Evidence map›Paper›PMID 37917972›Full record

ArticleClinical and experimental immunology2024

Type 1 interferon auto-antibodies are elevated in patients with decompensated liver cirrhosis.

Gordon Greville, Sinead Cremen, Shauna O'Neill, Sarah Azarian, Gareth Brady, William McCormack, Adam H Dyer, Nollaig M Bourke, Olivier Touzelet, David Courtney and 5 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 46% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 1 country.

Gordon GrevilleDepartment of Biology, Kathleen Lonsdale Institute for Human Health Research, Maynooth University, Maynooth, Ireland.
Sinead CremenSchool of Medicine, University College Dublin, Dublin, Ireland.
Shauna O'NeillDepartment of Biology, Kathleen Lonsdale Institute for Human Health Research, Maynooth University, Maynooth, Ireland.
Sarah AzarianDepartment of Biology, Kathleen Lonsdale Institute for Human Health Research, Maynooth University, Maynooth, Ireland.
Gareth BradyDiscipline of Clinical Medicine, School of Medicine, Trinity Translational Medicine Institute, Trinity College Dublin, Dublin, Ireland.
William McCormackDiscipline of Clinical Medicine, School of Medicine, Trinity Translational Medicine Institute, Trinity College Dublin, Dublin, Ireland.
Adam H DyerDiscipline of Medical Gerontology, School of Medicine, Trinity Translational Medicine Institute, Trinity College Dublin, Dublin, Ireland.ORCID 0000-0003-1356-510X
Nollaig M BourkeDiscipline of Medical Gerontology, School of Medicine, Trinity Translational Medicine Institute, Trinity College Dublin, Dublin, Ireland.
Olivier TouzeletWellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, Northern Ireland.
David CourtneyWellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, Northern Ireland.
Ultan F PowerWellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, Northern Ireland.
Paul DowlingDepartment of Biology, Kathleen Lonsdale Institute for Human Health Research, Maynooth University, Maynooth, Ireland.
Tom K GallagherDepartment of Hepatopancreaticobiliary and Transplant Surgery, St. Vincent's University Hospital, Dublin, Ireland.
Connor G G BamfordWellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, Northern Ireland.
Mark W RobinsonDepartment of Biology, Kathleen Lonsdale Institute for Human Health Research, Maynooth University, Maynooth, Ireland.ORCID 0000-0002-7871-7103
National University of Ireland, Maynooth · IETrinity College Dublin · IESt. Vincent's University Hospital · IEUniversity College Dublin · IE

Funding

Medical Research Council MC_PC_19057Science Foundation Ireland 20/COV/8362
6 · The paper itself

Abstract

Patients with decompensated liver cirrhosis, in particular those classified as Childs-Pugh class C, are at increased risk of severe coronavirus disease-2019 (COVID-19) upon infection with severe acute respiratory coronavirus 2 (SARS-CoV-2). The biological mechanisms underlying this are unknown. We aimed to examine the levels of serum intrinsic antiviral proteins as well as alterations in the innate antiviral immune response in patients with decompensated liver cirrhosis. Serum from 53 SARS-CoV-2 unexposed and unvaccinated individuals, with decompensated liver cirrhosis undergoing assessment for liver transplantation, were screened using SARS-CoV-2 pseudoparticle and SARS-CoV-2 virus assays. The ability of serum to inhibit interferon (IFN) signalling was assessed using a cell-based reporter assay. Severity of liver disease was assessed using two clinical scoring systems, the Child-Pugh class and the MELD-Na score. In the presence of serum from SARS-CoV-2 unexposed patients with decompensated liver cirrhosis there was no association between SARS-CoV-2 pseudoparticle infection or live SARS-CoV-2 virus infection and severity of liver disease. Type I IFNs are a key component of the innate antiviral response. Serum from patients with decompensated liver cirrhosis contained elevated levels of auto-antibodies capable of binding IFN-α2b compared to healthy controls. High MELD-Na scores were associated with the ability of these auto-antibodies to neutralize type I IFN signalling by IFN-α2b but not IFN-β1a. Our results demonstrate that neutralizing auto-antibodies targeting IFN-α2b are increased in patients with high MELD-Na scores. The presence of neutralizing type I IFN-specific auto-antibodies may increase the likelihood of viral infections, including severe COVID-19, in patients with decompensated liver cirrhosis.

Indexed as

COVID-19Interferon Type ILiver DiseasesLiver TransplantationAntibodiesHumansLiver CirrhosisAntibodiesInterferon Type Iauto-antibodiesCOVID-19decompensated liver cirrhosisSARS-CoV-2type I interferon

Identifiers

PMID37917972
PMCPMC10847822
OpenAlexW4388209978

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.