Evidence map›Paper›PMID 41407770›Full record

ArticleScientific reports2025

The interferon-inducible MxB large GTPase attenuates hepatitis B virus replication by activating the RIG-I innate immunity signaling pathway.

Masazumi Onuki, Jun Inoue, Kotaro Doi, Masashi Ninomiya, Akitoshi Sano, Mio Tsuruoka, Kosuke Sato, Satoko Sawahashi, Keishi Ouchi, Kengo Watanabe and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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. 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

12 authors.

Masazumi OnukiDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Jun InoueDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan. jinoue-drgn@umin.net.
Kotaro DoiDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Masashi NinomiyaDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Akitoshi SanoDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Mio TsuruokaDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Kosuke SatoDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Satoko SawahashiDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Keishi OuchiDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Kengo WatanabeDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Mark A McNivenDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA.
Atsushi MasamuneDivision of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.

Funding

Japan Society for the Promotion of Science 19K08385 and 23K07390
6 · The paper itself

Abstract

The innate immune response has been reported to be perturbed by hepatitis B virus (HBV) infection. We hypothesized that the induction of the IFN-inducible dynamin family member, myxovirus resistance protein 2 (MxB), might support an innate immune response against HBV via mitochondrial alterations. The objective of this study was to elucidate the mechanism by which MxB suppresses HBV replication. Knockdown of MxB in HBV-expressing HepAD38 cells induced morphological changes in mitochondria. These cells exhibited a substantial increase in the release of enveloped HBV particles, as determined by immunoprecipitation or sucrose density-gradient centrifugation. The expression of envelope proteins L/M/SHBs was increased in the cells, and HBsAg in the culture supernatant was also increased by 4-10 fold. When cells were stimulated with poly(I: C), the downstream signaling of RIG-I including the mRNA of type I and III IFNs was suppressed. Mitochondrial antiviral signaling (MAVS) clustering, which is required for this pathway, was inhibited by MxB knockdown. In conclusion, these findings provide support for a new model implicating MxB-directed HBV inhibition initiated by downstream RIG-I signaling that could promote the formation of MAVS clusters in the mitochondria. Enhancement of this pathway could be a potential therapeutic option for suppressing HBV infection.

Indexed as

DEAD Box Protein 58Hepatitis B virusImmunity, InnateInterferonsMyxovirus Resistance ProteinsSignal TransductionVirus ReplicationAdaptor Proteins, Signal TransducingCell Line, TumorHepatitis BHepatitis B Surface AntigensHumansMitochondriaPoly I-CReceptors, ImmunologicAdaptor Proteins, Signal TransducingDEAD Box Protein 58Hepatitis B Surface AntigensInterferonsMAVS protein, humanMX2 protein, humanMyxovirus Resistance ProteinsPoly I-CReceptors, ImmunologicRIGI protein, humanHBVMAVSMitochondriaMxBRIG-I

Identifiers

PMID41407770
PMCPMC12711879

What OpenQuestion holds

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Read underepoch 390

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.