Evidence map›Paper›PMID 35141510›Full record

ArticleJHEP reports : innovation in hepatology2022

Inducers of the NF-κB pathways impair hepatitis delta virus replication and strongly decrease progeny infectivity

Maud Michelet, Dulce Alfaiate, Brieux Chardès, Caroline Pons, Suzanne Faure-Dupuy, Thomas Engleitner, Rayan Farhat, Tobias Riedl, Anne-Flore Legrand, Roland Rad and 6 more

Open access · goldAbstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. A novelJHEP reports : innovation in hepatology · 2025
    Article
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  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 2 countries.

Maud MicheletINSERM, U1052, Cancer Research Center of Lyon (CRCL), University of Lyon (UCBL1), CNRS UMR_5286, Centre Léon Bérard, Lyon, France.
Dulce AlfaiateDepartment of Infectious Diseases, Croix-Rousse Hospital, Hospices Civils de Lyon, Lyon, France.
Brieux ChardèsINSERM, U1052, Cancer Research Center of Lyon (CRCL), University of Lyon (UCBL1), CNRS UMR_5286, Centre Léon Bérard, Lyon, France.
Caroline PonsCIRI - Centre International de Recherche en Infectiologie, Univ Lyon, Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR5308, ENS Lyon, Lyon, 69007, France.
Suzanne Faure-DupuyDivision of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Thomas EngleitnerInstitute of Molecular Oncology and Functional Genomics, Rechts der Isar University Hospital, Munich, Germany.
Rayan FarhatINSERM, U1052, Cancer Research Center of Lyon (CRCL), University of Lyon (UCBL1), CNRS UMR_5286, Centre Léon Bérard, Lyon, France.
Tobias RiedlDivision of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Anne-Flore LegrandCIRI - Centre International de Recherche en Infectiologie, Univ Lyon, Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR5308, ENS Lyon, Lyon, 69007, France.
Roland RadInstitute of Molecular Oncology and Functional Genomics, Rechts der Isar University Hospital, Munich, Germany.
Michel RivoireINSERM, U1032, Centre Léon Bérard (CLB), Lyon, France.
Fabien ZoulimINSERM, U1052, Cancer Research Center of Lyon (CRCL), University of Lyon (UCBL1), CNRS UMR_5286, Centre Léon Bérard, Lyon, France.
Mathias HeikenwälderDivision of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Anna SalvettiCIRI - Centre International de Recherche en Infectiologie, Univ Lyon, Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR5308, ENS Lyon, Lyon, 69007, France.
David DurantelCIRI - Centre International de Recherche en Infectiologie, Univ Lyon, Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR5308, ENS Lyon, Lyon, 69007, France.
Julie LuciforaCIRI - Centre International de Recherche en Infectiologie, Univ Lyon, Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR5308, ENS Lyon, Lyon, 69007, France.
Université Claude Bernard Lyon 1 · FRGerman Cancer Research Center · DETUM Klinikum · DEHôpital de la Croix-Rousse · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsHDV superinfection of chronically HBV-infected patients is the most aggressive form of chronic viral hepatitis, with an accelerated progression towards fibrosis/cirrhosis and increased risk of liver failure, hepatocellular carcinoma, and death. While HDV infection is not susceptible to available direct anti-HBV drugs, suboptimal responses are obtained with interferon-α-based therapies, and the number of investigational drugs remains limited. We therefore analyzed the effect of several innate immune stimulators on HDV replication in infected hepatocytes.

methodsWe used

resultsWe describe here, for the first time, anti-HDV effects of Pam3CSK4 and BS1, agonists of Toll-like receptor (TLR)-1/2, and the lymphotoxin-β receptor (LTβR), respectively. Both types of agonists induced dose-dependent reductions of total intracellular HDV genome and antigenome RNA and of HDV protein levels, without toxicity in cells monoinfected with HDV or co/superinfected with HBV. Moreover, both molecules negatively affected HDV progeny release and strongly decreased their specific infectivity. The latter effect is particularly important since HDV is thought to persist in humans through constant propagation.

conclusionsImmune-modulators inducing NF-κB pathways in hepatocytes can inhibit HDV replication and should be further evaluated as a possible therapeutic approach in chronically HBV/HDV-infected patients. LAY SUMMARY: Hepatitis delta virus causes the most severe form of viral hepatitis. Despite positive recent developments, effective treatments remain a major clinical need. Herein, we show that immune-modulators that trigger the NF-κB pathways could be effective for the treatment of hepatitis delta infections.

Indexed as

antiviral activitydHepaRG, differentiated HepaRG cellsHDV-AG(s), HDV anti-genome(s)HDV-G(s), HDV genome(s)Hepatitis B virusHepatitis D virushepatocytesIFN, interferonIL-, interleukin-L-HDAg, large HDV antigenLTβR, lymphotoxin-β receptorlymphotoxin beta receptorNF-κBNTCP, Na+-taurocholate cotransporting polypeptidePeg-IFN-α, pegylated interferon-αPHH, primary human hepatocyterh, recombinant humanRNP, ribonucleoproteinS-HDAg, small HDV antigenTLR, Toll-like receptorTNF, tumor necrosis factortoll-like receptorvge, viral genome equivalent

Identifiers

PMID35141510
PMCPMC8792426
OpenAlexW4200579990

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.