Published online Feb 14, 2022. doi: 10.3748/wjg.v28.i6.683
Peer-review started: July 18, 2021
First decision: August 15, 2021
Revised: August 21, 2021
Accepted: January 19, 2022
Article in press: January 19, 2022
Published online: February 14, 2022
Processing time: 205 Days and 11.5 Hours
The intra and extracellular pathways of hepatic injury by coronavirus disease 2019 (COVID-19) are still being studied. Understanding them is important to treat this viral disease and other liver and biliary tract disorders. Thus, this paper aims to present three hypotheses about liver injury caused by COVID-19: (1) The interactions between severe acute respiratory syndrome coronavirus 2 spike protein and membrane receptors in the hepatocyte; (2) The dysbiosis and “gut-liver axis” disruption in patients with serious clinical presentations of COVID-19; and (3) The inflammatory response exacerbated through the production of interleukins such as interleukin-6. However, despite these new perspectives, the pathophysiological process of liver injury caused by COVID-19 is still complex and multifactorial. Thus, understanding all these variables is a challenge to science but also the key to propose individualized and effective patient therapies.
Core Tip: This paper aimed to present new hypotheses on the pathophysiology of liver injury caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Interactions between SARS-CoV-2 spike protein and other membrane receptors in the liver; “gut-liver axis” disruption and dysbiosis; and increased inflammatory process mediated by interleukin-6 and AT1R-metalloprotease 17 seem to be factors that contribute to such injury.