Evidence map›Paper›PMID 25557055›Full record

ArticleImmunity2015

The RNA sensor RIG-I dually functions as an innate sensor and direct antiviral factor for hepatitis B virus.

Seiichi Sato, Kai Li, Takeshi Kameyama, Takaya Hayashi, Yuji Ishida, Shuko Murakami, Tsunamasa Watanabe, Sayuki Iijima, Yu Sakurai, Koichi Watashi and 9 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 239 papers.

0numbers the graph read from it
0cells of the map it votes in
239citing papers in PubMed
16.3field-weighted citation impact, top 1% 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

239 citing papers in PubMed, 403 citations in OpenAlex.

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  15. Hepatitis B Virus Nucleocapsid Assembly.Journal of molecular biology · 2025
    Review
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179 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 6 institutions in 2 countries.

Seiichi SatoDivision of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan; Molecular Medical Biochemistry Unit, Biological Chemistry and Engineering Course, Graduate School of Chemical Sciences and Engineering, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan.
Kai LiDivision of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan; Molecular Medical Biochemistry Unit, Biological Chemistry and Engineering Course, Graduate School of Chemical Sciences and Engineering, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan.
Takeshi KameyamaDivision of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan; Molecular Medical Biochemistry Unit, Biological Chemistry and Engineering Course, Graduate School of Chemical Sciences and Engineering, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan.
Takaya HayashiResearch Center for Infection-Associated Cancer, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan.
Yuji IshidaPhoenixBio Co., Ltd., Higashihiroshima, Hiroshima 739-0046, Japan.
Shuko MurakamiDepartment of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467-8601, Japan.
Tsunamasa WatanabeDepartment of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467-8601, Japan.
Sayuki IijimaDepartment of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467-8601, Japan.
Yu SakuraiLaboratory of Innovative Nanomedicine, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido 060-0812, Japan.
Koichi WatashiDepartment of Virology II, National Institute of Infectious Diseases, Tokyo 208-0011, Japan.
Susumu TsutsumiDepartment of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467-8601, Japan.
Yusuke SatoLaboratory of Innovative Nanomedicine, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido 060-0812, Japan.
Hidetaka AkitaLaboratory of Innovative Nanomedicine, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido 060-0812, Japan.
Takaji WakitaDepartment of Virology II, National Institute of Infectious Diseases, Tokyo 208-0011, Japan.
Charles M RiceLaboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY 10065, USA.
Hideyoshi HarashimaLaboratory of Innovative Nanomedicine, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido 060-0812, Japan.
Michinori KoharaDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan.
Yasuhito TanakaDepartment of Virology and Liver Unit, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467-8601, Japan.
Akinori TakaokaDivision of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan; Molecular Medical Biochemistry Unit, Biological Chemistry and Engineering Course, Graduate School of Chemical Sciences and Engineering, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan. Electronic address: takaoka@igm.hokudai.ac.jp.
Hokkaido University · JPNagoya City University · JPNational Institute of Infectious Diseases · JPPhoenixBio (Japan) · JPRockefeller University · USTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Host innate recognition triggers key immune responses for viral elimination. The sensing mechanism of hepatitis B virus (HBV), a DNA virus, and the subsequent downstream signaling events remain to be fully clarified. Here we found that type III but not type I interferons are predominantly induced in human primary hepatocytes in response to HBV infection, through retinoic acid-inducible gene-I (RIG-I)-mediated sensing of the 5'-ε region of HBV pregenomic RNA. In addition, RIG-I could also counteract the interaction of HBV polymerase (P protein) with the 5'-ε region in an RNA-binding dependent manner, which consistently suppressed viral replication. Liposome-mediated delivery and vector-based expression of this ε region-derived RNA in liver abolished the HBV replication in human hepatocyte-chimeric mice. These findings identify an innate-recognition mechanism by which RIG-I dually functions as an HBV sensor activating innate signaling and to counteract viral polymerase in human hepatocytes.

Indexed as

AnimalsChild, PreschoolFemaleGene Products, polHepatitis B, ChronicHepatitis B virusHepatocytesHep G2 CellsHumansImmunity, InnateInterferonsLiverMembrane ProteinsMiceMice, SCIDNerve Tissue ProteinsGene Products, polInterferonsMembrane ProteinsNerve Tissue ProteinsP protein, Hepatitis B virusReceptors, Cell SurfaceRNA, ViralRobo3 protein, mouseRoundabout Proteins

Identifiers

PMID25557055
OpenAlexW1987376967

What OpenQuestion holds

Textmetadata
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.