Letter to the Editor
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 14, 2022; 28(6): 683-688
Published online Feb 14, 2022. doi: 10.3748/wjg.v28.i6.683
COVID-19, liver dysfunction and pathophysiology: A conceptual discussion
Jucier Gonçalves Júnior
Jucier Gonçalves Júnior, Department of Internal Medicine, Division of Rheumatology, São Paulo University, São Paulo 01246-903, State, Brazil
Author contributions: The author worked on all aspects of manuscript preparation and has read and approved the final manuscript; The author meets the criteria for authorship established by the International Committee of Medical Journal Editors.
Conflict-of-interest statement: The author declares no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Jucier Gonçalves Júnior, MD, PhD, Academic Research, Department of Internal Medicine, Division of Rheumatology, São Paulo University, Av. Dr. Arnaldo, 455, 3º Andar-Sala 3131 Cerqueira César, São Paulo 01246-903, State, Brazil. juciergjunior@hotmail.com
Received: July 18, 2021
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
Core Tip

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.