov 29.


The recent outbreak of coronavirus disease 2019 (COVID-19), caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has resulted in a world-wide pandemic. Disseminated lung injury with the development of acute respiratory distress syndrome (ARDS) is the main cause of mortality in COVID-19. Although liver failure does not seem to occur in the absence of pre-existing liver disease, hepatic involvement in COVID-19 may correlate with overall disease severity and serve as a prognostic factor for the development of ARDS. The spectrum of liver injury in COVID-19 may range from direct infection by SARS-CoV-2, indirect involvement by systemic inflammation, hypoxic changes, iatrogenic causes such as drugs and ventilation to exacerbation of underlying liver disease. This concise review discusses the potential pathophysiological mechanisms for SARS-CoV-2 hepatic tropism as well as acute and possibly long-term liver injury in COVID-19.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiotensin-Converting Enzyme 2 / physiology
  • COVID-19 / complications*
  • Cholestasis / etiology
  • Humans
  • Liver / virology*
  • Liver Diseases / etiology*
  • Non-alcoholic Fatty Liver Disease / etiology
  • SARS-CoV-2*
  • Viral Tropism*


  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2