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Review
. 2023 Mar 28;29(12):1838-1851.
doi: 10.3748/wjg.v29.i12.1838.

Autoimmune liver diseases and SARS-CoV-2

Costantino Sgamato  1 , Alba Rocco  2 , Debora Compare  1 , Stefano Minieri  1 , Stefano Andrea Marchitto  1 , Simone Maurea  3 , Gerardo Nardone  1
Affiliations
Review

Autoimmune liver diseases and SARS-CoV-2

Costantino Sgamato et al. World J Gastroenterol. .

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causing coronavirus disease 2019 (COVID-19), can trigger autoimmunity in genetically predisposed individuals through hyperstimulation of immune response and molecular mimicry. Here we summarise the current knowledge about auto-immune liver diseases (AILDs) and SARS-CoV-2, focusing on: (1) The risk of SARS-CoV-2 infection and the course of COVID-19 in patients affected by AILDs; (2) the role of SARS-CoV-2 in inducing liver damage and triggering AILDs; and (3) the ability of vaccines against SARS-CoV-2 to induce autoimmune responses in the liver. Data derived from the literature suggest that patients with AILDs do not carry an increased risk of SARS-Cov-2 infection but may develop a more severe course of COVID-19 if on treatment with steroids or thiopurine. Although SARS-CoV-2 infection can lead to the development of several autoimmune diseases, few reports correlate it to the appearance of de novo manifestation of immune-mediated liver diseases such as autoimmune hepatitis (AIH), primary biliary cholangitis (PBC) or AIH/PBC overlap syndrome. Different case series of an AIH-like syndrome with a good prognosis after SARS-CoV-2 vaccination have been described. Although the causal link between SARS-CoV-2 vaccines and AIH cannot be definitively established, these reports suggest that this association could be more than coincidental.

Keywords: Autoimmune hepatitis; Autoimmune liver disease; COVID-19; COVID-19 vaccine; SARS-CoV-2.

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Conflict of interest statement

Conflict-of-interest statement: Gerardo Nardone has served as a speaker and advisory board member for AG Pharma, Reckitt Benckiser, and has received research funding from SOFAR Spa and Alfasigma. No relevant conflicts of interest exist for the other authors.

Figures

Figure 1
Figure 1
The severe acute respiratory syndrome coronavirus 2 infection may lead to autoimmune liver disease through hyperstimulation of the immune system and molecular mimicry with human self-components. S1: Spike protein subunit 1; ACE2: Angiotensin-converting enzyme 2; TMPRSS2: Transmembrane Serine Protease 2; TH: T helper cells; IL: Interleukin; TNF-α: Tumour necrosis factor alfa; IFNγ: Interferon-gamma; APC: Antigen-presenting cell; GM-CSF: Granulocyte-macrophage colony-stimulating factor; IgG: Immunoglobulin G; SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2.
See this image and copyright information in PMC

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