Evidence map›Paper›PMID 37154158›Full record

ArticleJCI insight2023

Persistent hepatic IFN system activation in HBV-HDV infection determines viral replication dynamics and therapeutic response.

Takeshi Chida, Yuji Ishida, Sho Morioka, Go Sugahara, Christine Han, Bill Lam, Chihiro Yamasaki, Remi Sugahara, Meng Li, Yasuhito Tanaka and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Hepatitis Delta Virus and Hepatocellular Carcinoma.Pathogens (Basel, Switzerland) · 2024
    Review
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

13 authors at 5 institutions in 3 countries.

Takeshi ChidaDivision of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California (USC), Los Angeles, California, USA.
Yuji IshidaDivision of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California (USC), Los Angeles, California, USA.
Sho MoriokaPhoenixBio, Co., Ltd., Higashi-Hiroshima, Hiroshima, Japan.
Go SugaharaDivision of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California (USC), Los Angeles, California, USA.
Christine HanDivision of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California (USC), Los Angeles, California, USA.
Bill LamDivision of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California (USC), Los Angeles, California, USA.
Chihiro YamasakiPhoenixBio, Co., Ltd., Higashi-Hiroshima, Hiroshima, Japan.
Remi SugaharaDivision of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California (USC), Los Angeles, California, USA.
Meng LiBioinformatics Service, Norris Medical Library, USC, Los Angeles, California, USA.
Yasuhito TanakaDepartment of Gastroenterology and Hepatology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Kumamoto, Japan.
T Jake LiangLiver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH, Bethesda, Maryland, USA.
Chise TatenoPhoenixBio, Co., Ltd., Higashi-Hiroshima, Hiroshima, Japan.
Takeshi SaitoDivision of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California (USC), Los Angeles, California, USA.
University of Southern California · USPhoenixBio (Japan) · JPKumamoto University · JPNational Institute of Diabetes and Digestive and Kidney Diseases · USUSC Norris Comprehensive Cancer Center · US

Funding

Molecular Mechanisms Of Hepatitis B Viral Pathogenesis And PersistenceZIADK054500 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI LIANG, T. JAKE · 2009 to 2025
$20.3M
Innate Defense Program against HCVR01DK101773 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SAITO, TAKESHI · 2015 to 2019
$1.9M
Impact of Occult Hepatitis C Virus Infection in Progression of Liver DiseasesR21AI139954 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SAITO, TAKESHI · 2018 to 2019
$454k
NIAID NIH HHS R21 AI139954NIDDK NIH HHS R01 DK101773
6 · The paper itself

Abstract

Hepatitis delta virus (HDV), a satellite virus of HBV, is regarded as the most severe type of hepatitis virus because of the substantial morbidity and mortality. The IFN system is the first line of defense against viral infections and an essential element of antiviral immunity; however, the role of the hepatic IFN system in controlling HBV-HDV infection remains poorly understood. Herein, we showed that HDV infection of human hepatocytes induced a potent and persistent activation of the IFN system whereas HBV was inert in triggering hepatic antiviral response. Moreover, we demonstrated that HDV-induced constitutive activation of the hepatic IFN system resulted in a potent suppression of HBV while modestly inhibiting HDV. Thus, these pathogens are equipped with distinctive immunogenicity and varying sensitivity to the antiviral effectors of IFN, leading to the establishment of a paradoxical mode of viral interference wherein HDV, the superinfectant, outcompetes HBV, the primary pathogen. Furthermore, our study revealed that HDV-induced constitutive IFN system activation led to a state of IFN refractoriness, rendering therapeutic IFNs ineffective. The present study provides potentially novel insights into the role of the hepatic IFN system in regulating HBV-HDV infection dynamics and its therapeutic implications through elucidating the molecular basis underlying the inefficacy of IFN-based antiviral strategies against HBV-HDV infection.

Indexed as

Hepatitis B virusHepatitis Delta VirusAntiviral AgentsHepatocytesHumansVirus ReplicationAntiviral AgentsCytokinesHepatitisHepatologyInnate immunityVirology

Identifiers

PMID37154158
PMCPMC10243812
OpenAlexW4375954587

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.