Evidence map›Paper›PMID 31969598›Full record

ArticleScientific reports2020

Hepatitis C virus infection suppresses hepatitis B virus replication via the RIG-I-like helicase pathway.

Kazuhiro Murai, Hayato Hikita, Yugo Kai, Yasuteru Kondo, Makoto Fukuoka, Keisuke Fukutomi, Akira Doi, Takuo Yamai, Tasuku Nakabori, Ryo Fukuda and 9 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Occult hepatitis B virus infection.Nature reviews. Gastroenterology & hepatology · 2026
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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

19 authors at 5 institutions in 1 country.

Kazuhiro MuraiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Hayato HikitaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Yugo KaiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Yasuteru KondoDepartment of Hepatology, Sendai Kousei Hospital, Sendai, Japan.ORCID http://orcid.org/0000-0001-5935-4346
Makoto FukuokaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Keisuke FukutomiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Akira DoiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Takuo YamaiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Tasuku NakaboriDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Ryo FukudaDepartment of Hepatology, Sendai Kousei Hospital, Sendai, Japan.
Takeshi TakahashiLaboratory Animal Research Department, Biomedical Research Laboratory, Central Institute for Experimental Animals, Kawasaki, Japan.
Kei MiyakawaDepartment of Microbiology, Yokohama City University School of Medicine, Yokohama, Japan.
Hiroshi SuemizuLaboratory Animal Research Department, Biomedical Research Laboratory, Central Institute for Experimental Animals, Kawasaki, Japan.ORCID http://orcid.org/0000-0002-3706-2454
Akihide RyoDepartment of Microbiology, Yokohama City University School of Medicine, Yokohama, Japan.
Ryoko YamadaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Takahiro KodamaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.ORCID http://orcid.org/0000-0002-6250-1324
Ryotaro SakamoriDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.ORCID http://orcid.org/0000-0002-1580-607X
Tomohide TatsumiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan.
Tetsuo TakeharaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Osaka, Japan. takehara@gh.med.osaka-u.ac.jp.
The University of Osaka · JPCentral Institute for Experimental Animals · JPSendai Kousei Hospital · JPYokohama City University · JPOsaka University of Pharmaceutical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanisms of hepatitis B virus (HBV) reactivation after hepatitis C virus (HCV) elimination by direct-acting antiviral (DAA) treatment in HBV/HCV-co-infected patients remain unclear. We examined RIG-I-like helicase (RLH) pathway activation by HBV mono-infection, HCV mono-infection or HBV/HCV co-infection and interference between HBV and HCV in primary human hepatocytes. Interference between HBV and HCV and HBV reactivation after DAA treatment in humanized-liver mice were assessed. HCV infection activated RLH pathway, as evidenced by RIG-I, ISG15 and ISG56 expression induction; HBV caused only RIG-I induction in vitro. RLH activation was also found in HBV/HCV-co-infected cells, and HBV replication were suppressed in HBV/HCV-co-infected than in HBV-mono-infected cells. siRNA-mediated double knockdown of ISG15 and ISG56 increased HBV replication in HBV/HCV-co-infected cells. HCV infection activated RLH pathway and suppressed HBV replication in humanized-liver mice. Subsequent elimination of HCV by DAA administration downregulated RLH pathway and upregulated HBV replication in mice. RLH pathway was activated in livers of chronic hepatitis C patients compared to those of chronic hepatitis B or non-B, non-C patients. The RLH pathway activation was downregulated by HCV elimination. In conclusion, HCV infection activated RLH pathway and suppressed HBV replication in human hepatocytes. HCV elimination upregulated HBV replication, probably through RLH pathway downregulation.

Indexed as

Signal TransductionVirus ReplicationAnimalsCells, CulturedCoinfectionDEAD Box Protein 58DEAD-box RNA HelicasesDown-RegulationHepatitis B virusHepatitis CHepatitis C, ChronicHepatocytesHumansLiverMiceReceptors, ImmunologicDEAD Box Protein 58DEAD-box RNA HelicasesReceptors, ImmunologicRIGI protein, human

Identifiers

PMID31969598
PMCPMC6976581
OpenAlexW3001297751

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.