Dysregulated liver function in SARS-CoV-2 infection: Current understanding and perspectives

Figure 1 Severe acute respiratory syndrome coronavirus 2 genome and its pathogenesis. A: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genome structure and its encoded proteins; B: Virion structure of SARS-CoV-2 illustrating viral structural proteins including spike protein (S), envelope protein (E), membrane protein (M), and nucleocapsid protein (N); C: SARS-CoV-2 entry to the target cells by binding the receptor-binding domain of S protein to cellular receptors, such as angiotensin-converting enzyme 2 and transmembrane protease serine 2. SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2; RBD: Receptor-binding domain; TMPRSS2: Transmembrane protease serine 2; ACE2: Angiotensin-converting enzyme 2.

Figure 2 Schematic diagram of the two mechanisms of severe acute respiratory syndrome coronavirus 2-induced liver dysfunction. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes direct liver injury through binding to the angiotensin-converting enzyme 2 receptor and transmembrane protease serine 2 expressed on cholangiocytes and hepatocytes. Indirect injury by cytokine storm. T cells are stimulated to secrete large quantities of cytokines including type I interferons, interleukin-6, and tumor necrosis factor-α following SARS-CoV-2 infection, leading to systemic excessive inflammation syndrome. ACE2: Angiotensin-converting enzyme 2; TMPRSS2: Transmembrane protease serine 2; TNF-α: Tumor necrosis factor-α; IL-6: Interleukin-6; IFN: Interferons.